Professional Documents
Culture Documents
4-2
December 3, 2013
Harrisons
Azotemia and
Urinary Abnormalities
Acute nephritis
Chronic renal
failure
Nephrotic
syndrome
Asymptomatic
urinary
abnormalities
Urinary tract
infection/pyelon
ephritis
IMPORTANT CLUES
TO DIAGNOSIS
Anuria
Oliguria
Documented recent
decline in GFR
Hematuria, RBC
casts
Azotemia, oliguria
Edema,
hypertension
Azotemia for >3
months
Prolonged
symptoms or signs
of uremia
Symptoms or signs
of renal
osteodystrophy
Kidneys reduced in
size bilaterally
Broad casts in
urinary sediment
Proteinuria >3.5 g
per 1.73 m2 per
24h
Hypoalbuminemia
Edema
Hyperlipidemia
Hematuria
Proteinuria (below
nephrotic range)
Sterile pyuria, casts
Bacteriuria >105
colonies/ml
Other infectious
agent documented
in urine
Pyuria, leukocyte
casts
COMMON
FINDINGS
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
Renal tubule
defects
Hypertension
Nephrolithiasis
Urinary tract
obstruction
Frequency, urgency
Bladder tenderness,
flank tenderness
Electrolyte disorders
Polyuria, nocturia
Renal calcification
Large kidneys
Renal transport
defects
Systolic/diastolic
hypertension
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
Hematuria
"Tubular"
proteinuria (<1
g/24h)
Enuresis
Proteinuria
Casts
Azotemia
Hematuria
Pyuria
Frequency,
urgency
Hematuria
Pyuria
Enuresis,
dysuria
AZOTEMIA
ASSESSMENT OF GLOMERULAR FILTRATION RATE
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Cockcroft-Gault
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Hepatorenal syndrome
Drugs such as NSAIDs
True or "effective" arterial hypovolemia leads to a fall
in mean arterial pressure, which in turn triggers a series of
neural and humoral responses that include:
o Activation of the sympathetic nervous
o Renin-angiotensinaldosterone system
o Antidiuretic hormone (ADH) release
GFR
is
maintained
by
prostaglandin-mediated
relaxation of afferent arterioles and angiotensin II
mediated constriction of efferent arterioles.
Once the mean arterial pressure falls below 80 mmHg,
there is a steep decline in GFR.
Blockade of prostaglandin production by NSAIDs can
result in severe vasoconstriction and acute renal failure
Blocking
angiotensin
action
with
angiotensinconverting enzyme (ACE) inhibitors or angiotensin
receptor blockers (ARBs) decreases efferent arteriolar
tone and in turn decreases glomerular capillary perfusion
pressure
Patients on NSAIDs and/or ACE inhibitors/ARBs are most
susceptible to hemodynamically mediated acute renal
failure when blood volume is reduced for any reason
Patients with bilateral renal artery stenosis (or stenosis
in a solitary kidney) are dependent on efferent arteriolar
vasoconstriction for maintenance of glomerular filtration
pressure and are particularly susceptible to a precipitous
decline in GFR when given ACE inhibitors or ARBs
Prolonged renal hypoperfusion may lead to acute tubular
necrosis (ATN). Prerenal analysis and urinary electrolytes
can be useful in distinguishing prerenal azotemia from ATN
The urine of patients with prerenal azotemia can be
predicted from the stimulatory actions of norepinephrine,
angiotensin II, ADH, and low tubule fluid flow rate on salt
and water reabsorption
In prerenal conditions tubules are intact, leading to:
o Concentrated urine (>500 mosmol)
o Avid Na retention (urine Na concentration <20 mM/L,
fractional excretion of Na <1%)
o UCr/PCr >40
The prerenal urine sediment is usually normal or has
occasional hyaline and granular casts, whereas the
sediment of ATN usually is filled with cellular debris and
dark (muddy brown) granular casts
Urine/plasma creatinine
(UCr/PCr)
>40
<20
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Approximate amount
Concentration
Daily
5-20 mg/dL
30 mg/dL
Less than 0.5
g/day
100 mg/dL
0.5-1 g/day
300 mg/dL
1-2 g/day
More than 2000
More than 2
mg/dL
g/day
APPROACH TO PATIENT
Investigation of proteinuria is often initiated by a positive
dipstick on routine urinalysis.
Conventional dipsticks detect predominantly albumin and
provide a semiquantitative assessment (trace, 1+, 2+, or
3+), which is influenced by urinary concentration as
reflected by urine specific gravity (minimum <1.005,
maximum 1.030).
More exact determination of proteinuria should employ a
spot morning protein/creatinine ratio (mg/g) or a 24h urine collection (mg/24 h).
Traditionally, healthy individuals excrete <150 mg/d of
total protein and <30 mg/d of albumin.
However, even at albuminuria levels <30 mg/d, risk for
progression
to
overt
nephropathy
or
subsequent
cardiovascular disease is increased.
The remainder of the protein in the urine is secreted by the
tubules (Tamm-Horsfall, IgA, and urokinase) or
represents small amounts of filtered 2-microglobulin,
apoproteins, enzymes, and peptide hormones
Another mechanism of proteinuria occurs when there is
excessive production of an abnormal protein that
exceeds the capacity of the tubule for reabsorption.
This most commonly occurs with plasma cell
dyscrasias, such as multiple myeloma, amyloidosis,
and lymphomas.
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