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NEPHROLOGY
FOURTH EDITION
EDGAR V. LERMA, MD, FACP, FASN, FNKF, FPSN (Hon)
Clinical Professor of Medicine
Section of Nephrology
University of Illinois at Chicago College of Medicine/Advocate Christ
Medical Center
Oak Lawn, Illinois
MATTHEW A. SPARKS, MD, FASN, FNKF

Assistant Professor of Medicine
Associate Program Director, Nephrology Fellowship
Duke University Medical Center;
Staff Physician
Durham VA Medical Center
Durham, North Carolina
JOEL M. TOPF, MD, FACP

Assistant Clinical Professor
Department of Medicine
Oakland University William Beaumont School of Medicine
Auburn Hills, Michigan
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
NEPHROLOGY SECRETS, FOURTH EDITION ISBN: 978-0-323-47871-7
Copyright © 2019 by Elsevier, Inc. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical,
including photocopying, recording, or any information storage and retrieval system, without permission in writing
from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies
and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing
Agency, can be found at our website: www.elsevier.com/permissions.
This book and the individual contributions contained in it are protected under copyright by the Publisher
(other than as may be noted herein).
Notices
Knowledge and best practice in this field are constantly changing. As new research and experience broaden our
understanding, changes in research methods, professional practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating
and using any information, methods, compounds, or experiments described herein. In using such informa-
tion or methods they should be mindful of their own safety and the safety of others, including parties for
whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the most
current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be
administered, to verify the recommended dose or formula, the method and duration of administration, and
contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of
their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient,
and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any
liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise,
or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.
Previous editions copyrighted 2012, 2003, and 1999.

Library of Congress Cataloging-in-Publication Data
Names: Lerma, Edgar V., editor. | Sparks, Matthew A., editor. | Topf, Joel
M., editor.
Title: Nephrology secrets / [edited by] Edgar V. Lerma, Matthew A. Sparks,
Joel M. Topf.
Description: Fourth edition. | Philadelphia, PA : Elsevier, [2019] |
Includes
bibliographical references and index.
Identifiers: LCCN 2017060071 | ISBN 9780323478717 (hardcover : alk. paper)
Subjects: | MESH: Kidney Diseases
Classification: LCC RC903 | NLM WJ 300 | DDC 616.6/1--dc23
LC record available at https://lccn.loc.gov/2017060071
International Standard Book Number: 978-0-323-47871-7
Content Strategist: James Merritt

Content Development Specialist: Meghan Andress
Publishing Services Manager: Catherine Jackson
Senior Project Manager: Rachel E. McMullen
Design Direction: Bridget Hoette
Printed in the United States of America

Last digit is the print number: 9 8 7 6 5 4 3 2 1
To all my mentors, and friends, at the University of Santo Tomas
Faculty of Medicine and Surgery in Manila, Philippines, and
Northwestern University Feinberg School of Medicine in Chicago, IL,
who have in one way or another influenced and guided me to
become the physician that I am . . .
To all the medical students, interns, and residents at Advocate Christ
Medical Center whom I have taught or learned from, especially those
who eventually decided to pursue nephrology as a career . . .
To my parents and my brothers, without whose unwavering love
and support through the good and challenging times I would not have
persevered and reached my goals in life . . .
Most especially, to my two lovely and precious daughters, Anastasia
Zofia and Isabella Ann, whose smiles and laughter constantly
provide me with unparalleled joy and happiness; and my very loving
and understanding wife, Michelle, who has always been supportive
of my endeavors both personally and professionally, and who sacrificed
a lot of time and exhibited unwavering patience as I devoted a
significant amount of time and effort to this project. Truly,
they always provide me with motivation and inspiration.
Edgar V. Lerma, MD, FACP, FASN, FNKF, FPSN (Hon)
Editing the fourth edition of Nephrology Secrets has been both

rewarding and educational. Thanks to Edgar and Joel for embarking
on this journey with me. I could not ask for a better editorial team.
Thanks to each of the chapter authors for taking time to research
and write excellent chapters. Thanks to all of my mentors, especially
Tom Andreoli, Bob Safirstein, and Tom Coffman. Thanks to the many
undergraduates, medical students, residents, fellows, and my
colleagues I have had the privilege to work with both at Duke
University Medical Center and the University of Arkansas for Medical
Sciences. You have all played an important role in my life and continue
to inspire and motivate me. Thanks to my family, my siblings Jeff,
Shannon, and my parents for their encouragement and support.
Especially thanks to my wife, Neha, and the twins, Meera and Ishan,
for their unequivocal support and love throughout this project.
Thank you to the many patients and family members I have had
the privilege to care for over the years. I sincerely hope this book
helps others on their journey in medicine.
Matthew A. Sparks, MD, FASN, FNKF
iii
My hike through medicine and nephrology has been filled with teachers
and mentors. It has been a rich and rewarding journey in ways that I
could never have imagined. During this journey there have been particular
people who have believed in me and have been willing to trust me on
this somewhat unconventional path. Ernest Yoder at Wayne State
School of Medicine, Mary Ciccarelli at Indiana University Med-Peds,
and Patrick Murray at the University of Chicago Nephrology Fellowship
immediately come to mind. After my formal education, Robert Provenzano
has been a tireless cheerleader and more importantly, he built
St Clair Specialty Physicians into the type of nephrology company
where a physician who saw private practice a bit differently
could thrive.
I probably owe the most to the online nephrology community that has
blossomed in the last few years to be an always-on, all-hours, cocktail
party, with interesting conversation and intelligent answers to the
questions that bombard us all in clinical nephrology. #NephTwitter, you
are the future of nephrology education. Don’t slow down; keep going
full speed ahead.
I want to thank my wife, Cathy. Without her I wouldn’t be able to do any
of this. She is understanding, helpful, and patient. She has excellent
instincts and continues to be an awesome partner. She is better than I
deserve. Thanks for everything. Cathy is a wonderful mother to our
twins, Simon and Laura, who are great kids and always put a smile on
my face. It has been a delight watching you mature into thoughtful and
kind adults. Keep doing what you are doing, you are going to be the
people this planet needs.
Finally, I am left with the impossible task of trying to express the
amount of gratitude I have for my parents and how much they have
given me. Nobody could have received a better childhood than my
parents gave me and my sister. My mom and dad have always helped
guide and support me. So many times they could have tried to block an
unconventional decision, but instead, they understood what I was trying
to do and supported and helped me along. Thanks.
Joel M. Topf, MD, FACP
iv
CONTRIBUTORS
Rajiv Agarwal, MD Michael Berkoben, MD, FACP

Professor of Medicine Associate Professor of Medicine
Division of Nephrology Division of Nephrology
Indiana University School of Medicine Duke University Medical Center
Indianapolis, Indiana Durham, North Carolina
Talal Alfaadhel, MBBS, FRCPC Scott D. Bieber, DO
Assistant Professor Clinical Associate Professor of Medicine
Department of Medicine University of Washington
King Saud University Medical City Seattle, Washington
King Saud University
Florian Buchkremer, MD
Riyadh, Saudi Arabia
Division of Nephrology, Dialysis & Transplantation
Martin J. Andersen, DO Kantonsspital Aarau
Assistant Professor of Clinical Medicine Aarau, Switzerland
Division of Nephrology
Anna Marie Burgner, MD, MEHP
Indiana University School of Medicine
Assistant Professor
Indianapolis, Indiana
Department of Nephrology and Hypertension
John Robert Asplin, MD Vanderbilt University Medical Center
Medical Director Nashville, Tennessee
Litholink Corp, Laboratory Corporation of Americ
James Brian Byrd, MD, MS
Holdings
Assistant Professor
Chicago, Illinois
Rupali S. Avasare MD University of Michigan
Assistant Professor of Medicine Ann Arbor, Michigan
Daniel Cattran, MD
Oregon Health and Science University
Professor of Medicine
Portland, Oregon
George L. Bakris, MD University Health Network;
Professor and Director, ASH Comprehensive Senior Scientist
Hypertension Center Toronto General Research Institute
Department of Medicine University Health Network
The University of Chicago Medicine Toronto, Ontario, Canada
Chicago, Illinois
Devasmita Choudhury, MD
Amar D. Bansal, MD Chief Renal Section
Division of Renal-Electrolyte Salem Veterans Affairs Medical Center
Section of Palliative Care and Medical Ethics Salem, Virginia;
University of Pennsylvania Associate Professor Medicine
Philadelphia, Pennsylvania University of Virginia
Charlottesville Virginia;
Pravir V. Baxi, MD Virginia Tech Carilion School of Medicine
Roanoke Virginia
Department of Internal Medicine
Rush University Medical Center
Chicago, Illinois
v
vi CONTRIBUTORS
Rolando Claure-Del Granado, MD, FASN Jennifer L. Ennis, MD, FACP

Professor of Medicine Medical Director
Head Division of Nephrology Litholink Corporation, a LabCorp Company;
Hospital Obrero #2 - C.N.S., Clinical Assistant Professor of Medicine
Universidad Mayor de San Simon School of Medicine Medicine, Division of Nephrology
Cochabamba, Bolivia University of Illinois at Chicago
Chicago, Illinois
Bradley M. Denker, MD
Associate Professor of Medicine Fernando C. Fervenza, MD, PhD
Harvard Medical School; Professor of Medicine
Clinical Chief Department of Nephrology and Hypertension
Renal Division Mayo Clinic
Beth Israel Deaconess Medical Center; Rochester, Minnesota
Chief of Nephrology
Robert A. Figlin, MD, FACP
Harvard Vanguard Medical Associates
Steven Spielberg Family Chair in Hematology
Boston, Massachusetts
Oncology;
Vimal K. Derebail, MD Professor of Medicine and Biomedical Sciences,
Assistant Professor of Medicine Director
UNC Kidney Center Division of Hematology Oncology;
University of North Carolina Deputy Director
Chapel Hill, North Carolina Integrated Oncology Service Line;
Deputy Director
Robert J. Desnick, PhD, MD Samuel Oschin Comprehensive Cancer Institute
Dean for Genetics and Genomic Medicine Cedars-Sinai Medical Center
Department of Genetics and Genomic Sciences Saperstein Critical Care Tower
Icahn School of Medicine at Mount Sinai Los Angeles, California
New York, New York
Zita Galvin, MD
Luca di Lullo, MD Liver Transplant Unit
Department of Nephrology and Dialysis Toronto General Hospital
L. Parodi–Delfino Hospital University Health Network
Colleferro, Italy Toronto, Ontario, Canada
John V. Duronville, MD Pranav S. Garimella, MD
Medical Instructor Division of Nephrology-Hypertension
Division of Nephrology University of California San Diego
Duke University Medical Center San Diego, California
Debbie S. Gipson, MS, MD
Garabed Eknoyan, MD Professor of Pediatrics
Selzman Institute of Kidney Health Department of Pediatrics
Section of Nephrology University of Michigan
Department of Medicine Ann Arbor, Michigan
Baylor College of Medicine
Houston, Texas Patrick E. Gipson, MD
Professor of Pediatrics
Mina El Kateb, MD University of Michigan
Transplant Nephrology Fellow Ann Arbor, Michigan
St John Hospital and Medical Center
Detroit, Michigan David S. Goldfarb, MD, FACP, FASN, FNKF
Professor of Medicine and Physiology
William J. Elliott, MD, PhD NYU School of Medicine;
Professor of Preventive Medicine, Internal Medicine Interim Division Chief
and Pharmacology
Department of Nephrology
Chair NYU Langone Medical Center
Department of Biomedical Sciences; New York, New York
Chief
Division of Pharmacology
Pacific Northwest University of Health Sciences
Yakima, Washington
CONTRIBUTORS vii
Arthur Greenberg, MD Jonathan Ashley Jefferson, MD, FRCP

Professor of Medicine, Emeritus Professor of Medicine
Department of Medicine University of Washington
Duke University Medical Center Seattle, Washington
Kamyar Kalantar-Zadeh, MD, MPH, PhD
Hermann Haller, MD Professor and Chief
Professor, Division of Nephrology and Hypertension
Director University of California Irvine Medical Center
Department of Nephrology and Hypertension Orange, California
Hannover Medical School
Elaine S. Kamil, MD
Hannover, Germany
Health Sciences Clinical Professor of Pediatrics
Swapnil Hiremath, MD, MPH David Geffen School of Medicine at UCLA;
Assistant Professor Department of Pediatric Nephrology
Department of Medicine Cedars-Sinai Medical Center
University of Ottawa; Los Angeles, California
Senior Clinical Investigator
Jon-Emile S. Kenny, MD
Clinical Epidemiology
Ottawa Hospital Research Institute
Department of Internal Medicine
Ottawa, Ontario, Canada
Icahn School of Medicine at Mount Sinai
Edward J. Horwitz, MD New York, New York;
Metrohealth Medical Center Masters Candidate
Case Western Reserve University School of Medicine Department of Learning, Informatics, Management
Cleveland, Ohio and Ethics
Karolinska Institutet
Susan Hou, MD Stockholm, Sweden
Department of Medicine Charbel C. Khoury, MD
Division of Nephrology and Hypertension Fellow
Loyola University Medical Center Department of Nephrology
Maywood, Illinois Brigham and Women’s Hospital;
Fellow
Lesley A. Inker, MD, MS Department of Nephrology
Associate Professor of Medicine Massachusetts General Hospital
Department of Medicine Boston, Massachusetts
Tufts University School of Medicine
Boston, Massachusetts Jatinder Kohli, MD
University of Pennsylvania School of Medicine
Maria V. Irazabal, MD Hospital of the University of Pennsylvania
Assistant Professor of Medicine Philadelphia Pennsylvania
Department of Internal Medicine Eugene C. Kovalik, MD, CM, FRCP(C), FACP, FASN
Mayo Clinic Associate Profesor of Medicine
Rochester, Minnesota Department of Medicine/Nephrology
Duke University Medical Center
Ashley Bruce Irish, MBBS, FRACP Durham, North Carolina
Consultant Nephrologist
Department of Nephrology and Transplantation Csaba P. Kovesdy, MD
Fiona Stanley Hospital; Fred Hatch Professor of Medicine
Clinical Professor Department of Medicine
Department of Medicine University of Tennessee Health Science Center;
University of Western Australia Nephrology Section Chief
Perth, Western Australia, Australia Memphis VA Medical Center
Memphis, Tennessee
Kenar D. Jhaveri, MD
Zucker School of Medicine at Hofstra/Northwell
Hempstead, New York
viii CONTRIBUTORS
Warren Kupin, MD Ravindra L. Mehta, MBBS, MD, DM, FACP, FASN

