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216 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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TABLE 10-6. Examples of Tests Available and Possible Results from Multitest Urine Dipstick
(Bayer Multistix 10 SG)
TEST RESULT
Leukocyte
Negative Trace Small + Moderate ++ Large +++
esterase
Nitrite Negative Positive
Urobilinogen Normal
0.2 mg/dL
Normal
1 mg/dL
2 mg/dL 4 mg/dL 8 mg/dL
Protein Negative Trace 30 mg/dL + 100 mg/dL ++ 300 mg/dL +++ 2,000 mg/dL ++++
pH 5 6 6.5 7 7.5 8 8.5
Blood (Hgb) Negative Nonhemolyzed
trace
1.000 1.005 1.010 1.015 1.020 1.025 1.030
Hemolyzed
trace
Small + Moderate ++ Large +++
gravity
Ketones Negative Trace 5 mg/dL Small
15 mg/dL
Moderate
40 mg/dL
Large 80 mg/dL Large 160 mg/dL
Bilirubin Negative Small + Moderate ++ Large +++
Glucose Negative 1/10 g/dL (trace)
100 mg/dL
Source: Adapted with permission from Multistix (various) Reagent Strips [product information]. Elkhart, IN: Bayer HealthCare LLC; 2005.
1/4 g/dL
250 mg/dL
1/2 g/dL
500 mg/dL
1 g/dL
1,000 mg/dL
2 g/dL
2,000 mg/dL
phosphate, and magnesium–ammonium phosphate stones; pHs
<5.5are associated with cystine and uric acid stones.
Specific Gravity
Normal range: 1.016 to 1.022 (normal uid intake)
e kidneys are responsible for maintaining the blood’s osmolality within a narrow range (285 to 300 mOsm/kg). To do
so, the kidneys must vary the osmolality of the urine over a
wide range. Although osmolality is the best measure of the
kidneys’ concentrating ability, determining osmolality is dicult. Fortunately, it correlates well with specic gravity when
urine contains normal constituents. Specic gravity is the ratio
of the weight of a given uid to the weight of an equal volume
of distilled water. Sodium, urea, sulfate, and phosphate contribute most to the specic gravity of urine. Because specic gravity
is related to the weight (and not the number) of particles in
solution, particles with a weight dierent from that of sodium
chloride (the solute usually in the highest concentration there)
can widen the disparity. Patients with normal kidney function
can dilute urine to approximately 1.001 and concentrate urine
to 1.035, which correlates to an osmolality of 50 to 1,000
mOsm/kg, respectively. A urinary specic gravity of 1.010 is
considered isosthenuric; that is, the urinary osmolality is the
same as plasma.
Specic gravity can be measured by reagent strips (dipstick),
a urinometer (hydrometer), or a refractometer. e reagent
71,72,74
strips change color based on the pKa change of the strips in
relation to the ionic concentration of the urine. e indicator
substance on the strip changes color, which can be then correlated to the specic gravity. Specic gravity measured by reagent
strips is not aected by high concentrations of substances such
as glucose, protein, or radiographic contrast media, which may
elevate readings with refractometers and urinometers. e urinometer is akin to a graduated buoy; it requires sucient urine
volume to oat freely. e reading is adjusted according to the
urine temperature. e refractometer uses the refractive index
as a basis and needs only a few milliliters of urine and no temperature adjustment.
