Renal arteriosclerosis (RA), also known as nephrosclerosis or hypertensive nephrosclerosis, is scarring of the kidney due to infiltration by fibrous connective tissue, usually caused by renovascular diseases or chronic hypertension. The associated vascular changes can potentiate ischemic injury. RA can be either benign or malignant. Benign RA is characterized by the gradual and continuous deterioration of renal arteries, resulting in progressive kidney damage. Malignant RA is also characterized by deteriorating arteries but at a much quicker pace, requiring prompt treatment to avoid serious life-threatening complications.

No specific cause of RA has been identified. Risk factors include African ancestry, mature age, severe hypertension, and underlying chronic kidney disease (especially diabetic nephropathy). There are genetic variants associated with RA.

Typical presentation consists of an African-American individual with a long-term history of hypertension, elevations in blood urea nitrogen (BUN) and plasma creatinine concentration that slowly progress over time, and mild proteinuria. Most common clinical symptoms are manifestations of severe hypertension and include blurry vision, confusion, headache, nausea, and vomiting. Most common clinical signs include hypertension-related organ damage, changes in retinal vessels, and left ventricular hypertrophy. Some complications include heart failure, stroke, and/or uremia.

The primary goal of treatment is to control blood pressure with the use of antihypertensive drugs to prevent progression to renal failure.