Professor of Medicine Professor of Clinical Medicine,
Miami Transplant Institute Associate Chair of Clinical Research,
Katz Family Division of Nephrology Director CREST and MAS in Clinical Research
University of Miami Program
Miami, Florida Department of Medicine
University of California San Diego
Ruediger W. Lehrich, MD San Diego, California
Associate Professor of Medicine,
Program Director Patrick H. Nachman, MD
Nephrology Fellowship, Marion Stedman Covington Distinguished Professor
Director of Home-Suitable Dialysis of Medicine
Duke University Medical Center UNC Kidney Center
Durham, North Carolina University of North Carolina
Chapel Hill, North Carolina
Clinical Professor of Medicine Carol Nadai, MD
Section of Nephrology Medical Oncologist Instituto de Oncologia do Parana
University of Illinois at Chicago College of Medicine/ Curitibia, Brazil
Advocate Christ Medical Center
Lavinia Aura Negrea, MD
Oak Lawn, Illinois
Associate Professor of Medicine
Moshe Levi, MD Department of Medicine
Professor of Biochemistry and Molecular & Cellular University Hospitals Case Medical Center
Biology Cleveland, Ohio
Georgetown University Medical Center
Lindsay E. Nicolle, MD
Aurora, Colorado
University of Manitoba
Joseph L. Lockridge, MD Winnipeg, Manitoba, Canada
Medical Director
Keith C. Norris, MD, PhD
Kidney Transplant Program
Professor
Portland VA Health Care System;
Director of Transplant Nephrology
David Geffen School of Medicine, UCLA
Fellowship Training Program,
Los Angeles, California
Oregon Health & Science University Alexander Novakovic, MD
Portland, Oregon Research Associate
Division of Genitourinary
Jennifer Lopez, BS
Malignancies Department of Medical Oncology &
Division of Pediatric Nephrology
Therapeutics Research
NYU Langone Health
City of Hope Comprehensive Cancer Center
New York, New York
Duarte, California
Etienne Macedo, MD, PhD
Ali J. Olyaei, PharmD
Assistant Adjunct Professor
Professor
University of California San Diego, School of
Medicine and Pharmacy Practice
Medicine
Division of Nephrology and Hypertension
San Diego, California
OSU/OHSU
Rajnish Mehrotra, MBBS, MD, MS Portland, Oregon
Sumanta Kumar Pal, MD
Associate Professor
University of Washington;
Department of Medical Oncology and Experimental
Section Head Nephrology
Therapeutics
Division of Genitourinary Malignancies
Harborview Medical Center
City of Hope Comprehensive Cancer Center
Seattle, Washington
Duarte, California
CONTRIBUTORS ix
Paul M. Palevsky MD Michael V. Rocco, MD, MSCE

Chief, Renal Section Vardaman M. Buckalew Jr. Professor of Internal
VA Pittsburgh Healthcare System; Medicine/Nephrology
Professor of Medicine and Clinical & Translational Internal Medicine, Section on Nephrology
Science Wake Forest School of Medicine
Department of Medicine Winston-Salem, North Carolina
University of Pittsburgh
Claudio Ronco, MD
Pittsburgh, Pennsylvania
Director
Ami M. Patel, MD Department of Nephrology
Assistant Professor of Medicine San Bortolo Hospital;
University of Maryland School of Medicine, Director
Baltimore VA Medical Center International Renal Research Institute
Baltimore, Maryland San Bortolo Hospital
Vicenza, Italy
Vikram Patney, MD
Nephrology and Hypertension Specialists, LLC Mark E. Rosenberg, MD, FASN
St. Louis, Missouri Vice Dean for Education and Academic Affairs
University of Minnesota Medical School
Mark A. Perazella, MD Lino Lakes, Minnesota
Section of Nephrology Mitchell H. Rosner, MD
Yale University School of Medicine; Professor of Medicine
Director, Acute Dialysis Unit, Department of Medicine
Medical Director, Yale Physician Associate University of Virginia Health System
Program, Charlottesville, Virginia
Medical Director, Yale PA Online Program
Michael R. Rudnick, MD, FACP, FASN
New Haven, Connecticut
Associate Professor of Medicine
Phuong-Chi T. Pham, MD University of Pennsylvania School of Medicine;
Olive View-UCLA Medical Center Chief
Los Angeles, California Nephrology Division
Penn Presbyterian Medical Center
Phuong-Thu T. Pham, MD Philadelphia, Pennsylvania
David Geffen School of Medicine at UCLA
Ronald Reagan UCLA Medical Center Ernesto Sabath, MD
Los Angeles, California Hospital General de Queretaro
Universidad Autonomo de Queretaro
Joseph B. Pryor, BS Santiade Queretaro, Mexico
School of Medicine
Oregon Health & Sciences University Mark J. Sarnak MD, MS
Portland, Oregon Tufts Medical Center
Boston, Massachusetts
C. Venkata S. Ram
Director Jane O. Schell, MD, MHS
Apollo Heart Institute for Blood Pressure Management Assistant Professor of Medicine
and Apollo Blood Pressure Clinics Division of Renal-Electrolyte
Hyderabad, India University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania
Mahboob Rahman, MD
University Hospitals Cleveland Medical Center N. Winn Seay, MD
Case Western Reserve University School of Medicine Fellow, Division of Nephrology
Cleveland, Ohio Department of Medicine
Nathaniel Reisinger, MD Durham, North Carolina
Instructor and Clinical Ultrasound Fellow
Department of Emergency Medicine
Penn Medicine;
Moonlighting Nephrologist
Division of Renal, Electrolyte, and Hypertension
Penn Medicine
Philadelphia, Pennsylvania
x CONTRIBUTORS
John R. Sedor, MD Matthew A. Sparks, MD, FASN, FNKF