71,72,74
Several conditions can aect specic gravity. In general, urinary specic gravity should be considered abnormal if it is the
opposite (high versus low and vice versa) of that which should be
produced based on the concurrent plasma osmolality. Patients
who are volume depleted should present with a concentrated
urine (specic gravity ≥1.020) as a normal compensatory mechanism. Patients with prerenal disease will likely have relatively
concentrated urine, whereas patients with intrinsic damage to
the renal tubules are more likely to produce urine, which is isos
thenuric (the tubules are unable to dilute or concentrate the
urine, so the urine is the same concentration as the ltrate).
e urine of patients with diabetes insipidus has low values
(<1.005) despite a relatively hypertonic plasma. On the other
hand, patients with the syndrome of inappropriate syndrome
-
CHAPTER 10 • REnAl FunCTion And RElATEd TEsTs 217
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TABLE 10-7. Causes of Proteins in Urine
Mild proteinuria (<0.5 g/day)
High blood pressure
Lower UTI
Fever
Renal tubular damage
Exercise
Moderate proteinuria (0.5–3 g/day)
Congestive heart failure
Chronic glomerulonephritis
Acute glomerulonephritis
Diabetic nephropathy
Pyelonephritis
Multiple myeloma
Preeclampsia of pregnancy
Rhabdomyolysis
>3 g/day)
Glomerulonephritis
Amyloid
Chronic glomerulonephritis (severe)
Diabetic nephropathy
Lupus nephritis
Rhabdomyolysis
Source: Adapted with permission from Sacher RA, McPherson
Widmann’s Clinical
Interpretation of Laboratory Tests. 11th ed. Philadelphia, PA:
FA Davis Company; 2000:924–1014; Bosch X, Poch E, Grau JM.
Rhabdomyolysis and acute kidney injury. N Engl J Med.
2009;361(1):62–72.
of antidiuretic hormone (SIADH) have concentrated urine and
relatively hypotonic serum.
71,72,74
Urobilinogen
Normal range: 0.3 to 1 Ehrlich unit
Urobilinogen (formed by bacterial conversion of conjugated
bilirubin in the intestine) is normally present in urine and
increases when the turnover of heme pigments is abnormally
rapid, as in hemolytic anemia, congestive heart failure with liver
congestion, cirrhosis, viral hepatitis, and drug- induced hepatotoxicity. Elevated urobilinogen may be premonitory of early
hepatocellular injury, such as hepatitis, because it is evident in
urine before serum bilirubin levels increase. Alkaline urine is
also associated with increased urobilinogen concentrations
caused by enhanced renal elimination. Urobilinogen may
decrease (if previously elevated) in patients started on antibiotics
(eg, neomycin, chloramphenicol, and tetracycline) that reduce
the intestinal ora producing this substance. Urobilinogen is
usually absent in total biliary obstruction because the substance
cannot be formed. Increased urobilinogen in the absence of bilirubin in the urine suggests a hemolytic process.
Bilirubin
Normal range: negative
A dark yellow or greenish- brown color generally suggests bilirubin in the urine (bilirubinuria). Most test strips rely on the
reaction between bilirubin with a diazotized organic dye to
yield a distinct color. Bilirubinuria may be seen in patients with
intrahepatic cholestasis or obstruction of the bile duct (stones
or tumor). False- negative results may occur in patients taking
ascorbic acid.
Blood and Hemoglobin
Normal range: negative
Dipsticks for blood depend on the oxidation of an indicator dye
due to the peroxidase activity of hemoglobin. A dipstick test can
detect as few as one to two RBCs per high- power eld. Even
small amounts of blood noted on dipstick require further investigation. It is important to note that in addition to hemoglobin, myoglobin can also catalyze this reaction so that a positive
dipstick result for blood may indicate hematuria (blood),
hemoglobinuria (free hemoglobin in urine), or myoglobinuria.
Microscopic examination of the urine is needed to distinguish
hematuria. e presence of ascorbic acid in the urine may lead
to a false- negative result with these tests, which is usually associated with a fairly large oral intake of vitamin C.
72,74,78
Hemoglobinuria suggests the presence of intravascular
hemolysis or directed damage to the small blood vessels. e
presence of myoglobin in the urine is highly suggestive of rhabdomyolysis, the acute destruction of muscle cells. With rhabdomyolysis, myoglobin is cleared rapidly by the kidneys and can
be detected in the urine.
