Urinalysis in the diagnosis of renal disease
Theodore W Post, MD
Burton D Rose, MD
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Patients with renal disease may have a variety of different clinical
presentations. Some have symptoms that are directly referable to the kidney
(gross hematuria, flank pain) or to extrarenal sites of involvement (edema,
hypertensive, signs of uremia). Many patients, however, are asymptomatic and
are noted on routine examination to have an elevated plasma creatinine
concentration or an abnormal urinalysis.
Once renal disease is discovered, the presence or degree of renal dysfunction
is assessed and the underlying disorder is diagnosed. Although the history and
physical examination can be helpful, the most useful information is initially
obtained from estimation of the glomerular filtration rate (GFR) and
examination of the urinary sediment.
Estimation of the glomerular filtration rate (GFR) is used clinically to assess the
degree of renal impairment and to follow the course of the disease. (See
"Assessment of renal function: Plasma creatinine; BUN; and GFR"). However,
the GFR provides no information on the cause of the renal disease. This is
achieved by the the urinalysis and, if necessary, radiologic studies and/or renal
biopsy.
This card will provide an overview of the interpretation of the urinalysis in the
patient with renal disease. A general approach to the patient with renal
disease, including the utility of radiologic studies and renal biopsy are
discussed separately. (See "Approach to the patient with renal disease
including acute renal failure").
URINALYSIS – The major noninvasive diagnostic tool available to the clinician
is the urinalysis. Although examination of the urine can also provide some
information about disease severity, such a direct relationship between the
urinalysis and severity is not always present. In a patient with acute
glomerulonephritis, for example, normalization of the urinalysis represents
resolution of the active inflammatory process. However, this can reflect either
recovery or healing with irreversible glomerular scarring and nephron loss. In
this setting, repeat renal biopsy may be required to accurately estimate the
status of the renal disease [1].
Despite these potential limitations, a complete urinalysis should be performed
in all patients with renal disease. The specimen should be examined within 30
to 60 minutes of voiding; a midstream specimen is adequate in men, but the
external genitalia should first be cleaned in women to avoid contamination with
vaginal secretions. The urine should be centrifuged at 3000 rpm for three to
five minutes, and the supernatant then poured into a separate tube. A small
amount of sediment should be placed on a slide, while the supernatant should
be tested for color (particularly for color suggesting the presence of heme
pigments), protein, pH, concentration, and glucose.
Color – Normal urine is clear and light yellow in color; it is lighter when dilute
and darker when concentrated, such as after an overnight water restriction.
The urine may also be white (eg, due to pyuria or phosphate crystals), green
(eg, due to the administration of methylene blue, amitriptyline, or propofol [2]),
black (eg, due to malignancy or ochronosis), or shades of red or brown [3].
Although urine that is white, green, and black is extremely uncommon, the
intermittent excretion of red to brown urine is observed in a variety of clinical
settings [3,4]. The initial step in the evaluation of this problem is centrifugation
of the urine to see if the red color is in the urine sediment or the supernatant
(show figure 1).
• Hematuria is responsible if the red color is seen only in the urine sediment,
with the supernatant being clear.
If, on the other hand, it is the supernatant that is red, then the supernatant
should be tested for heme with a urine dipstick. (See "Red urine: Hematuria;
hemoglobinuria; myoglobinuria").
• A red supernatant that is negative for heme is a rare finding that can be
seen in several conditions, including porphyria, the use of the bladder
analgesic phenazopyridine, and the ingestion of beets in susceptible subjects.
• A red supernatant that is positive for heme is due to myoglobinuria or
hemoglobinuria. Hemoglobinuria and myoglobinuria can be usually be
distinguished by looking at the plasma which is red with hemoglobinuria and its
normal color with myoglobinuria.
Protein – The urine dipstick primarily detects albumin but not other proteins,
such as immunoglobulin light chains. This test is highly specific, but not very
sensitive for the detection of proteinuria; it becomes positive only when protein
excretion exceeds 300 to 500 mg/day. Thus, the urine dipstick is an insensitive
method to detect microalbuminuria, the earliest clinical manifestation of
diabetic nephropathy. In this setting, the development of a positive dipstick for
albumin is a relatively late event, occurring at a time when there is already
marked structural injury. (See "Microalbuminuria in diabetic nephropathy and
as risk factor for cardiovascular disease").