Professor Molecular Medicine Assistant Professor of Medicine
Cleveland Clinic Lerner College of Medicine Associate Program Director, Nephrology Fellowship
Case Western Reserve University; Duke University Medical Center;
Staff Staff Physician
Glickman Urology & Kidney Institute; Durham VA Medical Center
Staff Durham, North Carolina
Department of Pathobiology
Stuart M. Sprague, DO
Lerner Research Institute
NorthShore University HealthSystem
Cleveland, Ohio
Evanston, Illinois;
Akash Nair Sethi, DO Clincal Professor of Medicine
Fellow University of Chicago Pritzker School of Medicine
Renal, Electrolyte, and Hypertension Division Chicago, Illinois
Hosptial of the University of Pennsylvania
Susan Patricia Steigerwalt, MD
Philadelphia, Pennsylvania
Clinical Associate Professor
Anuja Shah, MD Cardiovascular Medicine
Department of Medicine University of Michigan
Division of Nephrology Ann Arbor, Michigan
Harbor-UCLA Medical Center
Hillel Sternlicht, MD
Torrance, California;
David Geffen School of Medicine at UCLA
Hofstra University School of Medicine
Los Angeles, California
Lori Shah, DO Lenox Hill Hospital-Northwell Health
Nephrology Fellow New York, New York
Vanderbilt University Medical Center
Marshall L. Stoller, MD
Nashville, Tennessee
San Francisco, California
Benjamin A. Sherer
Beje Thomas, MD
Clinical Fellow
Department of Urologic Surgery,
Laparoscopy/Endourology
University of Maryland School of Medicine
University of California San Francisco
Baltimore, Maryland
San Francisco, California
Hakan R. Toka, MD, PhD, FASN
Harpreet Singh, MD
Manatee Memorial Hospital
Medical Instructor
Graduate Medical Education
Bradenton, Florida
Rajalingam Sinniah, DSc, MD, PhD, FRCPI, FRCPA,
Assistant Clinical Professor
FRCPath
Clinical Professor of Pathology
Oakland University William Beaumont School of
School of Pathology and Laboratory Medicine
Medicine
The University of Western Australia;
Auburn Hills, Michigan
Consultant Pathologist,
Anatomic Pathology Vicente E. Torres, MD, PhD
Pathwest Laboratory Medicine Professor of Medicine
Fiona Stanley Hospital Department of Nephrology and Hypertension
Western Australia, Australia Mayo Clinic
Rochester, Minnesota
James A. Sloand, MD, FACP, FASN
Senior Medical Director, Global Therapeutic Area Howard Trachtman, MD
Lead, Peritoneal Dialysis Chief, Division of Pediatric Nephrology and
Renal Franchise Hypertension,
Baxter Healthcare Corporation Professor of Pediatrics
Deerfield, Illinois Division of Nephrology
NYU Langone Medical Center
New York, New York
CONTRIBUTORS xi
Carol Traynor, MB, BCh, BAO, BMedSci William L. Whittier, MD, FASN
Medical Instructor Associate Professor of Medicine
Duke University Medical Center Department of Internal Medicine
Durham, North Carolina Rush University Medical Center
Chicago, Illinois
Bryan M. Tucker, DO, MS
Assistant Professor of Medicine Jay B. Wish, MD
Department of Internal Medicine, Section Professor of Clinical Medicine
of Nephrology Department of Medicine
Wake Forest University School of Medicine Indiana University School of Medicine
Winston-Salem, North Carolina Indianapolis, Indiana
Beth A. Vogt, MD Florence Wong, MB, BS, MD, FRACP, FRCPC
Associate Professor Professor
Department of Pediatrics Department of Medicine, Division of
Case Western Reserve University; Gastroenterology
Attending Physician University of Toronto
Division of Nephrology Toronto, Ontario, Canada
Rainbow Babies and Children’s Hospital
David C. Wymer, MD, FACR, FACNM
Cleveland, Ohio
Associate Chair
Rimda Wanchoo, MD Radiology
Associate Professor of Medicine University of Florida;
Division of Nephrology Chief of Service, Imaging
Zucker School of Medicine at Hofstra/Northwell Department of Radiology
Hempstead, New York Malcom Randall VAMC
Gainesville, Florida
Matthew R. Weir, MD
Professor of Medicine David T.G. Wymer, MD
Department of Medicine, Resident
Director, Division of Nephrology Department of Radiology
University of Maryland School of Medicine Mount Sinai Medical Center
Baltimore, Maryland Miami Beach, Florida
Adam Whaley-Connell, DO Ladan Zand, MD
Associate Professor of Medicine Assistant Professor
Department of Medicine Department of Nephrology and Hypertension
Division of Nephrology and Hypertension Mayo Clinic
University of Missouri-Columbia School of Medicine; Rochester, Minnesota
Division of Endocrinology and Metabolism, and the
Research Service
Harry S. Truman Memorial Veterans Hospital
Columbia, Missouri
PREFACE
“Questions you will be asked on rounds, in the clinic, and on oral exams.”
This was the subtitle to the first Medical Secrets textbook by Anthony Zollo from 1991. This was click
bait before there was click bait. No medical student could resist a title like that. And it also is strangely
compelling for attendings and teachers. Doctors don’t get to peer inside the bedside teaching of other
attendings, and the chance to see the questions that others are asking is hard to resist.
The book in your hand is the fourth edition of Nephrology Secrets. It has been nearly a decade since
Lerma and Nissenson edited the third edition. All aspects of nephrology have evolved, and some topics have
been completely revolutionized. Since the third edition was published, the cause of idiopathic membranous
nephropathy has been elucidated, a genetic mutation explaining the high rate of kidney disease in African
Americans has been discovered. We have an effective therapy for hepatitis C and its downstream kidney
effects. Home dialysis modalities have recovered from being on the ropes and are now resurgent in both perito-
neal and hemodialysis. The biomedical revolution in oncology has uncovered novel kidney diseases. The mo-
lecular mechanism of preeclampsia, the most common glomerular disease on the planet, has been elucidated.
Nephrology is no longer the slow, methodical specialty of yore; it is fast moving and constantly changing.
Parallel to the changes in the science there has been a revolution in how nephrology educators
teach and are recognized. More and more teaching is shifting from the classroom and bedside to the
smartphone and internet. Therefore the current edition includes contributions from several individuals
who have honed their skills teaching in that space.
In keeping with the design of the original Medical Secrets, we have included questions on everyday
topics in addition to some “zebras” of particular academic interest. We hope that this book will be used
not only by nephrologists and nephrology fellows, medical residents and interns, and medical students but
also by primary care providers with particular interest in the art of homeostasis.
From personal experience, we know that very few people read a textbook from cover to cover. For
a variety of reasons, people skim through books as patient encounters and interests guide them. To
accommodate this reality, we tried to ensure that each chapter would be complete in itself. As a conse-
quence, there is unavoidable overlap among some of the information provided in many chapters. Indulge
this luxury; paper is cheap, and this makes the book a better information retrieval appliance.
Though only three names are on the cover, this book could not have been produced without a battalion
of contributors. First, and most obviously, we are in debt to all of the contributing authors who have spent
hours in producing high-quality, up-to-the-last-minute information that was rewarded with telephone, e-mail
and Twitter direct messages with suggestions, rewrites, and “spirited discussions.” The ISBN says fourth
edition, but if you ask the authors, they will tell you it was closer to a clean-sheet rewrite. We express our
sincere gratitude for all the authors’ openness to this collaboration. Namaste. Additionally, we would need to
express the highest gratitude to all the staff of Elsevier, most especially Meghan Andress, our Developmental
Editor, Rachel McMullen, our Senior Project Manager; and James Merritt, our Senior Acquisitions Editor, all of
whom have been very patient with our procrastinations and stubbornness.
Lastly, and philosophically, we thank our own teachers and our mentors, who devoted their time to
train and form us to become nephrologists and teachers. We thank the undergraduates, medical students,
residents, and fellows who have taught us how to teach. Lastly, we recognize and thank the patients,
who are the reason we are here. Knowledge without application is an empty vessel. Every page contains
information gleaned off the backs of patients. Their illness created this book, and on behalf of all the
contributors to this book, we fervently hope that the efforts may help alleviate their suffering, prevent
others from becoming similarly ill, and perhaps lead to their recovery.
@EdgarVLermaMD
Matthew A. Sparks, MD, FASN, FNKF
@Nephro_Sparks
@Kidney_Boy
xii
TOP 100 SECRETS
These secrets are 100 of the top board alerts. They summarize the concepts, principles,
and most salient details of nephrology.
1. The urine protein to creatinine (using a random urine specimen) ratio has been shown
to have a good correlation with the 24-hour urine protein determination.
2. The most common complication associated with a kidney biopsy is bleeding, though it
is usually self-limited and rarely life threatening.
3. The differential diagnosis of AKI includes prerenal azotemia, obstructive nephropathy,
and intrinsic forms of AKI.
4. Hepatorenal Syndrome (HRS) is a functional kidney failure that occurs in end-stage liver
cirrhosis with ascites.
5. The pharmacological treatment for HRS is a combination of albumin and vasoconstrictors,
but the definitive treatment is liver transplantation.
6. Due to the high incidence of drug-induced AKI, a thorough review of the medication list
should be performed in a patient at risk for AKI.
7. Sepsis is an important cause of AKI in critically ill patients and is associated with high
mortality rates.
8. Rapid (,3 hours after presentation) administration of appropriate antibiotics is associated
with improved outcomes and fewer cases of sepsis-associated AKI.
9. Early and vigorous volume resuscitation of patients with rhabdomyolysis (even before
extrication in crush syndrome) is important for preventing AKI.
10. AKI secondary to rhabdomyolysis usually occurs with creatine kinase levels greater
than 10,000 U/L.
11. Acute glomerulonephritis is a kidney injury syndrome characterized by the sudden
onset of edema, new or worsening hypertension, and an active urinary sediment.
12. Rapidly progressive glomerulonephritis is a clinical syndrome characterized by rapid
loss of kidney function that often results in ESKD.
13. Primary nephrotic syndrome is caused by one of the following four diseases—minimal
change disease, focal segmental glomerulosclerosis, membranous nephropathy, or
membranoproliferative glomerulonephritis—and the diagnosis is made based on a
combination of clinical features, kidney biopsy findings, laboratory findings, and genetic
testing.
14. Diuresis after relief of urinary obstruction may result from a physiologic excretion of
water and urea, but can become pathologic. Patients should have electrolytes checked
and replaced regularly, with free access to oral fluids. If necessary, the type and amount
of intravenous fluids should be determined by serum and urinary electrolyte levels.
15. Struvite stones are due to infection with bacteria that contain the enzyme urease;
Proteus mirabilis often has urease, Escherichia coli almost never has urease activity.
16. Uric acid stones are radiolucent on routine x-ray but are easily visualized by computed
tomography scan.
17. Uric acid stones are almost always due to overly acidic urine and therefore the treatment
of choice is alkali salts, not allopurinol.
xviii
TOP 100 SECRETS xix
18. Enteric hyperoxaluria requires that the patient have an intact colon because it is the
sight of pathologic oxalate overabsorption.
19. Low calcium diets are not recommended in the treatment of patients with hypercalciuria,
because a low calcium diet may contribute to bone demineralization.
20. The leading causes of CKD are diabetes, hypertension, glomerulonephritis, and cystic
kidney disease, with about 40% of all cases due to diabetes.
21. The target hemoglobin level for patients receiving erythropoiesis-stimulating agent (ESA)
therapy should be individualized based on transfusion avoidance, quality of life, physical
activity, and ESA responsiveness, and should not exceed 12 g/dL.
22. Most patients receiving ESAs will require iron supplementation; however, oral iron
supplements are often ineffective because of poor absorption and the magnitude of
iron requirements.
23. Decreased kidney function is associated with abnormalities of mineral metabolism that
results in decreased skeletal strength, bone pain, and abnormal calcification of the
blood vessels and soft tissues.
24. Cardiovascular disease is the primary cause of death in patients with CKD, and is
dramatically accelerated in CKD. Unfortunately, much of what is known about CVD may
not apply to patients with CKD, so physicians should prioritize evidence performed in
this special population.
25. Dyslipidemia is nearly universal in CKD and transplant. Kidney Disease Improving
Global Outcomes (KDIGO) guidelines recommend that patients with CKD over the age
of 50 and patients with a kidney transplant be treated with a statin.
26. Patients with progressive CKD opting for hemodialysis should have a timely evaluation
for vascular access to ensure it is ready when dialysis starts. An arteriovenous fistula
requires several months to mature.
27. Minimal change disease (MCD) is the cause of nephrotic syndrome in approximately
90% of children younger than 6 years of age, in approximately 65% of older children,
and in approximately 20% to 30% of adolescents. In adults, only approximately 10%
to 25% of nephrotic syndrome results from MCD, but it represents the third most
common cause of primary nephrotic syndrome in adults after membranous nephropa-
thy and FSGS.
28. Categorizing focal segmental glomerulosclerosis (FSGS) as genetic, secondary, or
primary may inform type of treatment offered and influence posttransplant disease
recurrence.
29. Patients with FSGS and high-risk APOL1 are at greater risk of ESKD than patients with
a low-risk APOL2 genotype.
30. Membranous nephropathy is a cause of nephrotic syndrome that can be either primary
or secondary to other diseases (malignancy, hepatitis B, lupus). Eighty percent of
idiopathic (primary) membranous has increased anti-PLA 2R antibody levels.
31. IgA nephropathy is the most common primary glomerulonephritis. It is a nephritic
syndrome that classically presents with hematuria. There is wide variability in kidney
outcomes, from benign microscopic hematuria to rapidly progressive crescentic
glomerular nephritis.
32. MPGN develops secondary to immune complex deposition or abnormalities in the
alternate pathway of complement; it can progress to ESKD over 10 to 15 years.
33. There is no proven therapy for MPGN. It can recur in up to 30% of kidney transplant
recipients.
34. Diabetic retinopathy is present in almost all patients with type 1 diabetes mellitus and
diabetic nephropathy.
xx TOP 100 SECRETS
35. Early diagnosis of lupus nephritis is imperative because kidney function at the time of
biopsy correlates with remission.
36. Anti-neutrophil cytoplasmic autoantibodies (ANCAs) are present in 90% of pauci-immune
glomerulonephritis and are pathogenic for these diseases.
37. Induction therapy for ANCA vasculitis rests on the use of corticosteroids in combination
with cyclophosphamide or rituximab. Plasma exchange should be considered in
patients with severe pulmonary hemorrhage, advanced kidney disease, or concomitant
anti-glomerular basement membrane disease.
38. Postinfectious streptococcal glomerulonephritis occurs 7 to 21 days after a streptococcal
infection (shorter for pharyngitis, longer for skin infections). It presents with acute nephritis
and is generally self-limiting, without a defined role for immunomodulation.
39. The presence or absence of hepatitis B e antigen (HbeAg) is important with regard to
the type of glomerular disease that may develop. Patients positive for both HbeAg and
hepatitis B surface antigen are highly infectious and have a greater risk of kidney disease.
40. Hepatitis C–related glomerulonephritis is associated with type 2 cryoglobulinemia, resulting
in activation of the classical complement pathway (low C3 and C4) with MPGN.
41. HIV-associated nephropathy (HIVAN) occurs almost exclusively in patients of black race
who have high-risk APOL1 genotypes.
42. HAART is the primary treatment for HIVAN and may lead to complete histologic reversal,
but HAART is not as successful in HIV immune complex disease of the kidney (HIVICK).
43. Both rhabdomyolysis and tumor lysis syndrome can cause profound electrolyte
abnormalities (hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia)
as a result of the release of intracellular constituents.
44. Rasburicase, a recombinant uric oxidase, rapidly lowers uric acid levels and is commonly
used in the prevention of AKI secondary to tumor lysis syndrome.
45. Myeloma cast nephropathy is a medical emergency and requires immediate diagnosis
and early institution of therapy in order to prevent irreversible kidney failure.
46. Kidney injury in myeloma is principally related to the light chain component of immuno-
globulin because, unlike heavy chains, light chains are freely filtered at the glomerulus
and reabsorbed in the proximal tubule.
47. Bortezomib-based chemotherapy regimens are recommended as the optimal management
of AKI and myeloma
48. The measurement of serum-free light chains is the preferred study if suspecting
myeloma and kidney disease due to light chain excess.
49. Patients with amyloidosis usually present with edema and nephrotic syndrome.
50. Treatments for metastatic renal cell carcinoma can be nephrotoxic—VEGF inhibitors
can cause proteinuria, and programmed death-1 inhibitors can cause an autoimmune
nephritis.
51. Thrombotic microangiopathies (TMAs) present with microangiopathic hemolytic anemia,
thrombocytopenia, and altering degrees of kidney failure and neurologic dysfunction.
The major causes of TMA are Shiga toxin–associated hemolytic uremia syndrome
(ST-HUS), atypical hemolytic uremia syndrome (aHUS), and thrombotic thrombocytopenic
purpura (TTP).
52. Fabry disease is an X-linked lysosomal storage disease that is unrecognized in 0.2% of
patients with ESKD that can be detected in males by their marked decrease or absent
plasma a-galactosidase-A activity.
53. Alport syndrome is associated with microscopic hematuria, proteinuria, sensorineural
hearing loss, and progressive loss of kidney function.
TOP 100 SECRETS xxi
54. Thin basement membrane nephropathy (TBMN) is a benign autosomal-dominant

