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Kidneys may be damaged by a variety of injuries; data helpful in the evaluation of kidney disease include estimation of disease duration, examination of the urine and quantification of urinary protein excretion, and estimation of the glomerular filtration rate (eGFR). Additionally, renal imaging (most often ultrasonography) can be helpful. Kidney biopsy may be performed in select cases as noted below and particularly when glomerulonephritis is suspected.


Kidney disease can be acute or chronic. Acute kidney injury (AKI) is worsening of kidney function over hours to days, resulting in retention of waste products (such as urea nitrogen) and creatinine in the blood. Retention of these substances is called azotemia. Chronic kidney disease (CKD) is the abnormal loss of kidney function over months to years. Differentiating between AKI and CKD is important for diagnosis and treatment, and certain clues may help distinguish the two. For instance, oliguria is only observed in AKI, whereas anemia (from low kidney erythropoietin production) suggests CKD. Additionally, small kidney size on ultrasound or other imaging is more consistent with CKD, whereas normal to large kidney size can be seen with both acute and chronic disease.


Examination of the urine can provide important clues to underlying kidney disease. A urine specimen should be collected in midstream or by bladder catheterization and examined within 1 hour after collection to avoid destruction of formed elements. Urinalysis includes a dipstick examination followed by microscopy if the dipstick has positive findings. The dipstick examination measures urinary pH, specific gravity, protein, hemoglobin, glucose, ketones, bilirubin, nitrites, and leukocyte esterase. Microscopy of centrifuged urinary sediment permits examination of formed elements—crystals, cells, casts, and infectious organisms. A bland (normal) sediment is common, especially in CKD and acute nonparenchymal disorders, such as limited effective blood flow to the kidney or urinary obstruction. Urinary casts form when urine flow is slow, leading to precipitation of Tamm-Horsfall mucoprotein in the renal tubule; if there are many red or white blood cells in the urine, cellular casts may form. The presence of protein on dipstick examination strongly suggests underlying glomerular disease. If the glomerular basement membrane (GBM) is damaged (eg, by inflammation), red blood cells may leak into the urinary space and appear dysmorphic (also called acanthocytes). Thus, proteinuria, hematuria with acanthocytes, and red blood cells casts (eFigure 22–1) are highly suggestive of glomerulonephritis. Heavy proteinuria and lipiduria are consistent with nephrotic syndrome. Pigmented granular casts (also termed “muddy brown casts”) and renal tubular epithelial cells alone or in casts are hallmarks of acute tubular necrosis (ATN). White blood cells (including neutrophils and eosinophils), white blood cell casts (Table 22–1), and proteinuria of varying degree can be seen with pyelonephritis and interstitial nephritis; Wright and Hansel stains can detect eosinophiluria. Pyuria alone can indicate a urinary tract infection. Proteinuria and hematuria are discussed more thoroughly below.

eFigure 22–1.

Red blood cell ...

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