APPROACH TO PATIENT WITH DISEASES OF THE

KIDNEY AND URINARY TRACT

Marie Fe A. Vergara- Lim Dy, MD
February 20, 2014; 1:00-3:00 PM
Internal Medicine
4, 2014, 3:00-5:00
PM
10 February
KIDNEY DISEASE
SYNDROMES

Acute and Rapidly Progressive Renal Failure

Pediatrics

Acute Nephritis
Chronic Renal Failure
Nephrotic Syndrome
Asymptomatic Urinary Abnormalities
Urinary Tract Infection

Renal Tubule Defects

Hypertension
Nephrolithiasis
Urinary Tract Obstruction
Kidney Disease Syndromes are mostly
secondary complications to other diseases.

Function of the Kidney

Manifold tasks of the kidney

Your kidney is responsible for the removal of metabolic end product such as BUN, creatinine and other toxins.
The kidney also functions to balance your water that maintains electrolyte balance that is important in blood
pressure control.
Also, the kidney is the site for vitamin D activation and Calcium balance thus involves in the bone structure. It is
responsible for excretion of phosphorus.
It has a function to maintain normal acid balance. Excretion of hydrogen and reabsorption of bicarbonate.
Last but not the least, it produces erythropoietin that is important in the formation of red blood cells.

Kidneys are able to do this function through the process of glomerular filtration in the glomerulus, tubular reabsorption and
secretion. Blood is delivered in the aorta t0 renal arteries down to afferent arterioles then enter to glomerular arteries.
Glomerular capillaries will produce ultrafiltrate of plasma devoid of large molecules. Blood and other molecules will go back to
main circulation through efferent arterioles. Ultrafiltrate of the plasma that is formed will go to the glomerulus to the tubules.
Inside the tubules, there will be reabsorption, secretion of water, electrolyte and formation of urine. Once urine is formed it will
pass through the renal pelvis, down to the ureter, urinary bladder and out in the urethra. Any disturbances along the way, as
well as the abnormality in the anatomy of the renal vessels, glomerulus, renal tubules, tubulo-interstitium, urinary tract will
result in the sign and symptoms of your kidney patients. When you combined the symptoms, you will be able to identify your
renal syndromes.

1. ACUTE & RAPIDLY PROGRESSIVE RENAL FAILURE (ARF/RPRF)

It is the decline in glomerular filtration rate (GFR)
happens over days (ARF) or weeks (RPRF)
Acute Renal Failure: Maximum of 12 weeks
Reversible
Chronic Renal failure: >12 weeks
Progressive renal disease
CLINICAL CLUES FOR ARF/RPRF
Anuria or oliguria
Uremia of recent onset
Azotemia (Increased BUN & Creatinine)
Symptoms (Abdominal pain, decreased in
sensorium, pruritus, gastritis)
Alteration of sleep-wake cycle
Edema
Hypertension
Electrolyte imbalances
Urinary sediments
Causes of AKI:

Transcriber/s:RemirrNolasco& Charles Obdianela

Formatting: Jun-jun Mendoza
Editor: Marie Mae Pantolla

Acute tubular necrosis

Urinary Obstruction
Nephrotoxins
Causes of RPRF:
Vasculitis
Crescentic GN
HUS
Malignant nephrosclerosis
Cryoglobulinemia
RIFLE
Used to evaluate ARF
Risk of renal dysfunction
Injury to the kidney
Failure of kidney function
Loss of kidney function
End stage kidney disease (ESKD)