condition associated with microscopic hematuria without proteinuria, hearing loss, or
progressive kidney failure.
55. The classical triad of fever, maculopapular rash, and peripheral eosinophilia is seen in
only a minority of cases (,10%) of acute tubulointerstitial nephritis (ATIN).
56. Drug-induced ATIN is not dose dependent. A repeat exposure to the same drug can
potentially lead to a recurrence of the disease process.
57. Asymptomatic bacteriuria should be treated only when present in pregnant women, or
patients undergoing traumatic genitourinary procedures.
58. The major physiologic change in the kidney during pregnancy is a 50% increase in GFR.
59. The most important predictor of maternal and fetal problems when pregnancy occurs
in women with preexisting kidney disease including prematurity, fetal loss, and loss of
kidney function is prepregnancy kidney function.
60. Patients with sickle cell nephropathy may be particularly vulnerable to develop AKI as a
result of hemodynamic insults, toxins, acute pyelonephritis, and urinary tract obstruction.
61. The rate of uremic toxin removal is determined by the time on dialysis, the blood and
dialysate flow rates, and the efficiency of the dialyzer.
62. For patients receiving hemodialysis three times per week, it is recommended that the
minimum delivered single pool Kt/V dose of dialysis is 1.2 and that the minimum treatment
time of time should be 3 hours if residual kidney function is less than 2 mL/min.
63. Home hemodialysis provides a number of clinical benefits when compared with
in-center hemodialysis, including decreased left ventricular mass, better volume
control, improved serum phosphorous levels, less antihypertensive medication use,
and improved quality of life.
64. Initiating incident patients on peritoneal dialysis (PD; i.e., “PD First”) offers survival and
other clinical benefits, particularly in situations where renal replacement is unplanned or
a central venous catheter would otherwise be used.
65. In patients with ESKD achieving recommended renal replacement therapy parameters a
high serum creatinine represents higher muscle mass and is associated with significantly
better outcomes.
66. A team-based, multifaceted approach to continuous quality improvement with regular
audit of infection rates and outcomes is essential to improving peritonitis rates in
patients undergoing PD. Training and re-training of both patients and nurse patient-
educators is a cornerstone of this effort.
67. In ANCA vasculitis, plasma exchange is presently recommended in addition to
corticosteroids and cyclophosphamide for patients presenting with advanced kidney
failure and/or pulmonary hemorrhage.
68. The new kidney transplant allocation system went into effect in December 2014. There
were significant changes to allow for longevity matching between donors and recipients
using the estimated posttransplant survival score and kidney donor profile index (KDPI)
score to maximize graft survival. Another change was giving patients a time credit for
time on renal replacement therapy.
69. The median time for waiting for a kidney transplant in the US is 3.6 years.
70. Living donor kidney transplantation offers the best long-term outcomes for patients with
ESKD.
71. Calcineurin inhibitors remain a cornerstone of immunosuppressive regiments in kidney
transplantation. They work by blocking calcineurin, an intricate protein in the signal
transduction pathway that activates signal 3. The two prototypes are tacrolimus and
cyclosporine, with tacrolimus being the primary drug of choice today.
xxii TOP 100 SECRETS
72. Chronic rejection, better defined as chronic antibody-mediated rejection, is the main
cause of late allograft loss and is histologically defined as transplant glomerulopathy.
73. Epstein-Barr virus is found in two-thirds of patients with posttransplant lymphoproliferative
disorder.
74. Quantification of BK virus DNA in plasma by polymerase chain reaction has a sensitivity
and specificity of 100% and 88%, respectively; a kidney transplant biopsy is still
needed to rule out other diagnoses and confirm the diagnosis of BK nephropathy.
75. In patients who have received a kidney transplant, proteinuria is associated with
cardiovascular events and mortality.
76. The traditional blood pressure target of ,140/90 mm Hg is now ,130/80 mm Hg for
everyone except those with a ,10% 10-year risk for cardiovascular events, where it is
still ,140/90.
77. No randomized trials to date have demonstrated a clear benefit for revascularization
over medical management alone in the treatment of atherosclerotic renal artery stenosis.
78. Although endocrine and secondary forms of hypertension are uncommon, about 20%
of patients with resistant hypertension can have their blood pressure controlled and
occasionally “cured” with specific forms of treatment. This cannot occur if secondary
forms of hypertension are not considered.
79. The most common form of secondary hypertension (,20% in some series) is associated
with obstructive sleep apnea, the treatment of which improves blood pressure and quality
of life.
80. Hypertensive emergencies occur when elevated blood pressure causes acute target-organ
damage and requires blood pressure to be reduced gradually within minutes to hours.
81. Initial antihypertensive drug therapy can be with a thiazide or thiazide-like diuretic, an
ACE inhibitor, an ARB, or a calcium channel blockers.
82. Spironolactone has emerged as the treatment of choice for treatment-resistant high
blood pressure, but requires careful monitoring of serum potassium and kidney
function.
83. Salt restriction is effective in reducing cardiovascular risk: reducing sodium consumption
to approximately 1000 mg daily can reduce cardiovascular events by 25%, and every
1000 mg increase in daily dietary sodium can increase the relative risk of nonfatal stoke,
myocardial infarction, and heart failure by 10%.
84. The Dietary Approaches to Stop Hypertension (DASH) diet, combined with sodium
restriction of 1.5 g daily, can improve systolic blood pressure by approximately
9 mm Hg.
85. Diuresis of patients with chronic obstructive pulmonary disease and cor pulmonale can
cause contraction alkalosis. Correction of contraction alkalosis with acetazolamide can
lead to improved ventilation.
86. In patients with volume contraction and metabolic alkalosis, the urine sodium concentration
may not be low. In this circumstance the urine chloride will typically be less than 15 mEq/L.
87. Abnormalities of serum potassium or bicarbonate, in the absence of diuretics, in
patients with difficult-to-treat hypertension should trigger an evaluation for monogenic
causes of hypertension.
88. Hypotonic hyponatremia arises from inadequate solute intake, excess electrolyte-free
water intake, or reduced excretion of electrolyte-free water. Urine osmolality can
distinguish the latter mechanism from the first two.
89. While acute hypotonic hyponatremia can be rapidly corrected, the rate of correction
of chronic hyponatremia should be limited to prevent the osmotic demyelination
syndrome.
TOP 100 SECRETS xxiii
90. In patients with severely symptomatic hyponatremia, raising the serum sodium
concentration by just 3 to 4 mEq/L by administering one to three 100 mL boluses of
3% saline completely abrogates the risk of seizures, tentorial herniation, non-cardiogenic
pulmonary edema, and other life-threatening complications.
91. Prediction equations for rate of rise of serum sodium concentration in response to
hypertonic saline infusions do not account for ongoing urinary water loss. Measuring
the serum sodium concentration change frequently when hypertonic saline is given is
essential to be certain that the response meets the anticipated target rate.
92. Hyponatremia should be presumed to be chronic unless its time of onset is definitely
known. This is especially true for hyponatremia developing prior to hospital presentation.
93. Definitive interventions to remove potassium from the body include hemodialysis or
increasing fecal excretion by using potassium binders.
94. Intravenous calcium prevents life-threatening consequences of cardiac arrhythmias
due to severe hyperkalemia by stabilizing the myocardial and conducting tissue cell
membranes. This effect is rapid but short-lived and hence should be followed by
definitive measures to lower serum potassium levels.
95. Hyperphosphatemia in the setting of normal kidney function: think excessive intake,
cellular breakdown, or hypoparathyroidism.
96. Always ensure magnesium is replete in patients with hypokalemia.
97. The current “Surviving Sepsis” guidelines recommend against administration of sodium
bicarbonate for arterial pH of 7.15 or more, and express uncertainty about whether
giving it when pH is lower has any utility.
98. Measuring the concentration of Cl2 in the urine is an excellent first step in the clinical
approach to patients with metabolic acidosis.
99. Hypokalemia plays a central role in the pathophysiology of metabolic alkalosis and
must be corrected to successfully correct metabolic alkalosis.
100. Palliative care can be provided at any time during the course of a serious illness and is
not synonymous with hospice, which is a Medicare benefit for patients with a terminal
illness or a prognosis less than 6 months.
I
Patient
Assessment
HISTORY AND PHYSICAL
CHAPTER 1
DIAGNOSIS
Swapnil Hiremath and Edgar V. Lerma
1. How do patients with kidney disease typically present?

Patients with kidney disease typically present in several ways:
• Abnormal blood laboratory studies (e.g., elevated blood urea nitrogen [BUN] and serum creatinine,
decreased estimated glomerular filtration rate, or abnormal serum electrolyte values)
• Asymptomatic urinary abnormalities (e.g., microscopic hematuria, proteinuria, microalbuminuria)
• Changes in urinary frequency or problems with urination (e.g., polyuria, hematuria, nocturia, urgency)
• New-onset hypertension
• Worsening edema in dependent areas
• Nonspecific symptomatologies (e.g., nausea, vomiting, malaise)
• At times, symptoms can be specific (e.g., ipsilateral flank pain in those with obstructing nephrolithiasis)
• Incidental discovery of anatomic kidney abnormalities on routine imaging studies (e.g., horseshoe
kidney, congenitally absent or ptotic kidney, asymmetric kidneys, angiomyolipoma, kidney mass,
polycystic kidneys)
• Symptoms related to underlying systemic disease (e.g., skin changes and/or rash with scleroderma,
vasculitis, systemic lupus erythematosus [SLE], arthritis due to gout, SLE, etc.)
2. What important features need to be elicited in the history of patients referred for kidney disease
evaluation?
• Previous diagnosis of kidney disease (e.g., previous documentation of BUN and serum creatinine
values)
• History of asymptomatic urinary abnormalities (e.g., hematuria, proteinuria)
• History of alterations in urinary frequency or urgency, etc.
• Change in the urinary character or appearance (e.g., smell, color, frothy appearance)
• History of diabetes (duration, severity, end-organ damage)
• History of hypertension (including cardiac history)
• Previous exposure to nephrotoxic medications (e.g., nonsteroidal antiinflammatory drugs [NSAIDs],
antibiotics such as aminoglycosides)
• Previous adverse reactions to renin-angiotensin-aldosterone system blocking agents (e.g., angiotensin-
converting enzyme inhibitors, angiotensin receptor antagonists)
• Recent gastrointestinal endoscopic procedures requiring bowel cleansing (risk of acute phosphate
nephropathy in those who use phosphate-containing enema)
• Recent exposure to contrast-requiring procedures (risk of contrast-induced acute kidney injury)
• Recent systemic infections or intercurrent illnesses
• Family history of kidney disease or any relative requiring some form of renal replacement therapy
(e.g., polycystic kidney disease [PKD], Alport syndrome)
• History of autoimmune diseases
• Recent changes in dose of a medication, or any new medication recently started
• Any over-the-counter medications used (e.g., NSAIDs) and/or herbal, natural supplements
3. Why is smoking history important in patients with kidney disease?
Chronic kidney disease has been shown to be closely related to cardiovascular disease and smoking.
The concept of smoking as an “independent” progression factor in kidney disease has been a subject
of interest in numerous investigations. Since 2003 several publications of clinical and experimental
data concerning the adverse kidney effects of smoking have drawn interest, including large, prospec-
tive, population-based, observational studies. These studies clearly demonstrate that smoking is a
relevant risk factor, and it does confer a significant increase in the risk for progression of kidney
dysfunction (i.e., elevation of serum creatinine) regardless of the underlying cause of the kidney
disease.
3
4 PATIENT ASSESSMENT
It has been suggested that urinary cotinine, a metabolite of nicotine, can potentially be used as
an objective measure of smoking exposure. Its use has not been studied in the population with
chronic kidney disease.
4. What familial diseases are characterized by kidney involvement?
• Autosomal dominant PKD (ADPKD) (chromosomes 4 and 16)
• Autosomal recessive PKD (linked to chromosome 6)
• Autosomal dominant tubulointerstitial kidney disease (previously known as familial juvenile hyperuri-
cemic nephropathy type 1, medullary cystic kidney disease type 2, and or uromodulin-associated
kidney disease, linked to chromosomes 1, 16, 17)
• Focal segmental glomerulosclerosis (linked to chromosomes 1, 9, 10, 11, 19)
• Hypertension
• Diabetes mellitus
• Fabry disease
• Alport syndrome
• Sickle cell nephropathy
• Familial hypercalcemic hypocalciuria
• Cystinuria
• HDR syndrome (syndrome of hypoparathyroidism, sensorineural hearing loss, and kidney disease;
also called Barakat syndrome; mapped to chromosome 10p)
• Liddle syndromes of apparent mineralocorticoid excess and other monogenic hypertension
• Bartter and Gitelman syndromes
• Congenital nephrotic syndrome (Finish and other variants, mapped to chromosomes 1, 3, 11, 19)
5. What are the common symptoms and signs that are seen in patients with advanced kidney
disease?
Chronic kidney disease is usually characterized by nonspecific signs and symptoms in the earlier
stages and can be detected only by an increase in serum creatinine.
Symptoms • Intractable hiccups
• Loss or decreased appetite (protein aversion) • Frothy” appearance of urine (usually results
• Easy fatigability from proteinuria)
• Generalized weakness • Decreased sexual interest (e.g., erectile
• Involuntary weight loss (resulting from dysfunction)
cachexia) or gain (resulting from fluid • Restless legs
retention) Signs
• Alterations in mentation (e.g., lethargy, • Elevated blood pressure (BP)
coma, difficulty concentrating) • Pallor (from anemia)
• Nausea and vomiting; dyspepsia • Volume overload (jugular venous distention,
• Metallic taste peripheral edema, pulmonary edema,
• Generalized itching or pruritus anasarca)
• Seizures • Friction rub (pericarditis)
• Difficulty breathing • Asterixis and myoclonus (uremic
• Edema encephalopathy)
6. What is a bedside diagnostic test that will suggest the presence of underlying diabetic nephropathy?
Funduscopy. It is believed that the similarities in the vascularization between the retina and the kidneys
account for the correlation of the typical microvascular complications commonly seen in patients with
diabetes mellitus.
Patients with type 2 diabetes with proliferative retinopathy often present with kidney involve-
ment, manifested by either microalbuminuria (in the earlier stages) or overt proteinuria. Therefore it is
recommended that all patients with diabetes and proliferative retinopathy undergo an evaluation of
kidney function including testing for microalbuminuria.
It must be remembered that although the presence of retinopathy does support a diabetic source
of proteinuria, the lack of diabetic retinopathy does not rule out diabetic nephropathy.
7. What are the common extrarenal manifestations associated with kidney diseases?
Dermatologic • Rheumatoid arthritis
• See Question 8 • Henoch-Schönlein purpura
• Cryoglobulinemia
Arthritis and/or Musculoskeletal Symptoms
• Sarcoidosis
• Lupus nephritis
HISTORY AND PHYSICAL DIAGNOSIS 5
• Amyloidosis nephropathy and antiphospholipid

