Nephrosclerosis and hypertension

Abstract

In patients with benign nephrosclerosis, the histologic changes are characterized by hyaline degeneration of afferent arterioles with reduced kidney size. Although the glomeruli are nearly intact in patients with adult essential hypertension, the greatest numbers of sclerotic glomeruli are seen in nephrosclerosis with the aging process. Aging undoubtedly plays a role. In the authors' experience, the kidney of an elderly subject, although with normotensive pressure and normal level of cholesterol, shows an increased mesangial matrix and hypertrophic vascular medial smooth muscle cells. Kidneys of elderly subjects also are associated with a large number of sclerotic glomeruli. Experimental evidence supports the notion that the pathogenesis of glomerulosclerosis with nephrosclerosis has been demonstrated as important factors: (1) the elevation of PG (glomerular hypertension); (2) mesangial dysfunction, such as mesangiolysis and increased mesangial matrix; and (3) genetic abnormalities (apoptosis) in mesangial cells with glomerular hypertension. Malignant nephrosclerosis is characterized histologically by vascular endothelial damage and fibrinoid necrosis of afferent and interlobular arteries. In an afferent arteriole or a glomerulus, NOS or endothelin produced in endothelial cells may play a role in the reduction or the maintenance of vascular tone. The frequency of malignant hypertension has decreased because of the effective treatment of essential hypertension with new antihypertensive agents: calcium antagonists, ACE inhibitors, and angiotensin II receptor antagonists. Therefore, the importance of the prevention of essential hypertension with these antihypertensive agents, by slowing and stopping the increase in blood pressure from mild hypertension, has received widespread recognition in the prevention of organ damage, such as cases of cardiovascular disease and ESRD. Thus, prevention of renal injuries is an important goal of antihypertensive therapy.