72
e clinical distinction between hematuria, hemoglobinuria, and myoglobinuria is important because the clinical conditions that cause them are very dierent. e color of the urine
is not specic; all three may lead to red or dark brown urine.
As noted with dipsticks for blood, all three conditions lead to
a positive test result. Microscopic analysis demonstrates many
more erythrocytes with hematuria, but RBCs can be seen with
hemoglobinuria and myoglobinuria. Erythrocytes may be few
in hematuria because of lysis of the RBCs if the urine has a low
specic gravity (<1.005).
Leukocyte Esterase
Normal range: negative to trace
Many dipsticks can detect leukocyte esterase, give a semiquantitative estimate of pyuria (pus in the urine), and thus be considered an indirect test for UTIs. e presence of esterase activity
correlates well with signicant numbers of neutrophils (either
present or lysed) in the urine. e leukocyte esterase test is
important because the presence of actual neutrophils in the
urine is not a specic indicator for UTI.
72,74
218 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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TABLE 10-8. Factors Affecting Urine pH
URINE PH AND FACTORS CAUSES AND COMMENTS
Alkaline
Postprandial Specimens voided shortly after meals
Vegetarianism
Alkalosis (metabolic or respiratory) Hyperventilation, severe vomiting, GI suctioning
UTI Some bacteria (eg, Proteus) split urea to ammonia, which is alkalinizing
Renal tubular acidosis
Drugs Acetazolamide, bicarbonate salts, thiazides, citrate, and acetate salts
Acidic
Drugs Ammonium chloride, ascorbic acid (high dose), methenamine
Food Cranberries, prunes, plums, fruit juices
Ketoacidosis Diabetes mellitus, starvation, high fever
Metabolic acidosis Increased ammonium excretion and cellular hypoxia with lactic acid production
(shock)
Sleep Mild respiratory acidosis
SourceWidmann’s Clinical Interpretation
of Laboratory Tests. 11th ed. Philadelphia, PA: FA Davis Company; 2000:924–1014; McPherson RA, Ben-Ezra J, Zhao S. Basic examination
of urine. In: McPherson RA, Pincus MR, eds. Henry’s Clinical Diagnosis and Management by Laboratory Methods. 21st ed. Philadelphia, PA:
Saunders Elsevier; 2007:393–425.
Nitrite
Normal range: negative
e presence of nitrite in the urine is another indirect indicator of a UTI. Many organisms, such as Escherichia coli, Klebsi-
ella, Enterobacter, Proteus, Staphylococcus, and Pseudomonas, are
able to reduce nitrate to nitrite; thus, a positive urine test result
would suggest a UTI. If nitrite- positive, a culture of the urine
should be obtained. A rst- morning urine specimen is preferred
because an incubation period is necessary for bacteria to convert
urinary nitrate to nitrite. A positive test result is suggestive of a
UTI, but a negative test result cannot rule out a UTI (ie, the test
is specic but not highly sensitive). False- positive test results
may be caused by strips that are exposed to air. False- negative
results occur with infections caused by non–nitrite- producing
organisms (Enterococcus).
72,74
Additionally, certain medications may cause intentional
glycosuria through their mechanism of action. One notable
example includes the sodium- glucose cotransporter 2 inhibitor (SGLT2i) drug class, which is indicated primarily for type 2
diabetes mellitus but is supported by an increasing body of evi-
SGLT2i are proteins located on the proximal convoluted tubule
that are responsible for ~90% of ltered glucose reabsorption.
SGLT2i prevent glucose reabsorption and facilitate excretion
in the urine, resulting in intended glycosuria.
80,81
As a result of
various factors that aect or cause glycosuria, use of urinary
glucose to screen and monitor for diabetes is no longer a standard of care.