The semiquantitative categories on the dipstick should be used with caution
and only as a rough guide since urine concentration will affect the
measurement. A dilute urine, for example, will underestimate the degree of
proteinuria. False-positive results are common with many iodinated
radiocontrast agents [5]. Thus, the urine should not be tested for protein with
the dipstick for at least 24 hours after a contrast study.
Sulfosalicylic acid test – In contrast to the urine dipstick, SSA detects all
proteins in the urine [6]. This characteristic makes the SSA test particularly
useful in older patients who present with acute renal failure, a benign
urinalysis, and a negative or trace dipstick. In this setting, myeloma kidney, in
which immunoglobulin light chains form casts that obstruct the tubules, must
be excluded. A significantly positive SSA test in conjunction with a negative
dipstick usually indicates the presence of nonalbumin proteins in the urine,
most often immunoglobulin light chains. (See "Pathogenesis of myeloma
kidney"). Similar to the urine dipstick, radiocontrast agents can cause false
positive SSA results [4].
The sulfosalicylic acid (SSA) test is performed by mixing one part urine
supernatant (eg, 2.5 mL) with three parts 3 percent sulfosalicylic acid, and
grading the resultant turbidity according to the following schema (the numbers
in parentheses represent the approximate protein concentration) [3]:
0 = no turbidity (0 mg/dL)
trace = slight turbidity (1 to 10 mg/dL)
1+ = turbidity through which print can be read (15 to 30 mg/dL)
2+ = white cloud without precipitate through which heavy black lines on a
white background can be seen (40 to 100 mg/dL)
3+ = white cloud with fine precipitate through which heavy black lines cannot
be seen (150 to 350 mg/dL)
4+ = flocculent precipitate (>500 mg/dL)
Measurement of quantitative urinary protein excretion – Most patients with
persistent proteinuria should undergo a quantitative measurement of protein
excretion. This can be accomplished by a 24-hour urine measurement;
however, collecting these specimens may be cumbersome in ambulatory care
settings.
An alternative method using a random urine specimen has been described [79]. This test calculates the total protein-to-creatinine ratio (mg/mg). This ratio
correlates closely with daily protein excretion in g/1.73m2 of body surface area
(show figure 2). Thus, a ratio of 4.9 (as with respective urinary protein and
creatinine concentrations of 210 and 43 mg/dL) represents a daily protein
excretion of approximately 4.9 g/1.73 m2.
It is important to note the units of measurement in your laboratory. If the
urinary creatinine concentration is measured in mmol/L, the formula must be
amended as follows since 1 mg/dL equals 0.088 mmol/L (see "Measurement of
urinary protein excretion"):
Protein excretion @ (Urine [protein] x 0.088) ÷ Urine [creatinine]
(See "Estimation of protein excretion" for automatic calculation of protein
excretion using this method).
Normal urinary protein excretion should be less than 150 mg per day. Levels
above this (proteinuria) that persist beyond a single measurement should not
be ignored since it implies an abnormality in glomerular permeability.
In this circumstance, it is important to understand how to differentiate between
relatively benign (eg, orthostatic proteinuria) or common causes of proteinuria
(eg, diabetic proteinuria) and uncommon causes that require nephrology
consultation. The approach to this problem is discussed in detail elsewhere.
(See "Proteinuria: The primary care approach", see "Evaluation of isolated
proteinuria" and see "Overview of heavy proteinuria and the nephrotic
syndrome").
Hydrogen ion concentration – The urine hydrogen ion concentration, measured
as the pH, reflects the degree of acidification of the urine. The urine pH ranges
from 4.5 to 8.0, depending upon the systemic acid-base balance. The major
clinical use of the urine pH occurs in patients with metabolic acidosis. The
appropriate response to this disorder is to increase urinary acid excretion, with
the urine pH falling below 5.3 and usually below 5.0. A higher value may
indicate the presence of one of the forms of renal tubular acidosis. Distinction
between the various types of RTA can be made by measurement of the urine
pH and the fractional excretion of bicarbonate at different plasma bicarbonate
concentrations. (See "Overview of renal tubular acidosis").