• Multiple myeloma syndrome)
• Gouty nephropathy • Volume overload (congestive heart failure,
mitral stenosis)
Hemoptysis
• Acute kidney injury with community Hearing loss
acquired pneumonia • Hearing loss from aminoglycosides or loop
• Pulmonary renal syndrome diuretics in someone with kidney disease
Goodpasture syndrome (also called • Alport syndrome
anti-GBM disease) • Charcot-Marie-Tooth syndrome
Henoch-Schönlein purpura and immuno- • HDR syndrome (hypoparathyroidism,
globulin A nephropathy sensorineural hearing loss, and kidney
Anti-Neutrophil Cytoplasmic Antibody disease; also called Barakat syndrome)
(ANCA)-related vasculitides: Granulo- • Wolfram syndrome (diabetes insipidus,
matosis with polyangiitis (previously diabetes mellitus, optic atrophy)
called Wegener granulomatosis); • Bartter syndrome (type IV)
eosinophilic granulomatosis with Abdominal discomfort
polyangiitis (previously called Churg- • Henoch-Schönlein purpura
Strauss syndrome); microscopic • Cryoglobulinemia
polyangiitis; and pauci-immune • Microscopic polyangiitis
crescentic glomerulonephritis • ADPKD
Cryoglobulinemia
• Lupus nephritis with pneumonitis Cervicocranial aneurysms:
• Pulmonary thromboembolism/infarction • ADPKD (also with mitral valve prolapse)
related to hypercoagulability (membranous • Fibromuscular dysplasia
8. What is importance of itching in kidney diseases, and how do you treat it?
Pruritus or itching is among the most common symptom of ESKD. In severe cases, it can be unrelenting.
Although mostly benign in etiology (see xerosis, previous), it can lead to secondary complications, such as
excoriations and lichen simplex chronicus, which may be disfiguring in extreme cases.
The use of emollients, moisturizing lotions, keratolytic agents, and hydration have been commonly
recommended as conservative treatment.
In some cases, phototherapy (ultraviolet B radiation [UVB] administered as total body irradiation
3 times a week for a total of 8 to 10 sessions) has been shown to be helpful. It has been suggested
that UVB (wavelength 280 to 315 nm) inactivates certain pruritogenic chemicals and induces the
formation of metabolites with antipruritic effects. The risk of malignancy is fairly significant, especially
in fair-skinned individuals.
Topical capsaicin (0.025%), by reducing the levels of substance P in cutaneous type C sensory
nerve endings, has been useful for localized pruritus.
Topical tacrolimus (0.03% for 3 weeks, followed by 0.01% for another 3 weeks) may be beneficial
but can predispose to dermatologic malignancies, so it is not recommended as a first line therapy or
for prolonged use.
Gabapentin (100 to 300 mg after each dialysis treatment) also has antipruritic effects. Prominent
side effects include depression of the central nervous system.
m-opioid receptor antagonists, such as per os (PO) naltrexone, has antipruritic properties. In the
same family, intranasal butorphanol (a F06BF06B-opioid receptor agonist and m-opioid receptor
antagonist) is another option.
Other treatment options include PO-activated charcoal, selective serotonin antagonists (ondansetron
and granisetron), oral cromolyn, cholestyramine, thalidomide, erythropoietin, and intravenous lidocaine.
9. What is calciphylaxis?
Calcific uremic arteriolopathy (CUA), also known as calciphylaxis, is characterized by painful,
subcutaneous purpuric plaques and nodules. These nodules may necrose in advanced disease.
Although the skin manifestations are dramatic, it is useful to think of it as a systemic disease, and
treat aggressively, given its high fatality rate. When the extremities are involved, the lesions tend to
be bilateral and symmetric in distribution and often are described as a mottled or violaceous discoloration
with a reticular pattern, similar to livedo reticularis (seen in atheroembolic kidney disease, antiphospholipid
syndrome, and cryoglobulinemia). Of note, those with proximal lesions (trunk, buttocks, and thighs) tend
to have a worse prognosis compared with those with more distal lesions (forearms and fingers; calves
and toes).
Several known risk factors predispose to CUA—namely, poorly controlled secondary hyperpara-
thyroidism, uncontrolled diabetes mellitus, obesity, female sex, duration of renal replacement therapy,
history of skin trauma, and use of warfarin.
The increased expression of osteopontin and bone morphogenic protein 4 suggests the pivotal
role that inducers of vascular calcification play in its pathogenesis.
Suspicion is the key to early diagnosis. When identified in its earlier stages (nonulcerative),
initiation of therapeutic measures has been shown to improve prognosis.
Prevention is the key to management of CUA. Aggressive control of secondary hyperparathyroidism
(see Chapter 21) is pivotal.
Sodium thiosulfate is one of the therapies for established CUA. It is believed to work by two
mechanisms of action:
1. Chelates calcium from soft tissues
2. Antioxidant, inducing endothelial nitric oxide synthesis, thereby improving local blood flow and soft
tissue oxygenation.
A commonly used regimen is 5 to 25 g of intravenous (IV) Na thiosulfate administered toward the end
of dialysis for several weeks to months.
Bisphosphonates (IV pamidronate and ibandronate and PO etidronate) may be effective in altering
ectopic deposition of calcium phosphate and directly inhibiting calcification via the nuclear factor
F06BF06BB cascade, although there are limited data.
Hyperbaric oxygen therapy improves oxygen delivery to damaged tissues by increasing the par-
tial pressure of oxygen; it also promotes wound healing by supporting phagocytosis and angiogenesis
while decreasing tissue edema.
10. What is nephrogenic systemic fibrosis (NSF)?
NSF, previously known as nephrogenic fibrosing dermopathy, is characterized by progressive fibrosis
and thickening of the skin (similar to scleroderma), which is particularly painful, and also fibrosis in
other organs (e.g., pleura, diaphragm). The skin lesions appear as plaques, papules, or nodules
distributed in an asymmetric fashion over the distal extremities. The pathogenesis is deposition of
gadolinium (contrast material used in magnetic resonance imaging), which does not get cleared in the
presence of severe chronic kidney disease or acute kidney injury. The interval between exposure to
gadolinium and the early manifestations of NSF can range from 2 days to 18 months. This variability
is attributed to mobilization of gadolinium from bone over time. The risk of NSF appears to be higher
with the linear molecules (e.g., gadodiamide) compared with macro cyclic gadolinium molecules.
NSF has no effective treatment and a high fatality rate, so the primary focus is on prevention.
Gadolinium-enhanced scans should be avoided in patients with severe chronic kidney disease or
acute kidney injury. When gadolinium-enhanced scans are necessary, prophylactic measures that
have been described include the use of hemodialysis (HD; eliminates 92% of gadolinium after two HD
sessions; 99% after three HD sessions) in patients with advanced chronic kidney disease. Similarly,
an intensified regimen of peritoneal dialysis (PD) can remove gadolinium (90% of the gadolinium in
2 days with a regimen of 10 to 15 exchanges per day of PD). The effectiveness of these measures is
not clear.
11. What are the other common dermatologic manifestations of kidney disease?
Xerosis or dryness of the skin, especially on the extensor surfaces of the extremities, is common
among patients receiving dialysis. It can lead to generalized pruritus and can be uncomfortable.
Changes in pigmentation—in particular, hyperpigmentation—have been attributed to the
increased levels of melanocyte-stimulating hormone and the subsequent deposition of melanin in the
basal layer of the epidermis.
Some patients may have a “sallow” discoloration of the skin believed to be caused by deposition
of lipochrome pigment and carotenoids in the dermis and subcutaneous tissues.
Pallor is commonly associated with varying degrees of anemia as a result of chronic kidney
disease.
Uremic frost refers to the deposition of crystallized urea that is excreted from sweat in the
epidermis, seen in cases of untreated and advanced kidney disease.
Ecchymoses are commonly associated with uremic platelet dysfunction.
Lindsay nails, also known as “half and half nails,” refer to the whitish discoloration of the proximal
half of fingernails, believed to be a result of edema of the nail bed and underlying capillary network.
Acquired perforating dermatosis (Kyrle disease) is predominantly seen in African Americans
with diabetes mellitus. It is usually characterized by a linear confluence of papules with a central,
oyster shell–like keratotic plug, distributed on the trunk, proximal extremities, scalp, and face, and
HISTORY AND PHYSICAL DIAGNOSIS 7
the lesions are pruritic. Possible etiologies include an inflammatory skin reaction secondary to the
presence of uremic toxins, uric-acid deposits, or scratching-induced trauma.
Porphyria cutanea tarda (PCT) commonly presents as a vesiculobullous disease commonly
involving the dorsum of both hands and feet but can affect any sun-exposed areas. It is commonly
accompanied by sclerodermoid plaques (facial hyperpigmentation) and hypertrichosis. It is usually
secondary to increased levels of uroporphyrins.
Avoidance of sun exposure is the cornerstone of management. Other measures to decrease
uroporphyrin levels include the use of high-flux dialysis membranes (to improve dialysis efficacy) and
small-volume weekly phlebotomies in extreme, rare cases.
Common precipitating factors are alcohol intake, use of estrogen and iron supplementations,
and chronic infections (e.g., hepatitis B or C virus, human immunodeficiency virus).
One common differential diagnosis is pseudoporphyria, which is clinically similar to PCT with the
exception of normal uroporphyrin levels.
12. What are the causes of palpable kidneys?
Palpation for the kidneys is best performed bimanually, with one hand behind the patient in the costo-
vertebral angle and the other anteriorly just below the costal margin. They may be normally palpable
in very thin individuals. Pathologic causes include:
• ADPKD (both kidneys will be palpable)
• Large kidney tumors
• Obstruction of the urinary tract with severe hydronephrosis
• Very large kidney cyst(s)
13. What are the causes and significance of an abdominal bruit?
• Normal: Approximately 5%–25% of normal individuals may have a midsystolic bruit audible, with
the prevalence being higher in younger individuals.
• Renovascular disease: The characteristic bruit seen in renovascular hypertension, due to renal
artery stenosis, is an epigastric systodiastolic bruit. Although it has a low sensitivity, it has a high
specificity in the patient in whom one is suspecting renovascular hypertension. Renovascular
hypertension can be due to either atherosclerotic disease or fibromuscular dysplasia (typically
seen in young or middle-aged women). In fibromuscular dysplasia, extrarenal disease is common,
with cervicocranial and other abdominal arteries being involved in particular.
• Nonrenal causes of abdominal bruit include portal hypertension (periumbilical venous hum),
pancreatic neoplasia (epigastric bruit), splenic arteriovenous malformation (left upper quadrant),
hepatic carcinoma (right upper quadrant), and abdominal aortic aneurysms.
14. What are the other important aspects of physical examination in kidney disease?
• BP measurement is a keystone of assessment of kidney disease. High BP can be a cause or a
consequence of kidney disease. Proper measurement, with adequate resting, measurement of both
arms, and assessment of change with posture should be a part of BP measurement.
• Assessment of volume: This is important for any case of acute kidney injury to make decisions
about volume resuscitation, as well for advanced kidney disease to assess for volume overload.
Typical components include jugular venous pressure, orthostatic BP measurements, skin turgor,
and mucus membranes.
• Chest examination: Signs of volume overload (pulmonary edema); pericardial friction rub (in uremic
pericarditis)
• Musculoskeletal system: See “Arthritis” section earlier.
• Skin: Many diseases, especially autoimmune diseases, can be accompanied by a skin rash, such
as SLE and Henoch-Schönlein purpura. Kidney disease can also have skin manifestations (see
Question 11 for more details).
KEY PO I N T S
1. The similarities in the vascularization between the retina and the kidneys account for the correla-
tion of the typical microvascular complications commonly seen in patients with diabetes mellitus.
2. Tobacco abuse confers a significant increase in the risk for progression of kidney dysfunction,
regardless of the underlying cause of the kidney disease.
3. In patients with calciphylaxis, those with proximal lesions (trunk, buttocks, and thighs) tend to have
worse prognosis compared with those with more distal lesions (forearms and fingers; calves and toes).
Commonly Used Terms for Signs and Symptoms of Kidney Disease and their
Meaning and Significance
Term Meaning Significance

Oliguria Decreased urine output (,0.5 mL/ Volume depletion; kidney failure
kghour in children, ,400 mL/day
in adults)
Anuria Severely decreased urine output Kidney failure
(,100 mL/day)
Absolute anuria No (0 mL) urine output Blocked/kinked catheter, urinary obstruction
Dysuria Pain or burning while passing Urinary tract infections, stones, sexually
urine transmitted infections, interstitial
cystitis
Hematuria Presence of blood in urine; Gross: Source of blood can be urinary tract or
visible with naked eye glomerulus
Microscopic: only seen with
dipstick/urinanalysis
Proteinuria Presence of protein in urine, by Usually suggests intrinsic kidney disease
dipstick (trace or more) or
quantitation
Microalbuminuria Very small amounts of albumin in Sign of early diabetic kidney damage;
urine, usually missed by urine in nondiabetic conditions suggests
dipstick endothelial dysfunction
Polyuria Increased amount of urine Increased water intake; diabetes
(opposite of oliguria)
Nocturia Increased frequency of urine at Usually accompanies polyuria; also with
night chronic kidney disease (decreased
urinary concentrating ability)
Pollakiuria Frequent urination in the daytime Benign condition in children; accompanies
polyuria; neurogenic bladder; drugs
(e.g., tolvaptan)
Bibliography
Abu-Alfa, A. (2008). The impact of NSF on the care of patients with kidney disease. Journal of the American College of
Radiology, 5, 42–52.
Glynne, P., Deacon, A., Goldsmith, D., Pusey, C., & Clutterbuck, E. (1999). Bullous dermatoses in end-stage renal failure:
Porphyria or pseudoporphyria? American Journal of Kidney Diseases, 34, 155–160.
Jones-Burton, C., Vessal, G., Brown, J., Dowling, T. C., & Fink, J. C. (2007). Urinary cotinine as an objective measure of
cigarette smoking in chronic kidney disease. Nephrology, Dialysis, Transplantation, 22(7), 1950–1954.
Kuypers, D. R. (2009). Skin problems in chronic kidney disease. Nature Clinical Practice Nephrology, 5, 157–170.
National Kidney Foundation. (2002). K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification,
and stratification. American Journal of Kidney Diseases, 39(2 Suppl. 1), S1–S266.
Orth, S. R., & Hallan, S. I. (2008). Smoking: A risk factor for progression of chronic kidney disease and for cardiovascular
morbidity and mortality in renal patients—Absence of evidence or evidence of absence? Clinical Journal of the
American Society of Nephrology, 3, 226–236.
Penfield, J. G., & Reilly, R. F., Jr. (2007). What nephrologists need to know about gadolinium. Nature Clinical Practice
Nephrology, 3, 654–668.
CHAPTER 2
URINALYSIS
Swapnil Hiremath, Florian Buchkremer, and Edgar V. Lerma
1. What is uroscopy?
Uroscopy comes from the word “uroscopia,” meaning scientific examination of the urine. It is derived
from the Greek words ouron meaning urine and skopeo meaning to behold, contemplate, examine, or
inspect. Such analysis of the urine was historically termed uroscopy until the 17th century and is now
called “urinalysis.”
2. What is the proper way of collecting and handling a urine specimen for analysis?
When collecting the urine specimen, the first 200 mL of early-morning voided urine should be
discarded. In men a simple midstream urine collection should suffice, whereas in women the external
genitalia should be cleaned first, to avoid contamination with secretions, before collecting a midstream
specimen. The specimen should be collected in a clean but not necessarily sterile container.
Urine should be analyzed within 30 to 60 minutes of voiding; the initially uncentrifuged
specimen is analyzed for color, pH, specific gravity, blood, protein, and glucose. Subsequently, it is
centrifuged at 3000 rpm for 3 to 5 minutes. The sediment is then examined under the microscope for
various elements, such as red blood cells (RBCs) and RBC casts, white blood cells (WBCs) and WBC
casts, squamous epithelial cells, hyaline, and granular casts.
3. What are the typical elements in a urine dipstick?
See Table 2.1.
• Color: Normal urine color can vary from pale or light yellow to deep amber or dark yellow. The
color is due the pigment urochrome. Two important characteristics influence the color: its chemical
composition and concentration. In an individual who is volume depleted, urine concentration tends
to be elevated, giving rise to a darker-yellow urine. However, in a patient with diabetes insipidus,
the urinary concentrating ability is impaired, making the urine dilute and lighter yellow in color
even in the presence of volume depletion. Certain medications and foods alter the urine color
(Table 2.2). In porphyria cutanea tarda, the urine turns the color of port wine.
• Clarity or turbidity: The degree of turbidity or cloudiness is usually influenced by excess amounts
of cellular debris and casts but can also be secondary to proteinuria, crystals, or contamination
with vaginal discharge.
• pH: Normal urine pH ranges between 4.5 and 8.0. In a normal individual on a Western diet, the
average endogenous acid production is 1 mEq/kg per day, and the kidneys are responsible for
clearing this acid load, so urine is typically quite acidic, usually with a pH of 5 to 6. Urine pH is
useful in differentiating the different types of renal tubular acidosis (RTA), which is characterized by
the inability to acidify urine to a pH less than 5.5 (i.e., despite an overnight fast and acid loading).
Similarly, it also provides a clue to the causes and therapies for certain disease states (e.g.,
nephrolithiasis). Alkaline urine is usually seen in urinary tract infection (UTI) caused by urea-
splitting organisms (Proteus mirabilis), associated with magnesium–ammonium phosphate crystals and
staghorn calculi, whereas acidic urine is seen with uric acid calculi. Urine may also be deliberately (but
cautiously, to avoid metabolic alkalemia and hypocalcemia) alkalinized, to a pH greater than 6.5, for
therapeutic reasons, to aid in elimination of certain toxins (e.g., salicylates, barbiturates) or to prevent
the crystallization of uric acid in tumor lysis syndrome or myoglobin in rhabdomyolysis.
• Specific gravity: The urine specific gravity (1.005 to 1.025) reflects the ability of the kidneys to
concentrate urine. In patients with impaired urinary-concentrating ability (acute tubular necrosis,
sickle cell nephropathy, diabetes insipidus), the specific gravity tends to be low. Although imprecise
at times, it can reflect a person’s volume status.
• Blood: The urinary dipstick test for blood detects the peroxidase activity of RBCs; however,
myoglobin and hemoglobin also catalyze this reaction, so a positive dip stick may indicate
hematuria, hemoglobinuria (paroxysmal nocturnal hemoglobinuria, transfusion-related reactions,
infection with Plasmodium falciparum, infection with Clostridium welchii), or myoglobinuria
(rhabdomyolysis). In the presence of positive blood on dipstick analysis, the presence of RBCs on
urine microscopy confirms the diagnosis of hematuria (see Question 4 for more on this topic).
9
Table 2.1. Urine Dipstick Testing