72,74,75
Ketones in the urine typically indicate a derangement of car
bohydrate metabolism resulting in use of fatty acids as an energy
source. Ketonuria in association with glucose in the urine is suggestive of uncontrolled type 1 diabetes mellitus. Ketonuria can
Glucose and Ketones
Normal range: none
Although glucose is ltered in the glomerulus, it is almost
completely reabsorbed in the proximal tubule so that glucose
also occur with pregnancy, carbohydrate- free diets, and starvation. Aspirin has been reported to cause a false- negative ketone
test result, whereas levodopa and phenazopyridine may cause
false- positive ketone results (Minicase 3).
72,74,75
is generally absent in the urine. However, at glucose concentrations >180 mg/dL, the capacity to reabsorb glucose is exceeded
and glycosuria occurs. Glucose in the urine is suggestive of
diabetes mellitus although other less common conditions can
cause glycosuria.
Urinary Electrolytes
Like most laboratory tests, urinary electrolytes are rarely denitive for any diagnosis. ey can conrm suspicions of a particular medical problem from the history, physical examination, and
79
-
CHAPTER 10 • REnAl FunCTion And RElATEd TEsTs 219
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MINICASE 3
Glycosuria/Ketonuria
Mason L. is a 20- year- old man who presents to an urgent care facility
with reports of fatigue and nausea. He notes losing 10 lb despite
experiencing increased appetite and thirst over the past 3 months.
He describes increased frequency of urination but denies any pain
or burning sensations upon voiding.
URINALYSIS RESULT REFERENCE STANDARD/RANGES
Color Yellow Yellow
Specific gravity 1.020 1.016–1.022
Ketones 5+ Negative
Glucose 4+ Negative
pH 5 4.6–8
Blood Negative Negative
Protein Negative Negative
Nitrite Negative Negative
Leukocyte esterase Negative Negative-
Bacteria 0 0- trace
WBC 0 0-2/HPF
RBC 1/HPF 1-3/HPF
Epithelial cells 0 0-1/HPF
QUESTION: What condition is suggested by the patient’s
presentation and urinalysis results?
DISCUSSION: The patient requires further evaluation for type 1
diabetes mellitus and diabetic ketoacidosis. Glycosuria suggests
diabetes mellitus because glucose is usually completely reabsorbed
in the proximal tubule. Reports of polyphagia, polydipsia, and
polyuria are hallmark characteristics of hyperglycemia. Type 1
diabetes mellitus is typically diagnosed in children, teens, and
young adults. The presence of ketones suggests uncontrolled type 1
trace
diabetes mellitus because of improper carbohydrate metabolism.
The subsequent catabolism of fatty acids for energy leads to weight
loss. Along with ketonuria, the patient’s symptoms of fatigue and
nausea prompt concerns for diabetic ketoacidosis.
other laboratory data. Along with the results of a urinalysis and
serum electrolytes, urinary electrolyte tests allow the practitioner to rule in or out possible diseases of the dierential diagnosis. ese tests are relatively simple to perform and widely used
in the clinical setting.
“Normal” values for urinary electrolytes are a bit of a misnomer because the kidneys should be retaining or excreting electrolytes based on intake and any endogenous production. Any
concentration in the urine is normal if it favors a normal uid
and serum electrolyte status. A related test, the urinary fractional excretion of sodium (%FENa), can assist with common
diagnostic dilemmas involving the kidneys’ ability to regulate
electrolytes.
Urinary Sodium and Potassium
e electrolyte that is most commonly measured in urine is
sodium. Occasionally, it is useful to measure potassium and
chloride. For these electrolytes, there is no conversion factor to
International System (SI) units because milliequivalents per liter
are equivalent to millimoles per liter.
Sodium
Normal range: varies widely
Regulation of urinary excretion of sodium maintains an eective systemic circulating volume. For this reason, the urinary
sodium concentration is oen used to assess volume status in
a patient. Less oen, a 24- hour assessment of sodium excretion (via a urine collection) can be used to assess adherence
to sodium restriction in a patient with hypertension and heart
82,83
failure.
should equal the amount of sodium taken in through the diet.