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 Creatinine value and Urine output are used as a basis to classify in which the patients belong.
Case: 42 female hypertensive. 2 months ago her serum Creatinine level was 74 (Normal level: up to 111-120). She
then returned to the clinic presenting with 1 week history of diarrhea and a current serum Creatinine level of 110.
From 74 to 110, her creatinine increased by >25% = RISK of Kidney failure
HINDI PURKET NORMAL EH NORMAL Dr. Lim
Normal Urine Output: 1-2cc/kg/hour
Minimal urine output that could still maintain Kidney function: 400mL
Oliguria = <400Ml
CAUSES OF ACUTE RENAL FAILURE
Prerenal
Above the level of the Kidney
Sudden and severe drop in blood pressure(shock) or interruption of blood flow to the kidneys from severe
injury or illness
Hypovolemia, Septic shock, cardiogenic shock, heart failure
Intrarenal
Direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply
Acute GN, tubules & interstitial diseases, sepsis and nephrotoxins
Postrenal
Sudden obstructionof urine flow due to enlarged prostate, kidney stones, bladder tumor, or injury
Obstruction in a solitary kidney
LABORATORY FINDINGS IN ACUTE RENAL FAILURE

In prerenal, kidneys are intact less blood flow/

volume entering the kidney more concentrated urine
(urine osmolality is more than 500). There is also sodium
retention that will result to urine sodium concentration
of less than 20 and greater BUN/ Crea ratio.
Transcriber/s:RemirrNolasco& Charles Obdianela
Formatting: Jun-jun Mendoza
Editor: Marie Mae Pantolla

Diagnostics
Urinalysis
GFR
BUN
Serum Creatinine
Neutrophil gelatinase associated lipocalin
(NGAL)
Renal tubules will produce Urinary
NGAL (usually increases after 2 hr of
injury, first to increase)
Normal NGAL is 300 400

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2. ACUTE NEPHRITIS (AGN & ATIN)

a. ACUTE GLOMERULONEPHRITIS (AGN)
Primarily affects the glomeruli but to a lesser
extent the renal tubules may also be involved
Immune-mediated inflammation of the
glomerulus
Primary vs. secondary
Damage to the glomerular wall allowing RBC and
plasma cells to enter the urinary space and into
the urine
Clinical Presentation:
Acute reduction in GFR similar to AKI
(associated with RPGN)
Nephritic Urinary Sediments:
Masyadongmadumi ang urine because
of the urinary sediments
Hematuria
RBC casts
Proteinuria
Volume expansion
Hypertension
Pulmonary congestion
Facial or peripheral edema

RBC casts denote glomerulonephritis

POST-STREPTOCOCCAL GN
Prototype of AGN
Infection with GAS brings about immune complex
deposition in the glomerular capillary membrane
Induces intense yet transient inflammatory
process
GFR falls but return to normal within weeks or
months
Good prognosis in children
Based on Dr.Limss experience: 2 out of 10 recover
completely some of them developed Chronic Kidney
Disease after illness especially in elderly.
OTHER CAUSES OF AGN
After bacterial or viral infections
Lupus nephritis
MPGN
HSP
IgA nephritis or Bergers Disease

Dysmorphic red cells

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Formatting: Jun-jun Mendoza
Editor: Marie Mae Pantolla

RENAL BIOPSY
Since we cant differentiate clinically via history, we
have to perform a biopsy.
Required for a definitive diagnosis and to
determine whether ARF/RPRF exists
Proliferative GN often with extracapillary crescent
formation
Treatment and prognosis depend on the definite
histologic pattern and types on immune complex and
immunoglobulins are deposited in the renal tissue

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b. ACUTE TUBULOINTERSTITIAL NEPHRITIS

Inflammation limited to the renal interstitium
Evidence of tubule cell injury : Electrolyte and
water imbalances
Hematuria, RBC casts, reduction in GFR, lesser
proteinuria compared to AGN
Leukocyturia (eosinophiluria) with peripheral
blood eosinophilia are common

Example of crescent formation in the glomerulus

CAUSES OF ACUTE TUBULOINTERSTITIAL NEPHRITIS (ATIN)
INFECTIONS
DRUGS
METABOLIC CAUSES
Bacterial:
Analgesic Nephropathy
Hypokalemia
Acute Pyelonephritis
Lithium Nephropathy
Hypercalcemia nephropathy
Rocky Mountain Spotted
Urate nephropathy
Fever
Oxalate Nephropathy

OTHER CAUSES
Heavy metals
Reflux nephropathy
Obstructive
nephropathy
Neoplastic diseases