MEASURED CLINICAL SIGNIFICANCE CAVEATS
Specific Expected value: 1.002–1.030 Increased values in the presence of
gravity ,1.005: inability to concentrate protein .1 g/L, ketoacids, iodinated
urine (e.g., diabetes insipidus, acute contrast media, dextran
tubular necrosis) Urine osmolality is a more exact
.1.030: SIAD, adrenal insufficiency, measure of urinary solutes
hypovolemia
pH Expected value: 5.5–6.5 Increased values when urine left
Alkaline: Diet (e.g., vegetarian), standing (increased ammonia synthesis)
renal tubular acidosis (type I or II),
salicylate overdose, acetazolamide,
alkali therapy
Acidic: diabetic ketoacidosis, diarrhea,
furosemide, systemic acidosis
Hemoglobin Expected value: Negative False negative: Presence of ascorbic
Positive due to presence of erythro- acid or formaldehyde, high nitrite
cytes, or free hemoglobin (e.g., with concentration, delayed examination, high
intravascular hemolysis) density of urine
False positive: Myoglobin, microbial
peroxidases, oxidizing detergents,
hydrochloric acid
Glucose Expected value: negative False negative: Presence of ascorbic
Positive in presence of glucose, acid, urinary tract infection
typical diabetes mellitus, or with False positive: Presence of oxidizing
reduced renal threshold for glucose detergents, hydrochloric acid
(e.g., proximal RTA, pregnancy, use
of sodium-glucose transporter
inhibitors, i.e., gliflozins)
Albumin Expected value: Negative False negative: Immunoglobulin light
Positive (1 or more): Proteinuria chains, hydrochloric acid, tubular
(glomerular disease) proteins, other globulins, colored urine
False positive: Alkaline urine (pH . 7.5),
quaternary ammonium detergents,
chlorhexidine, polyvinylpyrrolidone
Leukocyte Expected value: Negative False negative: Presence of ascorbic
esterase Positive indicates pyuria, which acid, recent treatment with gentamicin,
would indicate a urinary tract tetracycline, cephalosporins, nitrofuran-
infection, or other causes of sterile toin; proteinuria, glycosuria
pyuria (as discussed previously) False positive: Oxidizing detergents,
formaldehyde (0.4 g/L), sodium azide,
colored urine from beet ingestion, or
bilirubin
Nitrites Expected value: Negative False negative: Short bladder incubation
Positive in presence of bacteria that time, presence of ascorbic acid,
convert nitrates in urine to nitrites gram-positive bacteria
(typically gram-negative bacilli such False positive: colored urine
as E. coli, Klebsiella)
Ketones Expected value: Negative False negative: Test does not detect
Positive with ketonuria (e.g., presence of b-hydroxybutyrate
ketoacidosis due to diabetes, False positive: Free sulfhydryl groups
starvation; may also occur in (e.g., captopril), l-dopa, salicylates,
pregnancy, low-carbohydrate diets) phenothiazines, pigments in urine
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It was during the straggling march, caused by some of these
obstructions, that the catastrophe we have to narrate took place.
Again the troops were at times marching almost in file, and in rear of
the last company of Rifles were the two friends, Jerry and Dalton, and,
leaving their men to be led by their senior subalterns, they paced on
together, laughing from time to time, and talking of home and those who
awaited them there, now that the brief campaign was over, for homeward
now went the thoughts of all; but these two were unaware that their steps
were dogged and watched surely and stealthily.
As they made a little detour to avoid a more than usually deep pool
surrounded by some straggling palm-trees, they suddenly found themselves
face to face with at least a dozen of Ashantees—notably two of them the
fellows with the jawbones. They seemed to have sprung out of the earth, so
suddenly did they appear amid the eddying smoke and misty vapour; and
they at once struck Dalton down before he could utter a word.
Jerry instantly shot three in quick succession with his revolver, and,
knowing the reports would at once summon succour, he shouted cheerily,
and dragged Dalton to his feet, but at the same moment was struck down
senseless by a tremendous blow on the head, and falling—falling, he knew
not where—remembered no more...
In short, he had tumbled into a species of nullah or hollow, completely

fringed round with enormous boughs and luxuriant greenery, where he lay
hidden and undiscovered by the riflemen whom his pistol-shots summoned,
and who searched the whole vicinity in vain, till they could delay no longer,
as the waters were rising fast. They carried off with them Dalton, who was
severely wounded by dagger-blades, and whose haversack had been cut
away, and taken, and with it, of course, the unlucky scarabœus.
And so, while poor Jerry lay where we have described, the army pushed
on its homeward way, and ere long found the obstructions increase as the
night advanced. Where there had been a small stream at one place the water
was three hundred yards wide and five feet deep. With great toil the
Engineers bridged this by felling a huge tree, over which the white troops
defiled slowly, while the carriers and others had to splash their way through
as best they could, and many of the shorter men disappeared under the
surface more than once.
A worse obstruction still was encountered at Ordah, where the water

had risen two feet above the bridge built by the Engineers, and was more
than five feet deep in the mid-channel, and there the shorter men had all to
be assisted by their comrades who could swim. Another day crept on, and
by five o'clock in the afternoon the whole of the white troops had succeeded
in crossing the half-hidden bridge; but darkness was coming on, the river
was rising fast, and for all they knew the Ashantees, infuriated by the
destruction of Coomassie, might be pouring in wild hordes upon their rear!
Dalton's wounds had been dressed, but ere that was done he had lost so
much blood that his chances of recovery seemed very precarious; and
meanwhile how fared Jerry Wilmot?
When he struggled back to consciousness, and half raised himself out of

the place in which he lay by grasping the branch of a bush, he found
himself alone, and surrounded by dead silence. Not a sound fell on his ear,
and at a little distance he could see the red smouldering flames of
Coomassie. But where were the troops?
'Oh, God, help me!' he wailed out. 'Gone—gone, and I am left alone and
helpless behind them!'
There was a gleam of moonlight now, and after several futile efforts, for
his senses reeled like those of one intoxicated, he made out the hour on his
watch.
'Midnight—and they have been six hours on the march!'
He had been in a state of semi-unconsciousness for some two hours.

The sense—the conviction that he must instantly do something—attempt to
overtake them, made him struggle up desperately, feebly, and half blinded
in his own blood.
'Oh, Lord,' thought Jerry, 'I shall lose the little reason I have left! Why
did Dalton covet that infernal beetle!'
Alone—alone at Coomassie. Was not this some horrible nightmare, and
not a reality, crushing and bewildering? for but two fates seemed to await
him. If he did not die of hunger in the wilderness, he would be sure to be
tracked and taken; and then, if not killed at once, he would be doomed to a
lingering death by torture in Coomassie, or what remained of it—tortures
such as devils alone could devise.
He made an attempt to stand, but all power of volition seemed to have

left him; he fell again into the leafy hollow, and for a time remembered no
more.
CHAPTER III.
THE LOST ONE.
And where all this time was Alison Cheyne, after whom—as the chief
of our dramatis personæ—we must needs look now?
When consciousness returned to her, after wildly grasping the bell in the
porte-cochère of a large house on that night of snow and terror, and when,
fluttering, her white eyelids unclosed, after what seemed a long sleep, she
looked round her like a little scared bird, in utter bewilderment, and,
believing that she was dreaming, closed them again.
A bell ringing at a distance roused her, and she looked again, and
became convinced that what she looked on was no dream, and her eyes
wandered about with a dazed expression.
She was in a little room, with whitewashed walls, and a floor of plain
polished wood, on which lay a tiny patch of faded carpet. The sunbeams
were creeping through the closed blinds, and a fire burned cheerfully in a
little black iron stove. She lay in a pretty bed, with the softest of pillows and
sheets; it was of plain iron, and without curtains.
Above the mantelpiece, in a simple frame, hung an engraving from

Rubens' picture of 'St. Theresa interceding for the Souls in Purgatory,' the
three principal souls being—in a spirit of waggery—faithful portraits of the
artist's three wives. On one side of this was a little Madonna on a bracket,
with a red crystal lamp hung before it; on the other a crucifix, below which
was a tiny font of Antwerp china.
Other ornaments—save a few flowers in a vase—the apartment had

none, and its furniture—two cane-seated chairs and a deal table—was of the
simplest kind.
In one of the chairs sat a young woman dressed like a nun, with a black
robe and white hood, a large bronze crucifix and wooden beads at her cord
girdle; her down-cast face had a sweet, placid, and even beautiful
expression, and she was sedulously working, with the whitest of hands, at a
large piece of gold embroidery on cloth of silver—a portion of a priest's
vestments apparently, while glancing attentively from time to time down on
her patient or up at two pretty little love-birds in a brass cage.
Alison took in all these details at one rapid glance, and great terror
seized her that something strange had befallen her, that she was in the care
of a nursing sister.
'Where am I?' she said, faintly.
'Thank heaven, you speak, and rationally at last,' said her attendant,
casting aside her embroidery and coming softly to her side, laid her cool
hand gently on Alison's forehead. 'Pauvre enfant! pauvre enfant!' she
repeated, caressingly.
'But where am I, and who are you?' asked Alison, in a weak but
impatient manner.
'I am Sister Lisette, and you are safe, safe with friends, and ere long
your own people will soon be here to inquire for you.'
'My friends,' she murmured, with a puzzled expression, as her thoughts
now went back to her father's sick-room in the Hôtel St. Antoine; to
Cadbury, at the thought of which she shivered; to the Bal Masqué at the
theatre; the Café au Progrès, and the insolence of 'Captain Smith;' her flight
through the snowy streets; her fall at the door of a house, the nature of
which she knew not; all these things floated dimly and dreamily before her
now, though they seemed to have happened but a few hours ago.
'How fortunate that you had the power to ring our bell before you
fainted, child,' said the nun, caressing her and kissing her cheek. 'You might
have died in the snow otherwise.'
'Last night?'
'No—child—it was several nights ago.'
'Several?'
'Yes.'
'Oh, papa, papa! has he been here?' cried Alison, feebly, in great anguish
of mind, yet unable from weakness to raise her head from the pillow.
'No, for doubtless he knew not where you were.'
'Oh, he will be dead—dead with terror!' wailed Alison. 'Am I in a

