Histologic sections of a kidney reveal patchy necrosis of epithelial cells of both the proximal and distal tubules with flattening of the epithelial cells, rupture of the basement membrane (tubulorrhexis), and marked interstitial edema. Acute inflammatory cells are not seen. What is the best diagnosis?
Acute tubular necrosis (ATN) may produce oliguria, decreased glomerular filtration rate (GFR), increased fractional excretion of sodium, and an abnormal urinary sediment. ATN may be caused by renal ischemia (ischemic ATN) or chemical toxins (toxic ATN). Renal ischemia is the most common cause of ATN, while toxic ATN may be caused by antibiotics (such as aminoglycosides and amphotericin B), heavy metals (such as cisplatin), radiographic agents, and endogenous toxins (such as myoglobin and hemoglobin). Both ischemic ATN and toxic ATN are characterized by the finding of eosinophilic hyalin or pigmented granular casts in the urine. Histologically, both ischemic and toxic ATN reveal interstitial edema, flattening of the tubular epithelial cells, and tubular epithelial cell necrosis. One difference between these two etiologies is that the tubular epithelial cell necrosis is extensive with toxic ATN, while the necrosis with ischemic ATN is patchy with interposed unaffected segments. This can be quite variable, however, and ceain causes may be associated with damage to specific poions of the kidney. Both ischemia and heavy metals primarily damage the epithelial cells of the proximal straight tubules, while aminoglycosides primarily affect the proximal convoluted tubule. Reference: Robbins & Cotran Pathologic Basis of Disease, 9edition
Acute pyelonephritis
Acute tubular necrosis
Chronic glomerulonephritis
Chronic pyelonephritis
miscellaneous