Viral:
Cytomegalovirus
CLINICAL FEATURES OF ACUTE DRUG-INDUCED TIN
SIGNS AND SYMPTOMS
LABORATORY FINDINGS
Fever (85-100%)
Hematuria (95%)
Maculopapular Rash (25Eosinophilia (80%)
50%)
Sterile pyuria
Arthralgias
Low-grade proteinuria
Uremic Symptoms
Eosinophiluria
WBC casts

3. CHRONIC KIDNEY DISEASE

Progressive and irreversible destruction of
nephrons resulting in reduction in GFR for at least
3-6 months regardless of cause
Proofs of Chronicity
Bilaterally small kidneys
Renal osteodystrophy
Symptoms of uremia
Broad casts on urinalysis
Nonspecific evidences of Chronicity in renal
failure
Also present in AKI
Anemia
Hyperphosphatemia
Hypocalcemia
Proteinuria
Pagtinanongkangpasyente: Doc ano pong chances
nagagaling pa angasawako?, the proper answer would be
HINDI NA PO

CLINICAL FEATURES
Dermal: Pruritus, easy bruisability, edema
CVS: Dyspnea on exertion, retrosternal pain
on inspiration (pericarditis)
GIT: Anorexia, nausea, vomiting
GUT: Nocturia, oliguria, impotence
Neuromuscular: Restless legs, irritability,
inability to concentrate, insomnia,
decreased libido
INSOMNIA is the first clinical symptom,
alteration in sleeping pattern could be an early
sign of CKD
PE Findings
General: Sallow, debilitated appearance
Dermal: Pallor, ecchymoses, excoriations,
edema, xerosis
HEENT: Uriniferous breath
Pulmonary: Rales, pleural effusion
CVS: Hypertension, flow murmur or
pericardial friction rub, cardiomegaly
Neurologic: Stupor, asterixis, myoclonus,
neuropathy

Broad casts
Transcriber/s:RemirrNolasco& Charles Obdianela
Formatting: Jun-jun Mendoza
Editor: Marie Mae Pantolla

DLSHSI Medicine Batch 2016|4

 Common causes of acute deterioration of renal

function:
Volume depletion
Urinary tract obstruction
Drug-induces nephrotoxicity
Exacerbation of underlying renal disease
AKI is reversible
CKD is non-reversible
Diabetics lose hope -> take herbal meds ->
exacerbate further kidney diseases because they are
avoiding medications -> Kidney failure accelerates

MANAGEMENT OF CKD IS STAGE DEPENDENT

STAGE 1
GFR = <90-60
STAGE 2
GFR = 60-45
STAGE 3
GFR = 45-30
STAGE 4
GFR = 29-15
STAGE 5
GFR = <15
needs renal replacement
AKI ON TOP OF CKD (NICE TO KNOW!)
The acute component of the renal failure must be
evaluated as this is potentially reversible

4. NEPHROTIC SYNDROME
Massive proteinuria alone has come to define the
syndrome, since this finding connotes a serious
renal disease whether or not the protein losses
lead to hypoalbuminemia, lipid disturbances, or
edema
Hypercholesterolemia (> 200 mg/dl)
Hypoalbuminemia (< 3.5 g/dl)
Edema and anasarca
Lipiduria
Proteinuria of >3.5g/1.73 m2 surface area/ 24
hours of mainly albumin
Mnemonic: HHELP

PRIMARY NEPHROTIC
SYNDROME
Orthostatic or postural
proteinuria (benign)
Membranous
glomerulonephritis
Idiopathic MPGN
FSGS
IgA nephropathy
MCD
Proliferative GN

CAUSES OF NEPHROTIC SYNDROME

Minimal Change Disease
Idiopathic Membranous glomerulopathy
Focal and Segmental Glomerulosclerosis
Diabetic nephropathy
CLINICAL FEATURES
Edema, anasarca leading to dyspnea
Urine contains fewer cellular elements
Acute changes in GFR and urine volume are
uncommon
Hematuria, invariable
SECONDARY NEPHROTIC SYNDROME

