Gross Findings Light Microscopy

"Benign" nephrosclerosis results in small kidneys with finely granular surface and thinned cortex in late stages. Malignant (accelerated) nephro-sclerosis grossly shows petechial hemorrhage of the subcapsular surface, with mottling and occasional areas of infarct. Microscopically, in "benign" arterionephrosclerosis there is vascular wall medial thickening with frequent afferent arteriolar hyaline deposits, and varying degree of intimal fibrosis. The hyalinization is due to endothelial injury and increased pressure, leading to an insudate of plasma macromolecules. There are associated focal glomerular ischemic changes with variable thickening and wrinkling of the basement membrane, and/or global sclerosis, tubular atrophy, and interstitial fibrosis (Fig. 10.1). Global sclerosis more commonly is of the obsolescent type, with fibrous material obliterating Bowman's space. Solidified glomeruli, where the tuft is globally sclerosed without collagen in Bowman's space, has been called "decompensated" arterionephrosclerosis. Secondary focal segmental glomerulosclerosis (FSGS) may also occur, often with associated glomerular basement membrane (GBM) corrugation and filling of Bowman's space with fibrous material (4-10). These morphologic features hint that the segmental sclerotic process is secondary to hypertension-associated injury, rather than idio-pathic FSGS. The lesions of accelerated hypertension-associated consist of mucoid change of the arterioles, often with red blood cell (RBC) fragments within the wall. In malignant hypertension, arterioles show fibrinoid necrosis, and interlobular arteries have a concentric onion-skin pattern of intimal fibrosis, overlapping with the appearance of progressive systemic sclerosis

Figure 10.1. Arterial and arteriolar medial thickening, intimal and interstitial fibrosis, tubular atrophy and global sclerosis in arterionephrosclerosis (PAS).

and thrombotic microangiopathy (Fig. 10.2) (see below). There is proportional tubulointerstitial fibrosis in arterionephrosclerosis.

Immunofluorescence may show trapping of IgM and C3 in glomeruli, but there are no immune complex-type deposits. In malignant hypertension, fibrin/fibrinogen staining may be present in necrosed arterioles/arter-ies and injured glomeruli.

Figure 10.2. Vascular fibrinoid necrosis and thrombosis in malignant hypertension (Jones silver stain).

Electron microscopy confirms the corrugated, wrinkled GBM, and ischemic changes with increased lamina rara interna but without immune deposits. Hyaline may be present in sclerosed segments. Some foot process effacement may also be present, but it is usually not extensive.

Although none of the above lesions is pathognomonic, the constellation of these changes in the absence of other lesions of primary glomerular disease is indicative of arterionephrosclerosis.

Blood Pressure Health

Blood Pressure Health

Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...

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