The diagnostic use of the urine pH requires that the urine be sterile. Infection
with any pathogen that produces urease, such as Proteus mirabilis, can result
in a urine pH above 7.0 to 7.5. (See "Chapter 13B: Meaning of urine osmolality
and pH").
Osmolality and specific gravity – The solute concentration of the urine (or other
solution) is a function of the number of solute particles per unit volume; it is
most accurately measured by the osmolality of the solution. The plasma
osmolality is maintained within a very narrow range (approximately 285
mosmol/kg), principally because the kidney is able to excrete urine with an
osmolality markedly different from that of plasma. (See "Chapter 6B:
Antidiuretic hormone and water balance" and see "Chapter 9A: Water balance
and regulation of plasma osmolality").
Since the urinary concentration varies markedly based upon volume status, the
urine osmolality is useful only when correlated with the clinical state. This
measurement is most useful in the diagnosis of patients with hyponatremia,
hypernatremia, and polyuria. (See "Diagnosis of hyponatremia", see
"Diagnosis of hypernatremia", and see "Diagnosis of polyuria and diabetes
insipidus").
If an osmometer is unavailable, the concentration of the urine can be assessed
by measuring the specific gravity, which is defined as the weight of the solution
compared with that of an equal volume of distilled water. The specific gravity
generally varies with the osmolality. However, the presence of large molecules
in the urine, such as glucose or radiocontrast media, can produce large
changes in specific gravity with relatively little change in osmolality. (See
"Urine osmolality vs specific gravity").
Glucose – The presence of glucose in the urine as detected semiquantitatively
with a dipstick may be due to either the inability of the kidney to reabsorb
filtered glucose in the proximal tubule despite normal plasma levels (renal
glucosuria) or urinary spillage because of abnormally high plasma
concentrations. In patients with normal renal function, significant glucosuria
does not generally occur until the plasma glucose concentration is above 180
mg/dL (10 mmol/L).
Renal glucosuria can occur as an isolated defect but is more commonly
observed in association with additional manifestations of proximal dysfunction,
including hypophosphatemia, hypouricemia, renal tubular acidosis, and
aminoaciduria. This constellation is called the Fanconi syndrome and may
result from a variety of disorders, particularly multiple myeloma. (See "Types of
renal disease in multiple myeloma" and see "Etiology and diagnosis of type 1
and type 2 renal tubular acidosis").
The use of urinary glucose levels to screen for and monitor diabetes mellitus is
limited for a number of reasons. These include the relative insensitivity of the
measurement (since moderate hyperglycemia is required before a positive test
is obtained); its dependence upon the urine volume; and its value which
reflects the mean plasma glucose concentration and not the level at the time of
measurement. (See "Screening for diabetes mellitus" and see "Blood glucose
monitoring in management of diabetes mellitus").
Dipstick detection of hematuria and pyuria – Microscopic hematuria may be
discovered incidentally when heme (either red blood cells or hemoglobin) is
detected on a dipstick. Dipsticks for heme detect 1 to 2 red blood cells per high
power field and are therefore at least as sensitive as urine sediment
examination, but result in more false positive tests. By comparison, false
negative tests are unusual; as a result, a negative dipstick reliably excludes
abnormal hematuria [10]. Although red cells may be lysed in dilute urine, the
hemoglobin that is released will be detected by the dipstick. (See "Evaluation
of hematuria").
Dipsticks may also detect leukocyte esterase and nitrite, the former
corresponding to pyuria and the latter to Enterobacteriaceae which convert
urinary nitrate to nitrite. Although this test is a simple and inexpensive screen
for urinary tract infection, it may also detect pyuria not associated with
infection. (See "Urine sampling and culture in the diagnosis of urinary tract
infection"). Significant causes of sterile pyuria include interstitial nephritis, renal
tuberculosis, and nephrolithiasis.
Although the detection of hematuria and pyuria by dipstick may be useful as a
screening test, they cannot replace microscopic examination of the urine
sediment in patients with renal disease. Such examination permits the
detection of elements, such as red and white blood cell casts and epithelial
cells and/or casts, which cannot be found by dipstick alone.