Hereditary-familial
Autoimmune
Infectious
Drug-induced
Neoplastic

DM, Alports syndrome, sickle cell disease (DM: no.1

cause in the Philippines)
SLE, Goodpastures syndrome, Wegeners
granulomatosis, PAN, RA
Postinfectious GN, endocarditis, hepatitis B
NSAIDs, heroin, gold, Hg
Hodgkins disease, lymphomas, leukemia, MM

Evaluation of proteinuria
Patient with (+) protein in urine, you can request for 24 hr excretion of protein and creatinine or spot check of
BUN/crea ratio.
Microalbuminuria: less than 300mg, you can consider early DM, essential HTN, early stage of GN.
Macroalbuminuria: 300mg 3.5 g + cast in urine can be due to myeloma associated with kidney, CHF,
fever or exercise.
Nephrotic range proteinuria: consider DM, amyloidosis, late stage of minimal change disease, FSGS and
membranous

5. ASYMPTOMATIC URINARY ABNORMALITIES

Mild hematuria, pyuria, and cast or subnephrotic
proteinuria with no evidence of other
nephrologic syndromes
ISOLATED HEMATURIA
Is clue to:
Neoplasm (especially old patients)
Stone, infection in any part of the urinary
tract
Analgesic and sickle cell nephropathies
Transcriber/s:RemirrNolasco& Charles Obdianela
Formatting: Jun-jun Mendoza
Editor: Marie Mae Pantolla

Diagnostics that must be used:

IVP
Cystoscopy
Renal arteriography
Investigate before diagnosing asymptomatic
urinary abnormality
Nephronalhematuria
Urinary casts contains RBC or Hgb pigment
indicating damage to the nephron
Vehicular accident

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 Nephronalhematuria with proteinuria

Suggests a worse prognosis with high
tendency to progress to chronic renal failure
ISOLATED PROTEINURIA
Indicates little or no inflammatory reaction within
the glomeruli (DM, amyloidosis)
PYURIA (LEUKOCYTURIA)
Usually reflect infection and inflammation of the
lower urinary tract rather than parenchymal renal
disease
May be present in TIN, Lupus nephritis,
pyelonephritis, renal transplant rejection
WBC cast establishes the kidney as the site of
inflammation
Causes Sterile Pyuria:
Recent bacterial urinary infection being
treated with antibiotics
Glucocorticoid therapy

Acute febrile episodes

Cyclophosphamide administration
Pregnancy
GU trauma
Prostatitis and cystourethritis
All forms of TIN
2 weeks gap between antibiotics
Urine culture: Gold standard for UTI
Sterile pyuria can mean UTI
TB patients: Request urine AFB in 5 different urine
collections

PERSISTENT STERILE PYURIA

Unusual infections
TB (common cause in the PH)
Fungi
Atypical mycobacteria
Haemophilusinfluenzae
Anaerobic or fastidious bacteria

6. URINARY TRACT INFECTION

Demonstration in urine of pathogenic organism
Bacterial colony counts >105 organisms/ml
urine
> 102(100) colonies/mL in symptomatic
patients and urine obtained by suprapubic
aspiration or bladder catheterization
Kahit 100 CFU lang, pwedenamag start
ang treatment. DO NOT wait for it to
reach 105CFU.
CLINICAL MANIFESTATIONS as to site of involvement
Bladder & Urethral Inflammation
Dysuria, frequency, urgency and
suprapubic tenderness
Prostatitis
Frequency, dysuria, urgency with
prostate that is boggy and tender
Renal Parenchymal Infection:
Flank pain, chills, fever, nausea and
vomiting, hypotension from sepsis and
leukocyte casts

WHO ARE AT RISK FOR UTI?