hospital?'
'No, child, in my house,' said the nun, sweetly.
'Your house?' queried Alison, with very open eyes.
'In the Beguinage, in the Rue Rouge.'
Thus it was that both Sir Ranald and Lord Cadbury had utterly failed to
trace her, and fortunate it was indeed for Alison that she had fallen into such
good hands as those of the Beguines, who are a religious order, altogether
peculiar to Belgium, each nun having a private residence of her own within
the general enclosure.
The clatter of the ponderous bell, as the pull left her hand, had soon
brought aid to her. She was denuded of her wet and sodden attire, put to bed
in the little mansion occupied by Sister Lisette, and, before the angelus bell
rang in the chapel next forenoon, she was in a highly feverish state, and in a
delirium which lasted several nights and days, with intermissions of fretful
sleep, during all of which time nothing coherent could be gleaned from her
as to her name, or where she resided, whence she came, and how it was that
she was abroad in the streets alone and in such a night.
Her little ravings led them to know that she was English; her costume,
and the delicacy and beauty of her person, that she was undoubtedly a lady;
but, save a ring or two, she had no purse, card-case, or aught to indicate
who she was; but the name of 'Alison' worked upon some of her clothing at
once interested deeply Sister Lisette, who was also an Alison, but adopted
the French diminutive of it.
The poor Beguines were quite uncertain what else they could do with
her, but keep her till she grew well enough to be questioned; so she
remained there in her little iron bed, tended by Lisette, unconscious and
fever-stricken, while the lengthening days passed slowly over her aching
head.
Nearly a fortnight passed before she began mentally to drift back to

consciousness, so terribly had all she had undergone of late—the collision
at sea with the Black Hound of Ostend, the nursing of her querulous father,
her separation from Bevil Goring, and the worry incident to Cadbury's
wooing, culminating in that night of terror in the streets—told upon her
sensitive nature and delicate frame.
A sweet picture she made, in her little white bed in the plain bare room
of the kind Beguine, who never left her even for prayers, but said them by
her side on her knees when the angelus or elevation bells rang. Among the
huge, soft pillows the slight figure of Alison was half buried, yet the soft
tints of her face and hair came out in a species of relief from them; the
former was pale—very pale—and there were dark circles under the eyes;
and the gentle young Beguine who watched her thought she had never
looked on anyone so lovely, and often sat on a tabourette at the side of the
couch, keeping her hand caressingly within her own, and counting the
jewels in her rings one by one as a child might have done.
'She has a gentle expression in her eyes, such as I have often seen in
those of a Sœur de Charité, and other nursing sisters,' was the dictum of the
reverend mother of the establishment, who came from time to time to visit
the fair waif who had been so suddenly cast upon their tenderness; and,
truth to tell, there was a great touch of melancholy about the eyes and
features of Alison Cheyne now, though certainly melancholy was by no
means one of her characteristics naturally.
The Beguines, we have said, are a religious order peculiar to Belgium,

and totally unlike any other in so far that they are bound by no vows; they
may return to the world whenever they please; but it is their boast that no
sister has ever been known to quit the order after having once entered it.
They attend to the sick in the Beguinage, and frequently go out as nurses in
the hospitals.
They were among the few religious communities not suppressed by

Joseph II. or swept away by the furious torrent of the French Revolution.
Each Beguinage—more especially in Ghent, where the sisterhood averages
six hundred in number—is a species of little town by itself, with streets and
squares, having gates, and sometimes surrounded by a moat as well as a
wall, especially at Bruges.
The sisters live generally in separate houses, on the doors of which are
inscribed, not the name of the occupant, but of some saint adopted as her
patron or protectress; and many of them are persons of rank and wealth;
hence it was in the private house of Sister Lisette that Alison found herself
now.
Many writers ascribe the institution of the Beguines to St. Begga,

widow and abbess, daughter of Pepin of Landen, whose husband, mayor of
the palace, was killed while hunting, after which she dedicated herself to a
penetential state of retirement, and built seven chapels on the Meuse, in
imitation of the seven great churches of Rome; and, according to the
martyrology, she died so long ago as 698. Others assert that the Beguines
were founded by Lambert de Begue or Balbus, a pious priest, of Liege, in
1170, and derive their name from him; but all this lies apart from our story.
Suffice it that, fortunately for herself, it was in the spacious Beguinage of
Antwerp that Alison found succour, shelter, and protection.
Alison had often seen nuns, but never spoken to or been intimate with
one before, and, as all she knew of such recluses was derived through the
medium of novels and romances, when strength returned to her she began to
invest Sister Lisette with the halo of fiction, and to suppose that she must
have some story—that a lost lover or a broken heart accounted for her sweet
sadness of face and her present vocation; and she was nearer the truth in her
guess than she imagined, for Sister Lisette had once been—for a brief time
—a happy wife, of which more anon; and when Alison grew stronger, and
was taken as far as the chapel, she was greatly impressed by all she saw and
heard there at vesper time, though the chanting of female voices only—
some of them from age far from melodious—was pleasing, and the sight of
such a large assemblage of recluses in black robes with white veils—the
ancient Flemish faille, which they yet retain—dimly illuminated by a few
votive lamps, had a strange, weird, and, to her eyes, mysterious effect.
The novices are distinguished by a different costume, and those who

have just taken the veil wear a chaplet round their heads.
But in all this we are anticipating, for at present Alison was weak as a
child, and prostrate with the effect of the short, sharp fever that had left her,
though it was apparent to those who watched her that the lines of her face
were fine, and they could see that, when well and happy, she must look very
beautiful.
In Sister Lisette Alison found an able nurse, for she had served as one in
the German war under the Red Cross; her soft, white hand had dressed
many a ghastly wound and closed many a glazing eye, and often amid the
horrors of Sedan and elsewhere the heads of the dying had rested on her
bosom, and with low, loving words she had soothed their moments of death
and agony—words that were sometimes taken for those of mother, or wife,
or some young love that was far, far away.
Sister Lisette seemed about five-and-twenty years of age; her face was
delicately fair, but the rich tint of her lips and the peach-like bloom of her
cheeks relieved it of all paleness. Her features were small and regular, but
very soft in their lines, and, at times, a singular sadness stole over them.
Her eyes were of the clearest and darkest hazel, and full of 'soul's light,'
imparted to her face a world of expression; but what the colour of her hair
(or what remained of it) was, it would be impossible to say, as every vestige
of it was closely hidden by her tightly-fitting white wimple.
'And I have been here for days and nights ill,' said Alison, faintly, as
consciousness came fully back to her, and Lisette, while propping her pretty
head upon her own breast, gave her soothing drink. 'Oh, what a trouble I
must have been to you!'
'No trouble at all, ma sœur,' replied the other, letting her head tenderly
down on the pillow, and smoothing out the latter.
'So long, so long, and without papa being informed,' exclaimed Alison,
as tears of dismay started to her eyes.
'Child, we know not his name—his address—even of his existence.'
Alison sighed deeply. She was too prostrate in body and even mind to
regard anything as very extraordinary, even her unusual surroundings in the
convent; yet she longed for her father to come to her, or to have tidings of
him; of aught else she said nothing.
'Oh, if I should die without seeing papa again!' said she, wringing her
hands.
'One can die but once,' said Sister Lisette, placidly. 'You are too strong
and too young to die, though those who die are sometimes better off than
those who are left in the world. You, at least, have all your life to look
forward to.'
'And you?'
'Mine is ended.'
'Ended!'
'In the world at least, as I shall go back to it no more.'
Seeing that Alison was in a fever of impatience to hear tidings of her

father, Sister Lisette, on obtaining his name and address at the Hôtel St.
Antoine, at once sent a messenger with that letter which, as we have
described, so greatly startled and agitated the old man; and Alison remained
in a fever of impatience, awaiting the return of that messenger who might
perhaps bring her very crushing tidings.
'Dearest papa will not lose a moment in coming to me,' she murmured,
partly to her nurse and partly to herself; but how, if he were too weak to
come or in despair at her loss had left Antwerp, or perhaps—oh Heavens!—
have sunk under it, and—died! And to see him again would be, of course, to
see that odious Lord Cadbury; and so she tormented herself till the
messenger returned with tidings that her father was well and had been out
and about for days, despairingly searching for her, and would be with her
very soon.
'Oh, thank God for that!' said Alison, and a hot shower of joyful tears
relieved her; and now she started up at every sound, and inquired again and
again the exact distance between the Beguinage and the Marche aux
Souliers.
'Ma sœur Alison, you must not speak so much and be so impatient,' said
the Beguine, holding up a finger.
'What—you know my name?'
'Yes, it is mine also.'
'But how?'
Then the Beguine told her how she had become aware of it; and that she
too was an Alison, Lison or Lisette—it was all one—and as she spoke her
hearer's memory went back to that day with the buckhounds on which our
story opens, when Bevil Goring expressed some surprise at her name, and
she had explained that it was an old Scoto-French one, and common to the
Cheynes of Essilmont; and as she thought of him she pressed his ring to her
lips, as if it had been some sacred relique.
'How well you speak English,' said Alison.
'Because I was educated in the English convent at Bruges,' replied the

sister; 'but hark, there is a voiture at the gate—monsieur has come!'
'Papa,' murmured Alison, in a choking voice, as she felt herself become

a very child again, and another minute saw his arms around her, and her
face upon his breast, while she indulged in a passionate fit of weeping, and
he with difficulty restrained his tears.
Alison then, after a little time, looked earnestly in his face, and was
shocked to see how wan, and thin, and pinched it had become; for indeed,
during the mystery that enveloped her disappearance, he had undergone
terrible mental agony and much bodily fatigue, for with all his selfishness
he loved Alison as the only link that bound him to earth.
Her narrative of how she missed Lord Cadbury in that crowded place,
the Théâtre des Variétés, to which she should never have gone, tallied
completely with that of the former; but it was not until next day that she
detailed fully the manner in which she had been lured by 'Captain Smith' to
the Café au Progrès, and the terror with which she had fled from that place
into the snowy street.
'Captain Smith!' exclaimed Sir Ranald through his set teeth, while his
eyes sparkled with rage. 'Could I but meet that person, old as I am, I would
give him cause long to remember the weight of my cane, the scoundrel. I
must write to Cadbury on the subject and inquire.'
'Write!—is Lord Cadbury gone?' asked Alison, timidly and hopefully.
'Yes, back to London; he was telegraphed for.'
Alison gave a sigh of relief.

'Shall we go home now, papa—I mean when I am well enough to be
about?'
Sir Ranald paused before replying. Had she relented towards Cadbury
with a desire to see him, or was it a longing to be near 'that fellow Goring'
which prompted the question? One fact seemed pretty evident, that she and
the latter knew nothing of each other's movements, and that she was utterly
oblivious of his being or having been in Antwerp.
'Home—to where?' he asked.
'Chilcote, papa.'
Her reply was perfectly straightforward, though it again suggested ideas

of Bevil Goring, but Sir Ranald deemed that he must have 'effectually
crushed that fellow's presumption by the rough tenor of their last meeting.'
'Chilcote it shall be then, perhaps,' said he.
'Oh, yes, papa; it is so quiet there, even amid our little troubles,' said
she, as he left her, when the Beguinage gates were closed for the evening;
'and all I want is peace and rest—peace and rest.'
'Shall you ever get them in this world?' asked Sister Lisette.
Alison regarded her wistfully, and said,
'Why not? Can you have led a stormy life?'
'Far from it. My life in the world was a happy one till one dire calamity
fell upon me, and drove me to find peace for ever here; but how true it is
"that it is vain to try to knit up the present with the past; each part of our
lives has its own pleasures and hopes." But now my pleasure is to do good
—my only hope to die soon and well.'
'And the calamity to which you refer?' asked Alison, softly, while
greatly interested by the singularly sweet and subdued manner of the young
Beguine.
'Was the death of my dear, dear husband,' replied the sister; and so,
while she sat stitching away at the shining garment, resplendent with gold
—a priest's vestment—for old Père Leopold of the Church of St. André, she
told Alison some of her experiences in life, and amid them, curious to
relate, there occurred repeatedly a name with which the reader is already
familiar.
Alison had a sweetly sympathetic way with her, and her namesake was
seized by one of the unaccountable fits of confidence that, come to most of
us at times to speak about herself, and tell the story of her own sorrows.
CHAPTER IV.
A YEAR OF JOY.
A very simple circumstance—an occasion of every-day life—a railway

journey, brought about the awful tragedy in her life, by which she was left a
widow at twenty, after being wedded a year—which she called a year of
joy, left without a near relation in the world but her brother, Victor Gabion,
a captain of Artillery, who, strange to say, was the source of all her sorrow.
'After leaving the English convent at Bruges, I returned to the house of

my guardian, M. Hoboken, a merchant in the Avenue du Commerce here.
My parents were dead; I had but one brother, Victor Gabion, to whose
brother officer Lucien I had been betrothed by them, and whom I had
known from his early boyhood, when we had been playmates together, and
before we came to those restrictions in intercourse peculiar to French and
Belgian society in later years.
'We had learned to love each other very much, Lucien and I, though
now we could only see each other at given times, and always in presence of
a third party; and each time I seemed to discover some fresh trait in his
disposition which rendered him more worthy of love and more worthy of
the tenderest affection.
'He was so handsome, my Lucien, so kind, so tender; and so good, so

