Morning Report

Chief Concern "I am here for diarrhea"

 • 42 year old woman with a history of recurrent
UTIs and nephrolithiasis who presents to the
hospital for a weeklong course of non-bloody
diarrhea and associated mild-moderate supra-
pubic abdominal pain. 
• She has also had nausea and non-bloody, non-
bilious clear emesis that has been improving. 
• Of note, she was prescribed antibiotics for a
previous urinary tract infection less than a
HPI month ago. She also received ceftriaxone
during a recent admission. Patient mentioned
that she has had recurrent UTIs despite
multiple antibiotic treatments.
• Reported prior to this admission a burning
sensation while urinating and flank pain.
However, dysuria had resolved. 
• Denies any subjective fever, chills, recent
travel, exposure to new foods or sick
individuals. 
 • PMH: Nephrolithiasis, Type II Diabetes
Mellitus, Hypertension, Rheumatoid
Arthritis, Asthma, Insomnia, Anxiety, and
Bipolar disorder
• PSH: LEEP (2010), D&C (4/2018) and 3 C-
sections (2011, 2013, 2015)
Past Medical • Medications: Montelukast, Fluticasone
History propionate / Salmeterol, Metformin,
Empagliflozin, Dulaglutide, Hydrochlorothi
azide, Amlodipine,Oxybutynin, Cephalexin
• Allergies: Amoxicillin [Hives reaction]
• Family History: CKD on Maternal side in
multiple family members. 
 SOCIAL DETERMINANTS OF HEALTH
​Economic Stability Neighborhood and Education Tobacco, EtOH, IDU Community and Health Care System
physical environment Social Context

Denies Alcohol. Lived in Michigan

10 pack year
Lives entire life. 
history. Quit 15 Iives
independently Lives at home with Graduated High years ago with family
without husband and her 3 school Smokes marijuana and has Molina Healthcare
economic children. immediate family
 insecurity 3 times per week.  in surrounding
Denied IVDU,
illicit drug use. area. 
What is our
Problem
Statement?
 • 42 year old female with a history of
nephrolithiasis, recurrent UTI, and repeated
antibiotic use who presents to the hospital for a
weeklong course of non-bloody diarrhea, N/V,
and associated mild-moderate supra-pubic
abdominal pain. 
• Recently was evaluated and told she may have a
stone in her kidney. 
• Last episode of diarrhea was this morning where
she had 5 episodes of runny stool.
HPI Refresher • Endorses nausea and non-bloody, non-bilious
clear emesis that has been improving. 
• Denies any fevers, chills, dysuria, burning
sensation while urinating, or flank pain. 
• Denies any recent travel, exposure to new foods,
or sick individuals.
• Recently received ceftriaxone and prescribed
antibiotics for urinary tract infection. Patient
mentions that she recurrent UTIs despite multiple
antibiotic treatments.
A middle-aged woman with a history
of nephrolithiasis, recurrent UTI, and
repeated antibiotic use, who presents
with subacute nausea, vomiting,
diarrhea and suprapubic pain
 Blood pressure: 146/87

HR: 76

Physical Exam - Temperature: 36.6OC

Vitals Respiratory Rate: 18

Saturation: 95% on room air. 

BMI: 57.6 (kg/m2)

 • General:  Alert and oriented.   Ambulation status: Assistive
devices ( Walker ).  Appearance: Morbidly obese.  Behavior:
Appropriate, Cooperative.  
• Eye:  Normal conjunctiva.  
• HENT:  Normocephalic, Atraumatic, Oral mucosa is moist.  
• Respiratory:  Lungs CTA bilaterally, No wheeze.  
• Cardiovascular:  Regular rate, Regular rhythm, S1
auscultated, S2 auscultated, No murmur, Normal peripheral
perfusion, No edema.  