Gender
Female due to anatomic reasons (shorter
urethra)
50 60% adult women report that they have
had UTI (>2x/yr = recurrent)
Affects 1-3% of female school children
Sexual intercourse 3x a week is associated
with 2.6 times greater risk of UTI
Pregnancy
Abnormality in the urinary tract due to:
Enlarged prostate (>40yrs old:NPH)
Stones
Vesicoureteral reflux
Neurogenic bladder
Immunocompromised state
Diabetes
Patients taking immunosuppressant
Indwelling catheter
RECURRENT UTI
Episodes of acute uncomplicated cystitis
documented by urine culture occurring >2x/year
in a non-pregnant woman with no known urinary
tract abnormality.
DIAGNOSTIC TEST

WBC cast
SIGNS AND SYMPTOMS
Upper Tract (Systemic)
Fever,chills, flank pains, CVA tenderness,
nausea and vomiting
Lower Tract (Localized)
Dysuria, frequency, urgency, gross
hematuria or hypogastric pain

Urinalysis
Dipstick for
leukocyte
esterase and
nitrates
Urine Gram
stain and
Culture with
sensitivity
Blood culture

ACUTE
CYSTITIS
YES
(if with signs
of vaginal
discharge or
irritation)
YES
(if no
response
after 3 days of
antibiotic)
NO

ACUTE
PYELONEPHRITIS
YES
(pyuria>5 wbc/hpf of
centrifuged urine)

YES
(>10,000cfu/mL)

YES if with sepsis

There is no need for urinalysis if it fit UTI symptoms. TREAT NA AGAD.

However, if patients present with vaginal discharge, Urinalysis is needed.

Transcriber/s:RemirrNolasco& Charles Obdianela

Formatting: Jun-jun Mendoza
Editor: Marie Mae Pantolla

DLSHSI Medicine Batch 2016|6

7. RENAL TUBULE DEFECTS

This syndrome encompasses a large number of
acquired and hereditary disorders, all of which
tend to affect renal tubules more than glomeruli
Impairment of secretion and/or reabsorption of
electrolytes and organic solutes and limit urinary
concentrating and diluting ability
Polyuria, nocturia, metabolic acidosis, and various
disorders of the fluid and electrolyte balance
HEREDITARY ANATOMIC DEFECTS
Polycystic kidney disease (PCKD), medullary
cystic disease and medullary sponge kidney
Hematuria, bacteriuria, flank pain, or unexplained
azotemia
Detected by ultrasonography of intravenous
pyelography

PCKD = most common hereditary kidney

anatomic defect
TUBULE TRANSPORT DYSFUNCTION
3 Patterns of Renal Dysfunction:
Proximal Tubular Dysfunction
RTA type II w/ or w/o Fanconis
syndrome
Distal Tubular Dysfunction
RTA type I
Salt wasting or
Hyperkalemia
Renal Medullary Dysfunction
Decreased concentrating ability with
polyuria & nocturia
RTA Type I and II are commonly found in
children

8. HYPERTENSION
Blood pressure > 140/90 on 2 separate office visits
JNC VII CLASSIFICATION

BP Classification
Normal
Pre-hypertension
Stage 1
Stage 2

Systolic BP (mm Hg)

<120
120-139
140-159
>160

Diastolic BP (mm Hg)

<80
80-89
90-99
>100

9. NEPHROLITHIASIS
Definite Diagnosis:
Passage of stone
Visualization by x-ray
Removed by surgery or cystoscopy
CT Stonogram is most useful in the
diagnosis
Suggestive of Diagnosis:
Renal colic
Painful hematuria
Unexplained pyuria, dysuria and frequency

Composition of Renal Stones

Calcium
Uric Acid
Cystine
Struvite

All are radiopaque except for uric acid

stones and are visible in routine
abdominal radiography.
Stones 0.4cm in size may pass freely in the tubules.
If more than that, if will be difficult to excrete it.
1 cm size of stone may need surgical removal

10. URINARY TRACT OBSTRUCTION

Anuria
In adults, almost always due to obstruction
of the bladder outflow
Blockage of upper urinary drainage from
both kidneys or from a solitary functioning
kidney
Bladder Outflow Obstruction
Large bladder after voiding
Nocturia, frequency, overflow incontinence,
slowing or hesitancy of micturition
Urethral stricture, tumor, stone, neurogenic
causes, prostatic hypertrophy
Upper Tract Obstruction