religious and true! He had that dark southern beauty which makes a man so
attractive to a fair woman, and, moreover, he possessed that charm which is
more attractive and dangerous still—he was interesting.'
Alison thought of her own fiancée, Bevil Goring, and believed she
could understand all this to the fullest extent.
'His means were ample and his position good, for, apart from his rank in
the artillery, he was the representative of the Volcarts, one of the seven
Families Patriciennes d'Anvers, whose seven coats-of-arms, all bearing a
fesse checky you may see at this hour carved in the ancient Steyne of
Antwerp. But why think of or boast of such things, when life, we are told, is
but a dream, and often a very painful and feverish one!
'I have told you that I was educated in the convent at Bruges with
English girls and English ladies. Hence I picked up among them some of
that genuine and honest freedom of action which they understood and
enjoyed; so when my betrothal to Lucien was fully known, and even the
time of our marriage stated, we contrived to have more than one pleasant
meeting unknown to my grim guardian, M. Hoboken, whose absorption in
business, and often long absence at the Bassin du Kattendyk, and even at
Flushing, afforded us facilities we could not otherwise have had.
'But in all this there was a dire fatality, and I shall never forget the day
that brought it about.
'M. Hoboken was to be absent at Flushing for two days, and madame
was an invalid—unable to go abroad. I met Lucien by appointment in one
of the solitary walks, in the quiet park near the Avenue du Commerce, with
a gift I had procured for him, when within a week of our marriage.
'"Look what I have brought for you!" said I, as I opened a morocco case
containing an armlet of silver, like an Indian bangle—you know what I
mean—flat and broad, and closed by a spring lock. In raised letters on the
outside was my name, Alison, with the date of our coming marriage.
'"You are my prisoner already," said I, laughingly, as I fitted the band

round his wrist, and the spring closed with a snap, thus it could neither fall
off nor pass over his hand.
'"My dear love!" he exclaimed, and pressed me passionately to his

breast.
'"Now, you are most completely mine," I whispered; "fettered for life—
as without my aid you can never get it off."
'"Why?"
'"Because I shall keep the key," said I, and coquettishly dropped it into
my bosom.
'"Even as you have the key to my heart," he added,
'After a pause he said,
'"M. Hoboken is still at Flushing?"
'"Yes—and does not return till to-morrow."
'"Très bien!" said Lucien, "by what hour, at the utmost, may Madame
Hoboken miss you—or require you?"
'"By seven certainly, and she supposes me to be at the Beguinage—and

so will ask no questions, to put me in a false position."
'"Seven—it wants eight hours of that time. See, Lisette, how lovely the
day is— how bright the sun, and how beautiful the white and pink hawthorn
that load the air with fragrance."
'"Well, what of that?"

'"Does not such a day make you long to leave dusty Antwerp behind
you, and to roam in the country?"
'"It does indeed; but I dare not think of such a thing—till—till next
week," I replied, coyly.
'"Lisette," said he, "were you ever at the village of Elewyt, where the
old château of Rubens stands, between Malines and Vilvorde? It is a lovely
place, and wild as lovely; not a soul would see us there. Come with me,
darling, and let us spend one happy day together."
'"I dare not—I dare not," as a vision of Madame Hoboken, grim, prim,
and full of proprieties, oppressed me, though I was secretly overwhelmed
with delight at the suggestion of this stolen and, to me, new kind of pleasure
—a whole beautiful summer afternoon to be spent hand in hand with
Lucien—hand in hand, as we were wont to be when children in the Place
Verte or on the Boulevards.
'"Come with me, sweet one," he whispered, "it will never—can never be
known. It is less than an hour by railway, and, amid the bosky thickets and
gardens of the old château we shall seem to leave the world behind us."
'So strong was the temptation to spend an untrammelled afternoon with

my betrothed—he who within a week was to be my husband—that I
yielded. I knew that I ran a dreadful risk in being seen alone with him, for
Antwerp is one of the most scandalous and gossipy towns in Belgium. In
this country the rules are very strict as regards the daily intercourse of ladies
and gentlemen, in the mere matters of meeting or conversing, as compared
with you in England, where the perfect freedom of the innocent is so great;
and hence, I doubt not, your happier marriages; for in Belgium, as in
France, we are forced to espouse those to whose inner lives we are
strangers, and to whose hearts, before marriage, we can have no key, if it is
ever found at all.
'A voiture took us to the train, and we took seats in separate carriages.
Already the simple, child-like expedition had an air of guilt, and a
tremulous fear possessed me as the train glided out of the station, through a
cutting in the fortifications at the Rue du Rempart—the wet fosse was left
behind, and we sped through the open country.
'Glorious was the summer day; exhaled by heat, the silvery mist was
curling up from the rich pastures, amid which the drowsy cattle stood knee-
deep, and from the fertile arable lands, over which the giant sails of the
windmills cast their shadows; but my heart—now that I was alone, though
separated from Lucien by only a carriage or two—sank lower and lower
with vague apprehension, and I restrained my tears with difficulty. I was
full of terrors, scruples, and fears an English girl, circumstanced as I was,
would fail to comprehend, and after traversing miles of dairy farms, where
the summer breeze played so sweetly on the long ripples of verdant grass,
we reached the little roadside station, where a path diverged to Elewyt. I
gathered courage when Lucien Volcarts joined me, and we found ourselves
indeed alone, for we were the only persons who quitted the train, which
steamed slowly—as all Belgian trains do—on its way to Vilvorde, and our
short but delicious day of rambling and planning, scheming and dreaming
out our future, hand clasped in hand, began.
'We saw the old château of Rubens, now falling fast to decay, amid its
trees, on the land of which he was seigneur, but we did not go near it, and
contented ourselves with wandering amid the sylvan scenery, all of which
had the charm of extreme novelty to me. The birds that flew overhead or
sung in the hedgerows; the thickets of beech and oak, casting shadows over
pools where the trout rose to catch the floating fly; the white, waxen-like
lilies floating also on their surface; a little stream pouring slowly between
gravel banks and sandstone rocks; deep water-cuts in which the Cuyp-like
cattle stood midleg for coolness; the quaint cottages, few and far apart; the
carillons playing in a distant spire, were all sources of delight to me—
delight all the more that I could turn from them ever and anon to look into
the tender and loving eyes of Lucien.
'At one of the cottages, which quite approached the dignity of a small
farm, we got some refreshment—bread, milk, and cheese—just as we had
been wont to do when children in charge of the same bonne, and the
recollection of that made us laugh and all the more enjoy such simple fare;
and truth to tell, though so near our marriage day, in the freedom of the hour
we felt very much as if we were happy children again; and long we lingered
in one spot, I remember, on a grassy bank under a bower of hawthorn,
where the flies buzzed and the bees hummed, and the village bells rang
softly out, but now it was their evening chime.
'Evening—that suggested thoughts of home and the necessity for

returning, and we had some miles to walk to the railway-station at Elewyt.
'"It is only five, dearest Lisette," urged Lucien, looking at his watch;
"and the train, which deposits us at Antwerp, is not due for an hour yet. In a
little time we shall go, petite."
'The die was cast, for a day of pleasure but marred by secret fears. I was
content to remain a little longer, and then we set out for the station. More
than once did my apprehensive heart, full of undefined forebodings, suggest
the sound of a coming train upon the air, and once, perhaps, it was real, for,
on reaching the hamlet of Elewyt, we found the station-gate shut and the
platform untenanted.
'Lucien looked at his watch and grew pale. The hands still stood at five
o'clock—it was now past seven, the hour at which I should have been at
Madame Hoboken's, and the last train had gone some minutes before.
'"Gone!" replied Lucien, in a bewildered tone, to his informant; "and the

next?"
"'Not till seven to-morrow morning—from Brussels viâ Vilvorde."
'Both of us were filled with dire dismay as we heard this. Could a

voiture, a vehicle of any kind, be procured? Alas! there was not such a thing
at Elewyt.
'We turned away with sickening hearts, and I must own that mine died
within me. How was I ever to face grim and grave Madame Hoboken? I felt
as if I had committed a terrible crime; I shed the bitterest tears, and I cannot
tell you, here at least, how sweetly Lucien strove to console and soothe me.
'"I must find you shelter for the night at yonder cottage, where we got
the milk, till train time to-morrow," said Lucien; "for myself, I must find it
where I may. Come, petite, take courage; a little time, and we shall be
blessedly independent of everyone."
'On seeing Lucien's well-filled purse, the woman at the cottage was
willing enough to accommodate us, especially on learning that we had lost
the train; but she filled me with fresh dismay on informing me, with a
cunning and penetrating glance there was no mistaking, that she had "but
one chambre à coucher, which she sometimes let to passing English people
and others who wished to avoid strangers; and you, monsieur——"
'"Oh! I will sleep in the stable, or anywhere, madame, provided you can
accommodate mademoiselle ma sœur," interrupted Lucien, colouring at the
necessary falsehood which he told for the first time in all his blameless life,
but it was one to protect me.
'Whether the landlady believed him or not I cannot say; but there was a
strange and saucy twinkle in her eyes, and while in attendance upon us she
provoked me by an air of discretion she adopted; from past experience
apparently she was far too discreet to make sudden irruptions on our tête-à-
tête evening, however innocent it was, in outward seeming as she no doubt
thought, and Lucien twisted his dark moustache angrily, as he muttered,
'"Sapristi! this hag does not live mid-way between Brussels and
Antwerp for nothing."
'"Darkness must be closing over Antwerp now, and all the lamps in the
Avenue du Commerce will be lighted throughout its spacious length and
breadth," was then my thought; "what would Madame Hoboken be thinking
and saying of my non-appearance? Had Monsieur Hoboken returned by
train from Flushing? Doubtless he had. Where would they be anxiously and
angrily suspecting I was?" If they supposed me to be remaining—as I had
more than once done if a night proved wet—when visiting here at the
Beguinage all would be well; but the morning might ere long produce
untoward revelations, and I wept as if my heart would break when once
again I was left alone, as my poor Lucien betook him to sleep in a loft
above the stables, deploring the malheur in which he had involved us both;
but he had no one to scold him save his colonel if he missed a parade, while
my life and whole future might be made a burden to me.
'Anyway, I was, from a Belgian point of view especially, in a dreadfully

false position. 'There could have been no mistake as to the hour of the fatal
train, though all public clocks in Belgium strike the hour half an hour
beforehand, thus at half-past eleven the clock announced twelve; and
luckily for me Lucien was in plain clothes, not en grande tenue as he
usually was, with sword and epaulettes on; consequently he would be less
remarked, and fortunately the rain fell heavily that night, which might
account for my remaining for shelter at the Beguinage.
'When morning came my spirits rose a little, and I was up betimes to

meet the early train. How lovely looked the opening summer day. The grass
in the fields, the herbs and flowers in the gardens all glittered in the rays of
the sun, as if the dew that moistened them had been diamonds, and the tops
of the firs seemed edged with silver. A golden and purple glow filled all the
eastern sky, and between it and earth the vapours of night were floating.
The birds were awake, and the bees hummed and the butterflies flitted
about.
'To me the country seemed new and charming, and its continuity of
horizontal lines, each rising beyond the other to the level horizon, where in
the distance rose the spires of Antwerp, gave a sense of vastness and
novelty.
'In different carriages Lucien and I returned to the city. We parted with
but a glance at the station, and with a palpitating heart I sought my
temporary home in the Avenue du Commerce—my mind a prey to dire
misgivings, full of the stolen summer day at Elewyt, the lost train, the
cottage amid the pastures, and Madame Hoboken to be confronted!
'My innocent secret made a very coward of me. Never had I told a
falsehood, and I felt as if I would rather die than tell one now. I had done
nothing to be ashamed of, and yet the inferences were terrible, especially in
society constituted as it is in Belgium.

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NEPHROLOGY SECRETS, FOURTH EDITION ISBN: 978-0-323-47871-7

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Editing the fourth edition of Nephrology Secrets has been both

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Warren Kupin, MD Ravindra L. Mehta, MBBS, MD, DM, FACP, FASN

Paul M. Palevsky MD Michael V. Rocco, MD, MSCE

John R. Sedor, MD Matthew A. Sparks, MD, FASN, FNKF

54. Thin basement membrane nephropathy (TBMN) is a benign autosomal-dominant

1. How do patients with kidney disease typically present?

• Amyloidosis nephropathy and antiphospholipid

Term Meaning Significance

Table 2.1. Urine Dipstick Testing

In short, he had tumbled into a species of nullah or hollow, completely

A worse obstruction still was encountered at Ordah, where the water

When he struggled back to consciousness, and half raised himself out of

'Midnight—and they have been six hours on the march!'

He had been in a state of semi-unconsciousness for some two hours.

He made an attempt to stand, but all power of volition seemed to have

THE LOST ONE.

Above the mantelpiece, in a simple frame, hung an engraving from

Other ornaments—save a few flowers in a vase—the apartment had

'Where am I?' she said, faintly.

'No—child—it was several nights ago.'

'No, for doubtless he knew not where you were.'

'Oh, he will be dead—dead with terror!' wailed Alison. 'Am I in a

'No, child, in my house,' said the nun, sweetly.

'Your house?' queried Alison, with very open eyes.

'In the Beguinage, in the Rue Rouge.'

Nearly a fortnight passed before she began mentally to drift back to

The Beguines, we have said, are a religious order peculiar to Belgium,

They were among the few religious communities not suppressed by

Many writers ascribe the institution of the Beguines to St. Begga,

The novices are distinguished by a different costume, and those who

'Child, we know not his name—his address—even of his existence.'

Seeing that Alison was in a fever of impatience to hear tidings of her

'What—you know my name?'

'Yes, it is mine also.'

'How well you speak English,' said Alison.

'Because I was educated in the English convent at Bruges,' replied the

'Papa,' murmured Alison, in a choking voice, as she felt herself become

'Write!—is Lord Cadbury gone?' asked Alison, timidly and hopefully.

'Yes, back to London; he was telegraphed for.'

Alison gave a sigh of relief.

'Home—to where?' he asked.

Her reply was perfectly straightforward, though it again suggested ideas

NEPHROLOGY SECRETS, FOURTH EDITION ISBN: 978-0-323-47871-7