Admitting • Gastrointestinal:  Normal bowel sounds, soft, distended,

mildly tender to palpation in suprapubic zone, normoactive

Physical Exam 
bowel sounds
• Genitourinary: Right CVA tenderness.
• Musculoskeletal: Normal range of motion.  Normal
strength.  No deformity.  Spine/torso exam Thoracic:
vertebrae level  thoracic, mild, tenderness. 
• Integumentary:  Warm, Intact.  
• Neurologic:  Alert, Oriented, Normal motor function, No
focal defects, numbness to the bottom of right foot
consistent with paresthesia .  
• Psychiatric:  Cooperative, Appropriate mood & affect,
Normal judgment.  
Differential
Diagnoses?
 • Nephrolithiasis
• Pyelonephritis
• Viral Gastroenteritis
Differential • CDI
Diagnosis • Medication-induced Diarrhea
• UTI
• Pancreatitis
 Labs
Mg – 1.7
Phos – 3.0
139 101 15
95 Ca – 8.3
3.9 30 1.15 AST – 54
ALT – 109
10.4 Lipase: 23 GGT - 21
8.3 312 ALP – 51
33.7
Alb – 3.1
MCV: 80.2  | RDW: 16.2 T. Bili – 0.48
Labs (cont)
• UA (5/8/23)
• Nitrite: negative
• LE: 3+ 
• rbcs: 2-5
• C. Diff Ag + Toxins A&B -
• Epithelial Cells: <5
Negative
• wbcs: 50-100
• Bacteria: 1+
• UCx (5/5/23): 
• >100k gram negative 
• E. Coli
 • CTAP 5/4
• Asymmetric left perinephric
stranding with subtle wedge-
shaped areas of hypoattenuation. 
Soft tissue stranding along the left
ureter.
• Non-obstructing staghorn calculus
Imaging in the lower pole the right kidney
measuring 1.5 cm.
• US Renal 5/9
• No hydronephrosis.
• 8 mm non- obstructing right lower
pole renal calculus.
• Hepatic steatosis.
 • Pyelonephritis due to non-
obstructing right renal pole
Final Diagnoses nephrolithiasis >8mm
• Medication-induced Diarrhea
 • Patient was admitted for Pyelonephritis
with nephrolithiasis and started on IV
Fluids and ceftriaxone
• Urology was consulted for management of
1.5cm nephrolithiasis. Renal US obtained
for hydronephrosis rule out
• Renal US resulted no hydronephrosis, i.e.
Hospital Course no obstruction and urology recommended
outpatient follow up after infection
resolved
• By day 3 of admission patient's symptoms
completely resolved and wanting to go
home
• Patient discharged with cefdinir with total
of 14 day course
Assessment And Plan
#Pyelonephritis likely due to seeding from non-obstructing 1.5cm nephrolithiasis at R inferior pole
• This patient originally arrived with suprapubic pain, N/V and has a history of recurrent urinary tract
infections without known etiology. On exam R CVA tenderness was present. Vitals were stable, although
she presented with fever during her previous admission. Together, this meets criteria for pyelonephritis.
• CT abdomen done on 05/05/23 shows 1.5 cm right sided struvite stone. UA this admission is suggestive
of active infection with 2+ leukocyte esterase, 50-100 WBCs, and microscopic hematuria; urine culture
from 05/05/23 grew e. coli. Given the unknown etiology of UTI's and presence of large stone, it is
possible that this kidney stone is acting as a source of infection.
• Kidney stone sizes of 1.5 cm do not pass on their own and may need urological evaluation; stones less
than 10 mm may respond to medical expulsive therapy with tamsulosin but larger stones may require
endoscopic stone fragmentation 
• Today, the patient is hemodynamically stable without pain. She was given 100cc/hr NS and encouraged to
drink plenty of water throughout the day. We repeated UA and urine culture and then started IV
ceftriaxone to cover for e.coli. After speaking with urology, repeat renal US was obtained to rule out
hydronephrosis. If there continues to be no sign of obstruction, urology will not intervene
Nephrolithiasis
• A 38-year-old man presents to the ED. He has three to four loose bowel movements
each day. He reports no fever, pain, or dysuria. He cannot remember his medications
but notes that one them 'helps me eat without having diarrhea' and a couple
of multivitamins.
• Physical examination and vital signs and the remainder of the examination are
unremarkable.

• What do you think is going on?

