Revascularization in atherosclerotic renal artery disease

A 69-year-old white male attorney was referred three years ago because of progressive hypertension and declining renal function. He had smoked two packs of cigarettes daily for the past 55 years. Modest hypertension had been successfully treated with a thiazide diuretic for several years. At age 51, an 8 cm abdominal aortic aneurysm was resected. His blood pressure had risen 4 years ago to levels between 170/108 mm Hg and 205/110 mm Hg despite increased medications: pindolol, 5 mg twice daily; prazosin, 5 mg twice daily; and indapamide, 2.5 mg daily. His serum creatinine rose from 0.9 mg/dl at age 52 to 2.0 mg/dl at age 66. He was aware of several episodes of confusion, which had been attributed to lacunar strokes, but he remained able to work and function normally. He had no history of myocardial infarction or angina; an electrocardiogram disclosed left-ventricular hypertrophy. Hyperlipidemia had been treated with lovastatin, cholestyramine, and niacin. His medical history included resection of cancer of the penis and recently detected adenocarcinoma of the prostate, for which radiation therapy had been planned. Physical examination revealed an alert and functional man. His blood pressure was 205/108 mm Hg; and the pulse was 75 beats/min. The weight was 195 lbs, the height, 69 inches. Ophthalmic examination demonstrated grade II retinopathy. No carotid bruits were heard. Cardiac examination revealed a fourth heart sound. An abdominal scar was present, a result of the abdominal aneurysm surgery. Epigastric and abdominal bruits were detected in every quadrant. Pulses in the lower extremities were diminished. Pitting edema was present at the ankles. Laboratory data disclosed: hematocrit, 42.8; hemoglobin, 14.9 g/dl; serum creatinine, 2.0 mg/dl; sodium, 140 mEq/liter; potassium, 3.8 mEq/ liter; uric acid, 8.4 mg/dl; albumin, 4.2 g/dl; calcium, 9.3 g/dl; PO4, 3.1 mg/dl; and glucose, 122 mg/dl. Total cholesterol was 180 mg/dl; triglycerides, 122 mg/dl; HDL, 38 mg/dl. Urinalysis disclosed 11 proteinuria. A chest radiograph demonstrated an elevated right hemidiaphram, scattered fibrosis, and a tortuous aorta. An electrocardiogram showed left-ventricular hypertrophy with strain pattern and was unchanged from previous tracings. A renal angiogram demonstrated single renal arteries bilaterally with high-grade stenoses at their origins (Fig. 1). Severe atheromatous changes were present in the abdominal aorta, as were postoperative changes of a straight graft repair of the infrarenal abdominal aorta. Bilateral common iliac artery aneurysms were found. High-grade stenosis was present at the origin of the celiac artery. Renal-vein renin values were as follows: right, 13.2 ng AI/ml/hr; left, 10.0 ng/AI/ml/hr; and inferior vena cava, 6.7 ng AI/ml/hr. Over the three years since he was originally seen, the antihypertensive regimen has comprised indapamide, 2.5 mg daily; pindolol, 5 mg twice daily; and hydralazine, 25 mg, and prazosin, 5 mg each three times daily. He continued to take cholestyramine; lovastatin, 40 mg qd; niacin, 1000 mg; glyburide, 1.25 mg daily, was added a year or so ago. Home blood pressure readings ranged between 140/75 mm Hg and 155/80 mm Hg. Ambulatory blood pressure readings indicated average values of 149/83 mm Hg. Serum creatinine was 2.2 mg/dl; creatinine clearance, 38 ml/min. Amaurosis fugax developed at age 69, which carotid endarterectomy corrected without complications. He continued to smoke. He completed radiation therapy for carcinoma of the prostate, for which he now has no evidence of disease. A magnetic resonance angiogram (MRA) with gadolinium contrast medium was performed to determine progression (or not) of the vascular lesions (Fig. 2). Aneurysmal dilation above the previous graft remained visible, but no progression in the renal artery lesions per se could be seen.