Renal Histopathology , Urine Cytology , and Cytopathology of Acute Renal Failure

Causes of acute renal failure can be divided into three categories: 1) prerenal, due to inadequate perfusion; 2) postrenal, due to obstruction of outflow; and 3) intrinsic, due to injury to renal parenchyma. Among the latter, diseases of, or injury to, glomeruli, vessels, interstitium, or tubules may lead to a decrease in glomerular filtration rate (GFR). Glomerular diseases that lead to acute renal failure are the proliferative glomerulonephritides, including postinfectious and membranoproliferative glomerulonephritis secondary to glomerular deposition of immune complexes. If glomerular injury is severe enough to damage the glomerular basement membrane, leakage of fibrin and other plasma proteins stimulates formation of cellular extracapillary “crescents” composed of epithelial cells and monocytes and macrophages. Crescents may form as a result of an inflammatory reaction to immune complexes formed to nonglomerular antigens; antibody reaction to intrinsic glomerular antigens, as in anti–glomerular basement membrane disease; and, in the absence of immune complexes, the pauci-immune processes, which include the small vessel vasculitides, including Wegener’s granulomatosis and microscopic polyarteritis. Immunohistologic examination and electron microscopy play important roles in the diagnosis of these processes. Extensive crescent formation is accompanied by rapidly progressive acute renal failure. The urine sediment in these diseases often contains red blood cells and red cell casts. Vascular diseases (involving veins, arteries, or arterioles and capillaries) can lead to hypoperfusion and acute renal failure. Venous thrombosis, most often due to trauma or a nephrotic state, and arterial thrombosis due to trauma or vasculitis, cause parenchymal ischemia and Lorraine C. Racusen Cynthia C. Nast