Kidney disease can be discovered incidentally during a routine medical evaluation or with evidence of kidney dysfunction, such as hypertension, edema, nausea, or hematuria. The initial approach in both situations should be to assess the cause and severity of renal abnormalities. In all cases, this evaluation includes (1) an estimation of disease duration, (2) a careful urinalysis, and (3) an assessment of the glomerular filtration rate (GFR). The history and physical examinations, though equally important, are variable among renal syndromes—thus, specific symptoms and signs are discussed under each disease entity.
ASSESSMENT OF KIDNEY DISEASE
Kidney disease may be acute or chronic. Acute kidney injury (AKI) is worsening of kidney function over hours to days, resulting in the retention of nitrogenous wastes (such as urea nitrogen) and creatinine in the blood. Retention of these substances is called azotemia. Chronic kidney disease (CKD) results from an abnormal loss of kidney function over months to years. Differentiating between the two is important for diagnosis, treatment, and outcome. Oliguria is unusual in CKD. Anemia (from low kidney erythropoietin production) is rare in the initial period of AKI. Small kidneys are more consistent with CKD, whereas normal to large-size kidneys can be seen with both chronic and acute 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 a centrifuged urinary sediment provides 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 are formed when urinary flow is slow, allowing for the precipitation of Tamm-Horsfall mucoprotein in the renal tubule; if there are significant numbers of red or white blood cells in the urine, cellular casts may be formed. The presence of proteinuria by dipstick strongly suggests underlying glomerular disease. If the glomerular basement membrane (GBM) is damaged, eg, by inflammation, red blood cells may squeeze across into the urinary space and will appear “dysmorphic” (also called “acanthocytes”). Thus, proteinuria, hematuria with acanthocytes, and possibly red blood cells casts (eFigure 22–1) are indicative of glomerulonephritis. Heavy proteinuria and lipiduria are consistent with the nephrotic syndrome. Pigmented granular casts (also termed “muddy brown casts”) and renal tubular epithelial cells alone or in casts suggest 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 interstitial nephritis and pyelonephritis; Wright ...