Transcriber/s:RemirrNolasco& Charles Obdianela

Formatting: Jun-jun Mendoza
Editor: Marie Mae Pantolla

Few symptoms especially when obstruction

is incomplete and unilateral
Normal volume of urine or even increased
because of defect in the renal concentrating
function
Urinary Tract Obstruction
Urinary Stasis secondary to obstruction
predisposes to recurrent urinary tract
infection.
Chronic urinary obstruction predisposes to
progressive loss of renal function

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Common Mechanical Causes of Urinary Tract Obstruction

Ureter
Bladder Outlet
Congenital

Ureteropelvic junction narrowing or

obstruction

Ureterovesical junction narrowing or

obstruction

and reflux

Ureterocele

Retrocaval ureter
Acquired Intrinsic Defects

Calculi

Inflammation

Infection

Trauma

Sloughed papillae

Tumor

Blood clots
Acquired Extrinsic Defects

Pregnant uterus

Retroperitoneal fibrosis

Aortic aneurysm

Uterine leiomyomata

Carcinoma of uterus, prostate, bladder,

colon,

rectum

Lymphoma

Pelvic inflammatory disease, endometriosis

Accidental surgical ligation

Urethra

Bladder neck obstruction

Ureterocele

Posterior urethral valves

Anterior urethral valves
Stricture
Meatal stenosis
Phimosis

Benign prostatic hyperplasia

Cancer of prostate
Cancer of bladder
Calculi
Diabetic neuropathy
Spinal cord disease
Anticholinergic drugs
Alpha adrenergic antagonsit

Stricture
Tumor
Calculi
Trauma
Phimosis

Carcinoma of cervix, colon

Trauma

Trauma

Harrisons principle of Internal Medicine, 18th edition, page 2396

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Formatting: Jun-jun Mendoza
Editor: Marie Mae Pantolla

DLSHSI Medicine Batch 2016|8

SUMMARY
SYNDROMES

IMPORTANT CLUES TO DIAGNOSIS

ACUTE OR RAPIDLY PROGRESSIVE

RENAL FAILURE

Anuria
Oliguria
Documented renal decline in GFR

ACUTE NEPHRITIS

Hematuria, RBC casts

Azotemia, oliguria
Edema,
Hypertension
Azotemia for >3 months
Prolonged symptoms or signs of uremia
Symptoms and signs of renal osteodystrophy
Kidneys reduced in size bilaterally Broad cast in
urinary sediments.
Proteinuria >3.5g/1.73 m2/24 hrs
Hypoalbuminemia
Edema
Hyperlipidemia
Hematuria
Proteinuria
Sterile pyuria, casts
Bacteriuria
Other infectious agent documented in the urine
Pyuria, leukocyte casts
Frequency, urgency
Bladder tenderness,
flank tenderness
Electrolyte disorder
Polyuria, nocturia
Renal calcification
Large kidneys
Renal transport defects
Systolic / diastolic hypertension

CHRONIC RENAL FAILURE

NEPHROTIC SYNDROME

ASYMPTOMATIC URINARY
ABNORMALITIES
URINARY TRACT INFECTION /
PYELONEPHRITIS

RENAL TUBULE DEFECTS

HYPERTENSION

NEPHROLITHIASIS

URINARY TRACT OBSTRUCTION

Previous history of stone passage or removal

Previous history of stone seen by X-ray
Renal colic
Azotemia, oliguria, anuria
Polyuria, nocturia, urinary retention
Slowing of urinary stream
Large prostate, large kidneys
Flank tenderness
Full bladder after voiding

FINDINGS THAT ARE

COMMON
Hypertension
Hematuria
Proteinuria, pyuria
Casts, edema
Proteinuria
Pyuria
Circulatory congestion
Proteinuria
Casts
Polyuria, Nocturia
Edema, hypertension
Electrolyte disorders
Casts
Lipiduria

Hematuria
Mild azotemia
Mild proteinuria
Fever

Hematuria
Tubular proteinuria
Enuresis

Proteinuria
Casts
Azotemia
Hematuria
Pyuria
Frequency, urgency
Hematuria
Pyuria
Enuresis
Dysuria

KEEP CALM AND Study.

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