Urinalysis in the diagnosis of renal disease

Authors Theodore W Post, MD Burton D Rose, MD Section Editor Gary C Curhan, MD, ScD Deputy Editor Alice M Sheridan, MD

Last literature review version 18.3: September 2010 | This topic last updated: April 30, 2009 (More)

INTRODUCTION Patients with renal disease 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 assessed and the underlying disorder is examination can be helpful, the most estimation of the glomerular filtration sediment.

presence or degree of renal dysfunction is diagnosed. Although the history and physical useful information is initially obtained from rate (GFR) and examination of the urinary

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 kidney function: Serum creatinine; BUN; and GFR".) However, the GFR provides no information on the cause of the renal disease. This is achieved by the urinalysis and, if necessary, radiologic studies and/or renal biopsy.

This topic will review 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 "Diagnostic approach to the patient with acute or chronic kidney disease".)

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 have a variety of other colors.

Red to brown urine The intermittent excretion of red to brown urine is observed in a variety of clinical settings [2,3]. 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 (picture 1).

Hematuria is responsible if the red color is seen only in the urine sediment, with the supernatant being clear. (See "Red to brown urine: Hematuria; hemoglobinuria; myoglobinuria".)

If, on the other hand, it is the supernatant that is red, then the supernatant should be tested for heme with a urine dipstick.

A red supernatant that is negative for heme is a rare finding that can be seen in several conditions (table 1). These include use of the bladder analgesic phenazopyridine or a variety of other medications, food dyes, the ingestion of beets in susceptible subjects, and porphyria (picture 2).A red supernatant that is positive for heme is usually 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. False positive heme reactions may be seen if semen is present in the urine, if the urine is alkaline (pH >9), or contaminated with oxidizing agents used to clean the perineum [4].

Other Rarely, the urine has other colors. These include:

White urine, which may be due to pyuria, phosphate crystals, chyluria [5,6], or propofol [7].Green urine, which may be due to the administration of methylene blue [8], propofol [9-11], or amitriptyline.Black urine, which may be due to hemoglobinuria [12,13] or to ochronosis, which is most often due to alkaptonuria (also called black urine disease). The black urine in ochronosis results from urinary excretion of homogentisic acid (HGA). The black color may only be apparent after the urine stands for some time, permitting oxidation of HGA. (See "Disorders of tyrosine metabolism", section on 'Alkaptonuria'.)Purple due to bacteriuria in patients with urinary catheters. (See "Urinary tract infection associated with urethral catheters", section on 'Purple urine bag syndrome'.)

In addition, other colors can occur in children with inborn errors of metabolism (table 1).

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 regular urine dipstick is an insensitive method to detect microalbuminuria, which is the earliest clinical manifestation of diabetic nephropathy and is associated with increased cardiovascular risk in patient with and without diabetes. In type 1 diabetes, the development of a positive dipstick for albumin is a relatively late event, occurring at a time when there is already substantial structural injury. There are also a variety of dipsticks that can be used to test for microalbuminuria, such as Clinitek Microalbumin Dipsticks and Micral-Test II test strips. (See "Microalbuminuria in type 1 diabetes mellitus", section on 'Detection' and "Microalbuminuria in type 2 diabetes mellitus", section on 'Detection' and "Microalbuminuria and cardiovascular disease".)

The semiquantitative categories on the dipsticks should be used with caution and only as a rough guide since, at a given of albumin excretion, the albumin concentration will vary with the urine volume. A dilute urine, for example, will underestimate the degree of proteinuria, while a highly concentrated urine may have a 3+ response on the regular dipstick but not be indicative of heavy proteinuria.

False-positive results are common with many iodinated radiocontrast agents [14]. 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 [15]. 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 and diagnosis of myeloma cast nephropathy (myeloma kidney)".) Similar to the urine dipstick, radiocontrast agents can cause false positive SSA results [3].

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) [2]:

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)

Quantitative measurement of 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 and preferred method is calculating the total protein-to-creatinine or albumin-to-creatinine ratio (mg/mg) on a urine sample [16-18]. (See "Measurement of urinary protein excretion".)

With elevated urinary protein levels, 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 "Evaluation of isolated proteinuria in adults" and "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 "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 "Evaluation of the patient with hyponatremia" and "Evaluation of the patient with hypernatremia" and "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 versus 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 "Etiology and diagnosis of distal (type 1) and proximal (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 "Blood glucose self-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 hemoglobin detect 1 to 2 RBCs per high powered field and are therefore at least as sensitive as urine sediment examination, but result in more false positive tests. False positive results may occur with alkaline urine with a pH greater than 9, contamination with oxidizing agents used to clean the perineum, and semen present in the urine after ejaculation.

By comparison, false negative tests are unusual; as a result, a negative dipstick reliably excludes abnormal hematuria [19]. Although red cells may be lysed in dilute urine, the hemoglobin that is released will be detected by the dipstick. (See "Evaluation of hematuria in adults".)

