Abstract

Chronic kidney disease (CKD) associated with hypertension disproportionately affects African Americans, and occurs at younger age (as young as 20s) and with faster progression than in whites. Men are affected more than women. Patients develop progressive proteinuria that is related to the severity of hypertension, and may even have nephrotic range proteinuria. Hypertension-associated CKD accounts for approximately 25% of patients reaching end-stage kidney disease. Intensive therapy with antihypertensive drugs, including renin-angiotensin blockade, slows progression. Malignant hypertension can present with additional findings including congestive heart failure, acute kidney injury, and microangiopathic hemolytic anemia. Light microscopy: Hypertension-associated kidney disease is characterized by arterionephrosclerosis, with medial thickening, intimal fibrosis, and tortuosity of mediumand large-sized arteries. There is medial thickening and hyalinosis of arterioles, frequently associated with global glomerulosclerosis and often seen in a solidified pattern. Secondary segmental sclerosis can occur, particularly in a perihilar location. There is proportional tubulointerstitial fibrosis. With accelerated hypertension-associated injury, there is mucoid change of the arteries. Endothelial swelling and red blood cell fragments may be present in the arterial wall, and medial hypertrophy of small interlobular arteries in a concentric pattern with luminal stricture, the so called “onion skinning,” may be seen. In malignant hypertension, fibrinoid necrosis of the wall of arterioles and/or interlobular arteries often occurs with red blood cell fragments and fibrin within the lumen. Glomerular involvement with fibrin thrombi is uncommon.

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