For example, a patient following a low- sodium diet should ingest
<90 mEq (90 mmol) of sodium per day and would, therefore,
have a 24- hour urine sodium <90 mEq (90 mmol) per day if
the patient is following the diet accurately. Sodium and water
balance is an extremely complex process, and only the most
common disorders that may alter sodium and water balance
(and hence urine sodium) are discussed here.
seen in clinical practice, and it is most oen observed in volume depletion (GI loss and diuretics) and in SIADH, which is
is is because the total urinary sodium excretion
Hyponatremia is the most common electrolyte disorder
220 BASIC SKILLS IN INTERPRETING LABORATORY DATA
mo
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()
https://t.me/med1917
not uncommon. In particular, SIADH can be seen in elderly
patienets who are maintained on drugs known to cause excess
secretion of ADH, such as selective serotonin reuptake inhibitors. Urine sodium concentrations of <20 mEq/L generally suggest volume depletion— the kidneys are responding to the low
volume by reabsorbing sodium. In the case of SIADH, which is
characterized by inappropriate retention of water in the distal
tubule, the urine sodium is generally >20 to 40 mEq/L.
Hypernatremia is less common and occurs when there is
limited access to free water because otherwise healthy adults
become thirsty in the face of hypernatremia. Diabetes insipidus,
which is characterized by a decreased production or response to
ADH, is another cause of hypernatremia. With diabetes insipidus, the urine sodium concentration is low despite the presence of clinical euvolemia. is is due to dilution of the urinary
sodium secondary to inappropriate loss of water in the urine.
83,84
Urine sodium concentrations are also useful in the diagnosis of AKI. In the presence of prerenal azotemia, urine sodium
concentrations are low because of the kidneys’ attempt to maintain volume and blood ow to the kidneys. On the other hand,
with acute tubular necrosis, the urinary sodium is generally
>40mEq/L because the damaged renal tubules are unable to
reabsorb sodium and concentrate urine.83 e fractional excretion of sodium (FENa) may be used to test the resorptive function
of renal tubules. Diuretics can also interfere with the assessment of urinary sodium. Even with volume depletion, urinary
sodium levels can be high due to the eect of the diuretic on
renal sodium handling.
83
%FENa test. Although assessment of urine sodium concentra-
tions is useful in determining volume status, concentration of
sodium in the urine is aected by the degree of water reabsorption in the tubules. e FENa is the percentage of sodium
(fraction) that is ltered in the glomerulus that eventually is
excreted in the urine and corrects for the amount of water in
the ltrate. An FENa can be estimated from a spot (random)
urine sample with a concomitant serum sample. e calculation is as follows:
U
=
NaSCr
SNaU
100
Cr
(12)
FENa%
( )
where UNa and SNa are urine and serum sodium in milliequivalents per liter or millimoles per liter and UCr and SCr are in milligrams per deciliter or micromoles per liter.
In the face of AKI, the FENa can be useful to discriminate
between a prerenal process (ie, volume depletion) and acute
tubular necrosis. In the hypovolemic, prerenal state, the kidneys conserve sodium and the FENa is <1%. With tubular damage, the FENa generally is >2% to 3%. As with the assessment of
urine sodium, the FENa can be aected by diuretic therapy and
may be somewhat high despite volume depletion.
82,83
hypokalemia, urinary potassium may provide useful information. Concentrations >10 mEq/L in a hypokalemic patient
usually mean that the kidneys are responsible for the loss. is
may occur with potassium- wasting diuretics, high- dose sodium
penicillin therapy (eg, ticarcillin/clavulanate and piperacillin/
tazobactam), metabolic acidosis or alkalosis, and renal tubular
acidosis. Concomitant hypokalemia and low urinary potassium (<10 mEq/L) suggest GI loss (including chronic laxative
abuse) as the cause of low serum potassium. In the setting of
hyperkalemia, assessment of urinary potassium concentrations
is less useful. Hyperkalemia is oen due to kidney failure (with
or without drugs that aect potassium homeostasis), so potassium concentrations in the urine would be low.83 A 24- hour
urine potassium measurement or the transtubular potassium
gradient (TTKG) may be used to dierentiate between renal
and nonrenal causes of potassium abnormalities. e TTKG
measures potassium secretion by the distal nephron corrected
for urine osmolality:
=× (13)
os
sm
TTKGKu/Ks S/U
where Ku and Ks are the concentrations of potassium in the
urine and serum and S
serum and urine, respectively.