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. Significant causes of sterile pyuria include interstitial nephritis, renal tuberculosis, and nephrolithiasis. (See "Urine sampling and culture in the diagnosis of urinary tract infection in adults".)

URINE SEDIMENT Hematuria and pyuria by dipstick may be useful as a screening test. However, a microscopic examination of the urine sediment is essential in the evaluation of renal disease, as it permits detection of elements which cannot be found by dipstick alone (eg, red and white blood cells and casts, and epithelial cells or casts). Small amounts of crystals, bacteria, cells, or casts 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 [20]. In addition, crystals of uric acid, calcium oxalate, or phosphate may occasionally be seen.

The specimen is ideally examined within 30 to 60 minutes of voiding. The urine should be centrifuged at 3000 rpm for three to five minutes, most of the supernatant poured out, and the pellet resuspended with gentle shaking of the tube. A small amount of the resuspended sediment is poured on the slide.

The urine sediment examination should be performed by a clinician trained in urine microscopy, as the diagnostic yield compared to a laboratory urinalysis may be substantially greater [21]. However, in a study using photograph images, there were only fair to moderate levels of agreement among nephrologists in identifying important structures [22].

Crystalluria 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 (picture 3A-B). (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 (picture 4A-B). (See "Risk factors for calcium stones in adults".)Cystine crystals Cystine crystals, with their characteristic hexagonal shape, are diagnostic of cystinuria (picture 5). (See "Cystine stones".)Magnesium ammonium phosphate crystals Magnesium ammonium phosphate (struvite) and calcium carbonate-apatite are the constituents of struvite stones (picture 6). (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 "Methanol and ethylene glycol poisoning" and "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 in adults".) Although normal urine is sterile, asymptomatic bacteriuria is increasingly recognized but is usually not treated. (See "Approach to the adult 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 The presence of hematuria can be benign or reflect serious underlying disease (figure 1). The evaluation of patients with hematuria is discussed in detail separately, but some of the major issues will be briefly reviewed here. (See "Evaluation of hematuria in adults".)

Hematuria may be grossly visible or microscopic. Microscopic hematuria is commonly defined as the presence of more than 2 red blood cells per high powered field in a spun urine sediment (picture 7) [23]. The color change in gross hematuria does not necessarily reflect a large 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 to brown urine: Hematuria; hemoglobinuria; myoglobinuria".)

Hematuria may be transient or persistent. Transient hematuria is relatively common in young subjects and is not usually indicative of disease in this population. However, even transient hematuria can represent underlying malignancy in patients over age 50. 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. (See "Evaluation of hematuria in adults", section on 'Transient or persistent hematuria'.)

Persistent hematuria should always be evaluated. Among the more common pathologic causes are kidney stones, malignancy, and glomerular disease. Thus, an important aspect of evaluation is determining whether the hematuria is glomerular in origin or extraglomerular. Findings strongly suggestive of glomerular disease are red cell casts, proteinuria, and dysmorphic red cells, particularly acanthocytes (picture 8A, 9). The small number of red cells in normal urine are also dysmorphic, suggesting a glomerular origin [24]. (See "Hematuria: Glomerular versus extraglomerular bleeding".)

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) (picture 10A). 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 in adults" and "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.

Novel assays Glomerular epithelial cells, or podocytes, are involved in maintenance of the filtration barrier in the glomerular capillary tuft, and are the principal site of injury or genetic abnormality in certain glomerulopathies. (See "Mechanisms of immune injury of the glomerulus" and "Pathogenesis and diagnosis of focal segmental glomerulosclerosis", section on 'Familial or genetic disease' and "Congenital and infantile nephrotic syndrome".)

Podocytes are normally absent or present in only very small quantities in the urine of individuals without kidney disease, or with inactive glomerular diseases [25], but excretion appears to increase with active disease, and decrease with treatment [2527]. It has been suggested that podocyturia may be a better marker of ongoing glomerular damage than proteinuria, but the test is not yet available clinically [28].

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 [29]. 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 (picture 8B). (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 (picture 11A-B). 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 (picture 12A-B).

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 (picture 13A-B). 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 (picture 10B).

Waxy casts Waxy casts are thought to be the last stage of the degeneration of a granular cast (picture 10C). 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 (table 2).

Hematuria with red cell casts, dysmorphic red cells, proteinuria, and/or lipiduria This constellation of findings is virtually diagnostic of glomerular disease or vasculitis (picture 13A-B, 8A-B, 9). However, he absence of these pathognomonic changes in patients with hematuria does not exclude these disorders. (See "Differential diagnosis of glomerular disease" and "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 (picture 12A-B, 16A). 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 [30]. 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 mol/L); how this occurs is not clear [31].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 (picture 10A-C, 11A-B). 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 in adults" and "Glomerular hematuria: IgA; Alport; thin basement membrane nephropathy".)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 kidney disease, disorders that should be considered include prerenal disease (as with congestive heart failure), urinary tract obstruction, benign nephrosclerosis, and tubular or interstitial diseases.