Figure 54

Benign and malignant nephrosclerosis. In benign nephrosclerosis the artery walls are thickened with intimai fibrosis and luminal narrowing. Arteriolar walls are thickened with insudative lesions, a process affecting afferent arterioles almost exclusively. Both of these processes, which can be quite patchy, result in chronic ischemia. A, In glomeruli, chronic ischemia is manifested by gradual capillary wall wrinkling, luminal narrowing, and shrinkage and solidification of the tufts. B, As these processes progress, collagen forms internal to Bowman's capsule, beginning at the vascu

FIGURE 5-3 (see Color Plate)

Disseminated intravascular coagulation. In disseminated intravascular coagulation, fibrin thrombi are typically found in many glomerular capillary lumina. In contrast to the thrombotic microangiopathies, in disseminated intravascular coagulation, fibrin is not primarily in vessel walls but in the lumina. Consequently, the capillary wall thickening, endothelial cell swelling, and fibrin accumulation in subendothelial locations are not features of this lesion. In the glomerulus illustrated, the fibrin is in many capillary lumina and appears as bright fuchsin positive (red) masses.

lar pole and growing as a collar around the wrinkled ischemic tufts. This collagen formation ultimately is associated with tubular atrophy and interstitial fibrosis.

In malignant nephrosclerosis the changes are virtually identical to those of thrombotic microangiopathies (Fig. 5-1 C). Malignant nephrosclerosis may be seen in essential hypertension, scleroder-ma, unilateral renovascular hypertension (with a contralateral or "unprotected" kidney), and as a complicating event in many chronic renal parenchymal diseases.

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