URINE SEDIMENT – Although microscopic examination of the urine sediment
in the patient with renal disease may reveal crystals, bacteria, cells, or casts,
the presence of small amounts of one or more of these elements may be
observed in healthy individuals. In a normal patient, for example, one high
power field may contain 0 to 4 white blood cells and 0 to 2 red blood cells, and
one cast may be observed in 10 to 20 low powered fields [11]. In addition,
crystals of uric acid, calcium oxalate, or phosphate may occasionally be seen.
Crystals – Whether crystals form in the urine depends upon a variety of
factors, including the degree of supersaturation of constituent molecules, the
urine pH, and the presence of inhibitors of crystallization. Many different forms
may be observed in normal patients and in those with defined disorders:
• Uric acid crystals – Uric acid crystals as well as amorphous urates are
observed in acid urine, a milieu which favors the conversion of the relatively
soluble urate salt into the insoluble uric acid (show sediment 1A-1B). (See
"Uric acid renal diseases").
• Calcium phosphate or calcium oxalate crystals – The formation of calcium
oxalate crystals is not dependent upon the urine pH, while calcium phosphate
crystals only form in a relatively alkaline urine (show sediment 2A-2B). (See
"Risk factors for idiopathic calcium stones").
• Cystine crystals – Cystine crystals, with their characteristic hexagonal
shape, are diagnostic of cystinuria (show sediment 3). (See "Cystine stones").
• Magnesium ammonium phosphate crystals – Magnesium ammonium
phosphate (struvite) and calcium carbonate-apatite are the constituents of
struvite stones (show sediment 4). (See "Pathogenesis and clinical
manifestations of struvite stones"). Normal urine is undersaturated with
ammonium phosphate and struvite stone formation occurs only when ammonia
production is increased and the urine pH is elevated to decrease the solubility
of phosphate. Both of these requirements may be met when urinary tract
infection occurs with a urease-producing organism, such as Proteus or
Klebsiella.
Although the observation of crystals in the urine is most frequently of little
diagnostic importance, there are several notable exceptions. These include the
presence of cystine or ammonium magnesium phosphate crystals (as
mentioned above), the combination of acute renal failure and calcium oxalate
crystals (a setting consistent with ethylene glycol ingestion), and the presence
of a larger number of uric acid crystals occurring in association with acute renal
failure (consistent with tumor lysis syndrome). (See "Management of methanol
and ethylene glycol intoxication" and see "Tumor lysis syndrome").
Bacteria – The presence of bacteria in a urine sediment is most frequently due
to contamination of the specimen upon collection. (See "Urine sampling and
culture in the diagnosis of urinary tract infection"). Although normal urine is
sterile, asymptomatic bacteriuria is increasingly recognized but is usually not
treated. (See "Approach to the patient with asymptomatic bacteriuria").
Cells – The cellular elements found in the urinary sediment include red blood
cells, white blood cells, and epithelial cells. Infrequently, tumor cells may also
be observed, thereby suggesting the diagnosis of genitourinary malignancy
(eg, bladder cancer) and/or infiltration of the renal parenchyma with malignant
cells (eg, lymphoma).
Hematuria – Transient hematuria is relatively common in young subjects and
is not indicative of disease. As an example, one study evaluated 1000 young
men who had yearly urinalyses between the ages of 18 and 33; hematuria was
seen in 39 percent on at least one occasion and 16 percent on two or more
occasions [12]. In another series of men over the age of 50 who were tested
weekly for three months, hematuria was present in 10 percent [13]. In this age
group, however, even transient hematuria may be important since it may
reflect a serious underlying condition, such as bladder cancer. (See
"Evaluation of hematuria").
Transient hematuria can also occur with urinary tract infection (eg, cystitis or
prostatitis. This is typically accompanied by pyuria and bacteriuria and patients
may often complain of dysuria.
Hematuria may be grossly visible or microscopic. The color change does not
necessarily reflect the degree of blood loss since as little as 1 mL of blood per
liter of urine can induce a visible color change. As previously mentioned, the
intermittent excretion of red to brown urine can be observed without red blood
cells. (See "Red urine: Hematuria; hemoglobinuria; myoglobinuria").
