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 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 (see Hypertensive Emergencies).
Risk factors include older age, poorly controlled moderate to severe hypertension, and 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
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 (see Symptoms and Signs). 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 or 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 is done only if other causes of renal failure must be excluded. It may show that kidney size is reduced. Renal biopsy is done only if the diagnosis remains unclear.
Prognosis usually depends on adequacy of BP control and degree of renal failure. Usually, renal impairment progresses slowly; after 5 to 10 yr, only 1 to 2% of patients develop clinically significant renal dysfunction.
Treatment involves strict BP control (see General Treatment). The BP goal is < 140/90 mm Hg, although < 130/80 mm Hg is more appropriate for patients with diabetes or chronic kidney disease. Most experts suggest low-dose thiazide diuretic therapy. Among patients with proteinuria, an ACE inhibitor or angiotensin II receptor blocker is added. Ca channel blockers and ß-blockers can be added as needed; most patients require combination therapy for BP control. Weight loss, exercise, and salt and water restriction also help control BP. Chronic renal failure should be managed (see Prognosis).
Last full review/revision April 2008 by Seyed-Ali Sadjadi, MD
Content last modified November 2013