 • Common problem in the U.S
population
• An estimated 7-11% of the
Nephrolithiasis population will develop
nephrolithiasis.
• 50% will have recurrent disease
 • Age
• Diet – High animal protein, high
sodium, low dietary calcium
• Caucasian descent
• Diabetes Mellitus
Risk Factors • Obesity / Metabolic syndrome
• Chronic diarrhea 
• Malabsorptive disease
• History of bypass (Roux-en-Y)
 • 'Colicky' or flank pain
• Hematuria
• Absence of hematuria does not rule out
nephrolithiasis.
• Dysuria
Presenting • Nausea
Symptoms • Vomiting

• Symptoms develop as the stones pass from

the pelvis into the ureter.
• Site of obstruction plays in a role in
terms of presentation. As the stone
moves the site of pain may change
as well. 

Upper ureter/kidney
• Flank pain or tenderness

Lower ureter
• Groin pain – Testicular / labial pain

• Important note depending on the

site it may mimic a more serious
condition. 
 Important to note
Nephrolithiasis can be noted
incidentally during abdominal
imaging.
 • Calcium
• Oxalate
• Phosphate
• Struvite
Types of Stones • Uric Acid
• Cystine

• Calcium stones make up 80% of cases

of nephrolithiasis.
 • Most common type of kidney stone.
• It is associated with elevated urine
calcium levels. This is often idiopathic
in nature.
• Can be associated with several
conditions – HyperPTH,
Calcium Oxalate  Sarcoidosis, Cushing syndrome,
hyperthyroidism, and Paget
disease. 
• Associated with hyperoxaluria,
hypocitraturia, and low dietary
calcium.
 • Due to elevated urinary pH
• Associated with distal RTA and
hyperparathyroidism
Calcium Phosphate  • Use of carbonic anhydrase inhibitors
(acetazolamide or topiramate) raise
urine pH and decrease citrate
excretion. 
 • In metabolic acidosis, urine citrate,
an inhibitor of crystallization
is reduced.
• Chronic diarrhea, RTA syndromes
• Volume depletion decreased urine
volume and increases urinary calcium
Mechanism of and oxalate secretion. 
stone formation • In malabsorptive states calcium binds
to fat instead of oxalate leaving it
to be re-absorbed and excreted in the
urine. 
• Also seen in low dietary calcium
states. 
 • More likely to be formed in
women.
• Associated with neurogenic
Struvite bladder or chronic indwelling
catheter use.
• Commonly associated with UTI.
 • Urea splitting bacteria – Proteus,
Klebsiella, and Pseudomonas. 
Mechanism of • Urea is split into ammonium
which precipitates into magnesium
stone formation ammonium phosphate stones
(struvite). 
 • Kidney obstruction.
• Infection.
• Acute or Chronic Kidney Injury.
Complications
• Persistent infection leads to
parenchymal injury, focal
scarring, and loss of cortex. 
 • Uncommon, representing less
than 10% of stones. 
• Associated with low urine pH
(acidic urine) which decreases
solubility. 
Uric Acid • Associated with increase urine
acid formation (think gout!).
• Although associated,
hyperuricosuria is not required. 
• Volume depletion is the most
common cause. 
 • Least common stone (1-2%).
• Due to cystinuria, an autosomal recessive
condition. 

• Mechanism of action
• Decreased proximal tubular re-absorption
Cystine  of filtered cystine which results in
increased urinary excretion and stone
precipitation. 

• Not to be confused with homocystinuria! (A

disorder with cystathionine beta synthase and
methionine).
 • What laboratory or imaging
Diagnosis studies would you order and
why?
 • Basic metabolic panel.
• Urinalysis with microscopic exam.
• CT-Abdomen / Pelvis without
Diagnostics contrast. 
• Ultrasound of kidney/bladder is an
available alternative. 
 Pain control

Management 

Stone passage
or removal
 • NSAIDs are first line.
• Toradol 
Pain control • Opioids can be utilized for those
who do not achieve adequate
pain control.
For stone passage, what is the range where stones are expected to
resolve spontaneously?

