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Although some patients with kidney disease experience evidence of their disease such as hypertension, edema, nausea, or hematuria that may lead to its discovery, kidney disease is often discovered incidentally during a routine medical evaluation. The initial approach to kidney disease is to assess the cause and severity of renal abnormalities. In all cases, this evaluation includes (1) estimation of disease duration, (2) careful examination of the urine, and (3) assessment of the glomerular filtration rate (GFR). The history and physical examination, though equally important, are variable among renal syndromes—thus, specific symptoms and signs are discussed under each disease entity.


Disease Duration

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 ...

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