Microscopic hematuria is commonly defined as the presence of more than 2
red blood cells per high powered field in a spun urine sediment (show
sediment 5) [6].
Evaluation of red cell morphology also may be helpful in the patient with
hematuria. The red cells are typically uniform and round (as in a peripheral
blood smear) with extrarenal bleeding, but usually have a dysmorphic
appearance with renal lesions [14,15], particularly glomerular diseases [15].
This change in morphology is manifested by blebs, budding, and segmental
loss of membrane, resulting in marked variability in red cell shape and a
reduction in mean red cell size (show sediment 6A-6B).
Persistent hematuria should be evaluated. Among the more common causes
are kidney stones, malignancy, and glomerular diseases (show figure 3). (See
"Evaluation of hematuria").
Pyuria – White cells are slightly larger than red cells and can be identified by
their characteristic granular cytoplasm and multilobed nuclei (since most are
neutrophils) (show sediment 7). Infection is the most common cause of pyuria
alone; the routine urine culture may be negative with tuberculous infection.
(See "Urine sampling and culture in the diagnosis of urinary tract infection" and
see "Renal disease in tuberculosis"). Pyuria has less diagnostic value if it
occurs in association with other cellular casts, additional cellular elements,
and/or proteinuria (see below).
In addition to neutrophils, eosinophils and lymphocytes may also be seen in
the urine. These cells can be identified by a Wright's stain of the sediment.
Although it has been proposed that the finding of eosinophiluria is relatively
specific and might be diagnostic of acute interstitial nephritis, the diagnostic
accuracy of urinary eosinophils is uncertain. (See "The significance of urinary
eosinophils"). Urinary lymphocytes may be observed in disorders associated
with infiltration of the kidney by lymphocytes, such as chronic tubulointerstitial
disease. (See "Renal disease in sarcoidosis").
Epithelial cells – Epithelial cells may appear in the urine after being shed from
anywhere within the genitourinary tract. However, only renal tubular cells are
diagnostically significant. Renal tubular cells are 1.5 to 3 times larger than
white cells and contain a round, large nucleus. Since it is difficult to distinguish
renal tubular cells from lower urinary tract cells, the presence of epithelial cells
in casts is the only reliable finding to indicate a renal origin of the cell. Although
an occasional finding of an epithelial cell cast is normal, increased numbers
suggest a number of disorders, including acute tubular necrosis,
pyelonephritis, and the nephrotic syndrome.
Casts – Casts conform to the shape of the renal tubule in which they formed
and are therefore cylindrical with regular margins. All casts have an organic
matrix composed primarily of Tamm-Horsfall mucoprotein.
Many different types of casts may be observed. Some can be found in normal
individuals, while others are diagnostic of significant renal disease [16]. The
observation of cells within a cast is highly significant since their presence is
diagnostic of an intrarenal origin.
Hyaline casts – Hyaline casts, which are only slightly more refractile than
water, are not indicative of disease and are primarily observed with small
volumes of concentrated urine or with diuretic therapy; they may occur at a
frequency of 10 casts per high powered field.
Red cell casts – The finding of red cell casts, even if only one is seen, is
virtually diagnostic of glomerulonephritis or vasculitis (show sediment 8). (See
"Hematuria: Glomerular versus extraglomerular bleeding").
White cell casts – The presence of white cell casts and pyuria alone is most
consistent with a tubulointerstitial disease or acute pyelonephritis (show
sediment 9A-9B). They may also be observed with many glomerular disorders.
Epithelial cell casts – Acute tubular necrosis and acute glomerulonephritis,
disorders in which epithelial cells are desquamated, may be associated with
epithelial cell casts (show sediment 10A-10B).
Fatty casts – Among patients with significant proteinuria, the degeneration of
cells within epithelial casts may result in a characteristic "Maltese cross"
appearance and a fatty cast (show sediment 11A-11B). These droplets are
composed of cholesterol esters and cholesterol, which may also be observed
free in the urine. (See "Significance of lipiduria").
Granular casts – Granular casts, which are observed in numerous disorders,
represent degenerating cellular casts or aggregated proteins (show sediment
12).
