Chapter 045. Azotemia and Urinary Abnormalities (Part 5) Approach to the patient with hematuria. RBC, red blood cell; WBC, white blood cell; GBM, glomerular basement membrane; ANCA, antineutrophil cytoplasmic antibody; VDRL, venereal disease research laboratory; ASLO, antistreptolysin O; UA, urinalysis; IVP, intravenous pyelography; CT, computed tomography. A detailed discussion of glomerulonephritis and diseases of the microvasculature can be found in Chap. 277. OLIGURIA AND ANURIA Oliguria refers to a 24-h urine output of <500 mL, and anuria is the complete absence of urine formation (<50 mL). Anuria can be caused by total urinary tract obstruction, total renal artery or vein occlusion, and shock (manifested by severe hypotension and intense renal vasoconstriction). Cortical necrosis, ATN, and rapidly progressive glomerulonephritis can occasionally cause anuria. Oliguria can accompany any cause of acute renal failure and carries a more serious prognosis for renal recovery in all conditions except prerenal azotemia. Nonoliguria refers to urine output >500 mL/d in patients with acute or chronic azotemia. With nonoliguric ATN, disturbances of potassium and hydrogen balance are less severe than in oliguric patients, and recovery to normal renal function is usually more rapid. Proteinuria The evaluation of proteinuria is shown schematically in Fig. 45-3 and is typically initiated after detection of proteinuria by dipstick examination. The dipstick measurement detects mostly albumin and gives false-positive results when pH > 7.0 and the urine is very concentrated or contaminated with blood. A very dilute urine may obscure significant proteinuria on dipstick examination, and proteinuria that is not predominantly albumin will be missed. This is particularly important for the detection of Bence-Jones proteins in the urine of patients with multiple myeloma. Tests to measure total urine concentration accurately rely on precipitation with sulfosalicylic or trichloracetic acids. Currently, ultrasensitive dipsticks are available to measure microalbuminuria (30–300 mg/d), an early marker of glomerular disease that has been shown to predict glomerular injury in early diabetic nephropathy (Fig. 45-3). Figure 45-3 [newpage] Approach to the patient with proteinuria. Investigation of proteinuria is often initiated by a positive dipstick on routine urinalysis. Conventional dipsticks detect predominantly albumin and cannot detect urinary albumin levels of 30–300 mg/d. However, more exact determination of proteinuria should employ a 24-h urine collection or a spot morning protein/creatinine ratio (mg/g). The pattern of proteinuria on UPEP (urine protein electrophoresis) can be classified as "glomerular," "tubular," or "abnormal" depending upon the origin of the urine proteins. Glomerular proteinuria is due to abnormal glomerular permeability. "Tubular proteins" such as Tamm-Horsfall are normally produced by the renal tubule and shed into the urine. Abnormal circulating proteins such as kappa or lambda light chains are readily filtered because of their small size. RBC, red blood cell; FSGS, focal segmental glomerulosclerosis; MPGN, membranoproliferative glomerulonephritis. The magnitude of proteinuria and the protein composition of the urine depend upon the mechanism of renal injury leading to protein losses. Both charge and size selectivity normally prevent virtually all plasma albumin, globulins, and other large-molecular-weight proteins from crossing the glomerular wall. However, if this barrier is disrupted, there can be leakage of plasma proteins into the urine (glomerular proteinuria; Fig. 45-3). Smaller proteins (<20 kDa) are freely filtered but are readily reabsorbed by the proximal tubule. Normal individuals excrete <150 mg/d of total protein and <30 mg/d of albumin. The remainder of the protein in the urine is secreted by the tubules (Tamm-Horsfall, IgA, and urokinase) or represents small amounts of filtered β 2 -microglobulin, apoproteins, enzymes, and peptide hormones. Another mechanism of proteinuria occurs when there is excessive production of an abnormal protein that exceeds the capacity of the tubule for reabsorption. This most commonly occurs with plasma cell dyscrasias such as multiple myeloma, amyloidosis, and lymphomas that are associated with monoclonal production of immunoglobulin light chains. . Chapter 045. Azotemia and Urinary Abnormalities (Part 5) Approach to the patient with hematuria. RBC, red blood cell; WBC,. by total urinary tract obstruction, total renal artery or vein occlusion, and shock (manifested by severe hypotension and intense renal vasoconstriction). Cortical necrosis, ATN, and rapidly. discussion of glomerulonephritis and diseases of the microvasculature can be found in Chap. 277. OLIGURIA AND ANURIA Oliguria refers to a 24-h urine output of <500 mL, and anuria is the complete