Hyaline arteriolosclerosis

Pathogenesis involves leakage of plasma proteins across injured endothelium and increased basement membrane matrix synthesis, depositing eosinophilic, glassy 'hyaline' material in the intima/media of arterioles. It is the small-vessel lesion of long-standing benign hypertension and of diabetes (where nonenzymatic glycosylation of basement membranes accelerates it), and is the hallmark of benign nephrosclerosis — kidneys become small with a finely granular cortical surface and patchy ischemic atrophy. In diabetes, hyaline arteriolosclerosis affects both the afferent and efferent arterioles (efferent involvement raises intraglomerular pressure and drives diabetic glomerulosclerosis with Kimmelstiel-Wilson nodules). Contrast with hyperplastic arteriolosclerosis: 'onion-skin' concentric smooth muscle proliferation seen in malignant hypertension, often with fibrinoid necrosis.