An early thrombus is seen in a small renal artery in a patient with patchy cortical infarction (original magnification X 250). The patient presented with acute renal failure. The thrombosis may be due to a hypercoaggulable state (eg, disseminated intravascular coaggulation) or endothelial injury (eg, hemolytic uremic syndrome). If the cortical necrosis is patchy, recovery of adequate renal function may occur .
A parenchymal infarct in a patient with renal vein thrombosis (hema-toxylin and eosin, original magnification X 200). A few surviving tubules and a rim of inflammatory cells are seen at the periphery of the infarct. Infarcts may also be seen with arterial thromboses, and with severe injury to the microvasculature, as occurs in thrombotic microangiopathies . If the process is extensive, acute cortical necrosis may occur, often leading to irreversible renal failure.
FIGURE 9-6 (see Color Plate)
FIGURE 9-6 (see Color Plate)
A fine-needle aspirate in renal infarction. A, Low magnification shows many degenerating cells with a "dirty background" containing cellular debris and scattered neutrophils. Compare to acute tubular necrosis, which has only scattered degenerated or necrotic cells without the extensive necrosis and cell debris. Neutrophils may be numerous if the edge of an infarct is aspirated (May-Grunwald Giemsa, original magnification X 40). B, Diffusely degenerated and necrotic cells with condensed and disrupted cytoplasm and pyknotic nuclei, and an adjacent neutrophil. No significant numbers of viable tubule epithelial cells remain (May-Grunwald Giemsa, original magnification X 160).
A small artery with severe inflammation in a patient with a small vessel vasculitis. The wall of the vessel is infiltrated by lymphocytes, plasma cells, and eosinophils (hematoxylin and eosin, original magnification X 250). The patient was p-ANCA positive. ANCA may play a pathogenic role in the vasculitis process . Vasculitis in the kidney is often part of a systemic syndrome, but may occur as an apparently renal-limited process.
FIGURE 9-8 (see Color Plate)
Microangiopathic changes in a small artery, with endothelial activation, evidenced by the large endothelial cells with hyperchro-matic nuclei and vacuolization. There is intimal edema with some cell proliferation, and a prominent band of fibrinoid necrosis is seen; the latter appears dark red-pink on this hematoxylin-eosin stain, and represents insudation of fibrin and plasma proteins into the wall of the injured vessel (original magnification X 250). The differential diagnosis includes hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, malignant hypertension, scleroderma, and drug toxicity, the latter due most commonly to mitomycin C or cyclosporine/FK506 .
A cast of necrotic tubular cells in urine sediment (Papanicolaou stain, original magnification X 400). The most likely causes of damage to the renal tubules with such findings in the urinary sediment are severe ischemia/infarction, or tubular necrosis due to exposure to toxins which injure the renal tubules. The latter include antibiotics, including aminoglycosides and cephalosporins, and chemotherapeutic agents.
Was this article helpful?