and U
osm
are the osmolarities of the
osm
85,86
A TTKG value of <6 suggests
a renal cause of hyperkalemia, whereas values >6 may indicate
extrarenal causes of hyperkalemia, such as increased potassium
intake, acidosis, or rhabdomyolysis.
87
SUMMARY
e kidneys play a major role in the regulation of uids, electrolytes, and the acid–base balance. Kidney function is aected
by the cardiovascular, pulmonary, endocrine, and central
nervous systems. erefore, abnormalities in these systems
may be reected in renal or urine tests. Urinalysis is useful as a
mirror for organ systems that generate substances (eg, blood/
biliary system and urobilinogen) ultimately eliminated in the
urine. Urinalysis allows indirect examination without invasive
procedures.
A rise in BUN without a simultaneous rise in SCr is not specic for kidney dysfunction. However, concomitant elevations in
BUN and SCr almost always reect some disturbance in the kidneys’ ability to clear substances from the body. Renal functions
should be estimated based on a patient’s SCr and demographic
characteristics using either the 2009 CKD-EPI or CockcroGault equation. ese equations are a more reliable index of
kidney function than SCr alone. Evolving evidence may show
better estimation of GFR with creatinine–cystatin-C equations.88
A thoughtful examination of urine (macroscopic, microscopic,
and chemical) is an indispensable tool in identifying kidney and
other pathologic processes that may be present in a patient.
Potassium
Normal range: varies widely
As is the case with sodium, urinary excretion of potassium
varies based on dietary intake and other factors that may aect
serum potassium concentrations. For patients with unexplained
ACKNOWLEDGMENTS
e authors acknowledge the contributions of Dr. Dominick P.
Trombetta, who authored this chapter in previous editions of
this textbook.
CHAPTER 10 • REnAl FunCTion And RElATEd TEsTs 221
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3. Dowling T. Evaluation of kidney. In: DiPiro JT, Yee GC, Posey L, et al, eds.
LEARNING POINTS
1. What is the relevance in knowing the eGFR?
ANSWER: The importance is in the assessment of whether the
based on estimates of GFR and ranges of albuminuria, and it
severity. Many medications are eliminated by renal excretion.
Inappropriate use of nephrotoxic drugs or inappropriate dosing
in patients with reduced renal function as evidenced by low eGFR
may contribute to adverse drug reactions. The eGFR may assist
the pharmacist in assessing medication use and determining
dose and frequency adjustment. Lastly, staging may help identify appropriate screening for other conditions and comorbidities, such as anemia and mineral and bone disorder, and prepare
patients for dialysis.
2.
Which is better to use for drug dosing, the CockcroftGault, MDRD, or CKD-EPI equation?
ANSWER: Either the CrCl using Cockcroft-Gault equation or
the eGFR multiplied by BSA may be used to calculate drug
doses for most patients. In some cases, manufacturer label-
such as for metformin and SGLT2 inhibitors; others use CrCl as
calculated by Cockcroft-Gault equation. Consider measuring
CrCl for patients who are considered at high risk (very young
and very old patients), for patients receiving drugs that have
a narrow therapeutic index, or for patients in whom estimations of kidney function vary or are likely to be inaccurate.
This is especially important in assessing patients for kidney
transplant.
3.
What is the clinical signicance of measuring albuminuria?
