Nephrosclerosis



Nephrosclerosis is one of the most common complications of essential hypertension and is a significant cause of end-stage renal failure. Two forms of the process can be described based on the severity and duration of the hypertension, the pathology of the vascular lesion in the kidney, and the eventual effect on renal and patient survival.

Benign nephrosclerosis is a misnomer that is used to describe a slow process of intrarenal vas­cular sclerosis and ischemic change that compli­cates the course of long-standing essential hyper­tension. The kidneys become progressively shrunken and the renal surfaces exhibit a fine, progressing to coarse, granular appearance.

Although all the intrarenal arteries show some signs of sclerotic thickening, the dominant lesion is at the level of the afferent arteriole. Hyaline thickening of the afferent arteriolar wall leads to a homogeneous, eosinophilic appearance of the vessel. The glomeruli have ischemic wrinkling of the basement membranes and become progres­sively sclerotic, while the tubules undergo atro­phy and are replaced by fibrotic tissue in the ab­sence of inflammation.

Minimal proteinuria occurs in some patients, but the urinary sediment is usually normal. A slow decline in GFR is generally the only feature of the disorder. End-stage renal failure due to nephro­sclerosis is more common in males and blacks, and nephrosclerosis has been estimated to ac­count for between 5 and 25 per cent of all cases of end-stage renal failure. Treatment is directed at early control of blood pressure elevations, but even late intervention may slow the progression of renal failure.
Malignant nephrosclerosis is the result of a gen­eralized necrotizing arteritis that is seen in con­junction with accelerated hypertension. Protein­uria, often with hematuria, occurs together with acute decreases in GFR. The diastolic blood pres­sure is usually, but not necessarily, above 120 mm Hg, and neuroretinal signs of encephalopathy, ret­inal arteriolar hemorrhage, and papilledema are almost always present. The entire syndrome is most common in black males and most often oc­curs as an acute exacerbation of essential hyper­tension.

The kidneys are generally contracted in size and have petechial hemorrhages on the surfaces. Two renal vascular lesions characterize malignant nephrosclerosis. The first lesion consists of fibri­noid necrosis, without inflammation, in the renal arterioles and sometimes extending into the glo­merular tufts. The second distinguishing lesion is the “onion skin” endothelial proliferation in small arteries. Concentric layers of collagen and proliferating endothelial cells contribute to this appearance. Similar changes are seen in the renal vessels in the hemolytic-uremic syndrome and the accelerated hypertension of scleroderma.

Prior to effective antihypertensive therapy, more than 75 per cent of persons with accelerated hypertension died of renal failure or cardiac fail­ure within one year. With effective control of the blood pressure, the prognosis is reversed, with less than 25 per cent of the patients suffering a renal or cardiac death within one year. Prompt and strict control of blood pressure is essential, and the course of renal failure can be arrested and even reversed. With long-term blood pressure nor­malization, the vascular lesions heal, demonstrat­ing the contributory role of pressure per se to the pathogenesis of the disorder.





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