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Benign Hypertensive Arteriolar Nephrosclerosis
Benign hypertensive arteriolar nephrosclerosis is progressive renal impairment caused by chronic, poorly controlled hypertension. Symptoms and signs of chronic kidney disease may develop (eg, anorexia, nausea, vomiting, pruritus, somnolence or confusion), as may signs of end-organ damage secondary to hypertension. Diagnosis is primarily clinical, supported by ultrasonography and routine laboratory test findings. Treatment is strict BP control and support of renal function.
Benign hypertensive arteriolar nephrosclerosis results when chronic hypertension damages small blood vessels, glomeruli, renal tubules, and interstitial tissues. As a result, progressive chronic kidney disease develops.
Benign nephrosclerosis progresses to end-stage renal disease in only a small percentage of patients. However, because chronic hypertension and benign nephrosclerosis are common, benign nephrosclerosis is one of the most common diagnoses in patients with end-stage renal disease. It is termed benign to distinguish it from malignant arteriolar nephrosclerosis, which is a synonym for hypertensive emergency.
Risk factors include
Poorly controlled moderate to severe hypertension
Other renal disorders (eg, diabetic nephropathy)
Blacks are at increased risk; it is unclear if the risk is increased because poorly treated hypertension is more common among blacks or because blacks are more genetically susceptible to hypertension-induced renal damage.
Symptoms and signs of chronic kidney disease, such as anorexia, nausea, vomiting, pruritus, somnolence or confusion, weight loss, and an unpleasant taste in the mouth, may develop. Signs of hypertension-related end-organ damage may occur in the vasculature of the eyes and in the skin, CNS, and periphery.
The diagnosis may be suspected when routine blood tests indicate deteriorating renal function (eg, elevated creatinine and BUN, hyperphosphatemia) in a hypertensive patient. Diagnosis is usually inferred because of the history and evidence of hypertension-related end-organ damage (eg, retinal changes, left ventricular hypertrophy) on physical examination. Hypertension should be present before onset of proteinuria and renal failure, and there should be no other clinically suspected cause of renal failure.
Urine testing should not suggest other causes of renal failure (eg, glomerulonephritis, hypertensive emergency). On urinalysis, there should be few cells or casts in the sediment, and protein excretion is usually < 1 g/day (it is occasionally higher and in the nephrotic range).
Ultrasonography should be done to exclude other causes of renal failure. It may show that kidney size is reduced. Renal biopsy is done only if the diagnosis remains unclear.
Treatment involves strict BP control. The BP goal is < 140/90 mm Hg, according to JNC 8 guidelines (1). Most experts suggest using an angiotensin II receptor blocker or an ACE inhibitor for patients who have proteinuria. Calcium channel blockers and thiazide diuretics can be used as first-line drugs; most patients require combination therapy for BP control. Weight loss, exercise, and salt and water restriction also help control BP. Chronic kidney disease should be managed.
James PA, Oparil S, Carter BL, et al. 2014 Evidence-based guideline for the management of high blood pressure in adults: Report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA 311(5):507-520, 2014.
Chronic hypertension can cause benign hypertensive arteriolar nephrosclerosis, resulting in chronic kidney disease and, infrequently, end-stage renal disease.
Suspect the diagnosis if chronic hypertension precedes onset of renal insufficiency.
Do ultrasonography to check for other causes of renal failure.
Treat most patients with an ACE inhibitor or angiotensin II receptor blocker and possibly other drugs.
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