And those that require intervention?

 • 5mm and 10mm
• Stones < 5mm are likely to
pass spontaneously. 
Stone passage • Approximately only 50% of
stones > 6mm will pass. 
• Stones > 10mm very unlikely
to pass spontaneously.
 • Alpha blockers – Tamsulosin 
• Up to 4 weeks
Medical • Calcium channel blockers –
Nifedipine
management
• Allopurinol
 • Indicated for any patients with:
• UTI
Urologic • AKI
Intervention • Stones > 10 mm.
• Lithotripsy
• Percutaneous nephrolithotomy
 If there are signs of
infection, what antibiotics
would you use to treat?
 • Cystitis
• First line agents 
• Nitrofurantoin - 100mg BID; 5
days for women, 7 days
for males
UTI • Fosfomycin – 3g PO one
time only. 
• Trimethoprim-
Sulfamethoxazole (DS
800/160mg) - 1 tab  BID for
7 days
 • Pyelonephritis 
• Fluoroquinolones 
• Ciprofloxacin 500mg PO BID
for 7 days 
• Levofloxacin 750mg PO
Pyelonephritis  daily for 7 days 
• Additional options 
• Trimethoprim-
Sulfamethoxazole 
• Third generation cephalosporin
• Severe sepsis or history of MDR?
• Cefepime / Piperacillin – Tazobactam
• ESBL?
• Meropenem or Imipenem
 • Absence of pain does not indicate
complete stone passage.
• If a patient passes their stone, they
should be instructed to keep the stone
Follow up and bring it in for analysis. 
• If imaging is required, the ideal is
modality for follow up is an
ultrasound. 
 • Emphasize importance of proper
hydration!
• This is important regardless
Prevention of stone composition
• Dietary adjustments as
necessary.
 • Prevention of nephrolithiasis via
lifestyle modifications: Hydration,
dietary adjustments
• In those symptomatic, the goals
are pain management and
Take Home Points determining intervention
depending on stone size
• The golden numbers are 5 and
10
• A 38-year-old man is evaluated after passing Calcium – 8.5 mg/dL
his second kidney stone. History is significant Creatinine – 0.7 mg/dL
for chronic pancreatitis secondary to a history
of alcohol abuse. He has three to four loose Electrolytes
bowel movements each day. He reports no Sodium – 137 mEq/L
fever, flank pain, or dysuria. There is no family Potassium – 3.5 mEq/L
history of kidney disease, Chloride – 104 mEq/L
hyperparathyroidism, or nephrolithiasis.
Bicarbonate – 21 mEq/L
Current medications are pancreatic enzymes
and multivitamins.
Urinalysis – pH 5.0; negative dipstick. Positive for
• Physical examination and vital signs and the calcium oxalate crystals. 
remainder of the examination are
unremarkable.

In addition to increasing fluid intake, which of the following is the most appropriate management?
A) Add allopurinol
B) Add potassium citrate
C) Add vitamin C
D) Decrease calcium intake
E) Increase protein intake
B) Potassium citrate
• In addition to increasing fluid intake, potassium citrate is appropriate to prevent future calcium
oxalate stones in this patient. Patients with chronic diarrhea and malabsorption are at increased
risk for forming calcium oxalate stones for three reasons. First, because of the diarrhea and
concomitant metabolic acidosis, urine citrate, an inhibitor of crystallization, is often reduced. In
addition, volume depletion from the diarrhea decreases urine volume and thus increases the
concentration of calcium and oxalate in the urine. Finally, in malabsorption, especially fat
malabsorption as occurs in chronic pancreatitis, enteric calcium binds to fat as opposed to
oxalate, leaving oxalate free to be absorbed and excreted in the urine. Although treatment should
be based on the metabolic evaluation in this patient, his low urine pH and low serum bicarbonate
level suggest that he has metabolic acidosis. Decreased systemic pH lowers urine citrate
excretion. Supplementation with citrate as a base equivalent will help correct the acidosis and
increase urine citrate, bind urinary calcium, and decrease the formation of calcium oxalate stones.
Thank you
References
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H1547961445
 
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