Waxy casts – Waxy casts are thought to be the last stage of the degeneration
of a granular cast (show sediment 13). Since this degenerative process is
probably slow, it is most likely observed in nephrons with very diminished flow.
Waxy casts are therefore most consistent with the presence of advanced renal
failure.
Broad casts – As with waxy casts, broad casts, which are wider than other
casts and tend to have a granular or waxy appearance, are thought to form in
the large tubules of nephrons with little flow. They are most often observed in
patients with advanced renal failure.
PATTERNS – The diagnostic value of the urinalysis in the patient with renal
disease lies in the association between different patterns of urinary findings
and different renal diseases. In many cases, the urinary findings point toward
one or only a few disorders (show table 1).
Hematuria with red cell casts, dysmorphic red cells, heavy proteinuria (greater
than 3.5 g/day), or lipiduria – Any of these findings, singly or in combination, is
virtually diagnostic of glomerular disease or vasculitis (show sediment 14A14D). The absence of these pathognomonic changes, however, does not
exclude these diagnoses. (See "Differential diagnosis of glomerular disease"
and see "Significance of lipiduria").
Multiple granular and epithelial cell casts with free epithelial cells – These
findings are strongly suggestive of acute tubular necrosis in a patient with
acute renal failure, although their absence does not exclude this diagnosis
(show sediment 15A-15C). In this setting, ischemic or toxic injury to the tubular
epithelial cells can lead to cell sloughing into the tubular lumen due either to
cell death or to defective cell-to-cell or cell-to-basement membrane adhesion
[17]. In addition to acute tubular necrosis, similar urinary abnormalities can
also be induced by marked hyperbilirubinemia alone (plasma bilirubin
concentration usually above 8 to 10 mg/dL or 136 to 170 µmol/L); how this
occurs is not clear [18].
Pyuria with white cell and granular or waxy casts and no or mild proteinuria –
This constellation is suggestive of tubular or interstitial disease or urinary tract
obstruction (show sediment 16A-16E). White cells and white cell casts can
also be seen in acute glomerulonephritis, particularly postinfectious
glomerulonephritis; in this setting, however, there are also other signs of
glomerular disease, such as hematuria, red cell casts, and proteinuria.
Hematuria and pyuria with no or variable casts (excluding red cell casts) –
These findings may be seen in acute interstitial nephritis, glomerular disease,
vasculitis, obstruction, and renal infarction. Eosinophiluria may also be seen
with acute interstitial nephritis, but the absence of this finding does not exclude
the diagnosis. (See "The significance of urinary eosinophils").
Hematuria alone – The significance of isolated hematuria (ie, without other
cellular elements or casts, including red cell casts) varies with the clinical
setting. It is suggestive of vasculitis or obstruction In the patient with acute
renal failure, and of urolithiasis in the patient with flank pain. It can also be
found with mild glomerular disease (particularly postinfectious
glomerulonephritis, IgA nephropathy, thin basement membrane disease, and
hereditary nephritis), polycystic kidney disease, and with extrarenal disorders
such as tumors, and prostatic disease. (See "Evaluation of hematuria" and see
"Glomerular hematuria: IgA; Alport; thin basement membrane disease").
Pyuria alone – Assuming no contamination with vaginal secretions (which is
unlikely if there are no large vaginal epithelial cells in the sediment), pyuria
alone is usually indicative of urinary tract infection (including tuberculosis).
Sterile pyuria suggests some form of tubulointerstitial disease, such as
analgesic nephropathy.
Normal or near-normal (few cells with little or no casts or proteinuria; hyaline
casts are not an abnormal finding) – In patients with acute renal failure, a
relatively normal urinalysis suggests prerenal disease, urinary tract obstruction,
hypercalcemia, myeloma kidney (although the SSA test should be markedly
positive), some cases of acute tubular necrosis, or a vascular disease with
glomerular ischemia but not infarction (scleroderma, atheroemboli [which are
irregularly shaped and do not completely occlude vessels], and rare cases of
polyarteritis nodosa affecting the renal arteries but not the glomeruli).
With chronic renal disease, disorders that should be considered include
prerenal disease (as with congestive heart failure), urinary tract obstruction,
benign nephrosclerosis, and tubular or interstitial diseases.
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