ANSWER: Under normal conditions, a small amount of total
low molecular weight serum globulins are then generally reabsorbed in the proximal tubule, which means only small amounts
are detected in the urine. The presence of albumin in the urine
may suggest glomerular dysfunction, and albuminuria and GFR
categories are used to classify CKD. Additionally, the category
of albuminuria should be considered when assessing CKD prognosis. The ACR ratio is recommended to assess kidney damage
in addition to the GFR. However, proteinuria may be intermittent and benign when caused by transient factors. As a result,
be recommended to distinguish between benign and pathologic
albuminuria.
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224 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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QUICKVIEW | BUN
PARAMETER DESCRIPTION COMMENTS
Common reference range
Adults
Children
Critical value 100 mg/dL (35.7 mmol/L) Associated with uremic syndrome in
Inherent activity Extremely high BUN levels lead to uremia, which
Location
Production Urea is byproduct of hepatic protein metabolism;
Storage Not applicable
Secretion/excretion
8–23 mg/dL (2.9–8.2 mmol/L)
5–18 mg/dL (1.8–6.4 mmol/L)
includes symptoms of nausea, vomiting, and other
metabolic and endocrine abnormalities
source of protein can be exogenous (eg, protein in diet)
or endogenous (eg, breakdown of RBCs or muscle cells)
undergoes proximal tubule reabsorption
BUN represents concentration of
nitrogen in serum
Usually measured with creatinine to
assess renal function
A normal BUN:creatinine ratio is 6:1
to 20:1; if ratio is >20:1, it suggests
prerenal etiology of renal failure;
if ratio is 10–20:1, it suggests
intrarenal etiology of renal failure
patients with severe renal failure
Urea is primary way that body
eliminates excess nitrogen
Percentage that is reabsorbed by
proximal tubule is inversely related
to patient’s intravascular volume; if
intravascular volume is lower than
normal, then percentage of BUN
reabsorbed in proximal tubule is
increased
Causes of abnormal values
High Prerenal causes: dehydration, blood loss, shock,
congestive heart failure, hypotension, increased protein
catabolism (due to fever, infection, severe burns)
Intrarenal causes: acute or chronic renal failure due to
any cause, glomerulonephritis, acute tubular necrosis,
severe hypertension
Postrenal causes: obstruction of ureter, bladder
neck, or urethra due to stones, enlarged prostate, or
stricture, respectively
Nonrenal causes: excessive amino acid infusions, upper
gastrointestinal tract bleeding
Drugs with antianabolic effects or protein catabolic
effects: corticosteroids, tetracyclines
Drugs that contribute to prerenal or intrarenal failure:
ACE inhibitor, acetaminophen, acyclovir, diuretics,
aminoglycosides, antibiotics, angiotensin II receptor
blockers, NSAIDs, radiographic contract media
CHAPTER 10 • REnAl FunCTion And RElATEd TEsTs 225
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QUICKVIEW | BUN
PARAMETER DESCRIPTION COMMENTS
Low Starving or malnourished patients with inadequate
Signs and symptoms
High level Azotemia refers to elevated BUN, which occurs when
Low level No symptoms
After event, time to….
Initial elevation Variable, depending on etiology of increase in BUN
Peak values Can exceed 100 mg/dL
(cont’d)
protein intake or patients with muscleExcess intravascular volume (eg, congestive heart
failure) or SIADH may dilute BUN and have low levels
Chloramphenicol, guanethidine, or streptomycin use
GFR is 20%–35% of normal
electrolyte, endocrine, neuromuscular, hematologic,
or dermatologic, and metabolic abnormalities; it
occurs when patient has overt renal failure and GFR is
<20%–25%
wasting disease
Normalization If prerenal or postrenal etiology of renal failure is
corrected, BUN will return to normal range quickly;
however, if intrarenal etiology of renal failure results
in permanent nephron injury, high levels of BUN may
persist; in this case, when uremia develops, patient
may be dialyzed, which will reduce BUN level
Causes of spurious
results
Avoid collecting blood specimens in tubes containing
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