Arteriovenous Communication of the Kidney in a Patient with Hypertension

Abstract

In the search for the cause of hypertension, renal investigations, from both a laboratory and a roentgen standpoint, are now routine. Intravenous pyelograms, with or without initial one-, two-, and three-minute films, renal wash-out pyelograms, and arteriograms are usually obtained. The author (S. B. F.) feels that, in spite of its rarity, one cause of renal hypertension, renal arteriovenous fistula, can probably be suspected on the basis of routine intravenous pyelography. A case report to substantiate this view follows. Case Reports A 43-year-old white woman was admitted to Mt. Sinai Hospital (Minneapolis) Nov. 25, 1962, because of cardiac decompensation. In 1953 she was examined at the Mayo Clinic for the evaluation of hypertension, which had recently been discovered. The regitine test was normal at that time. An abnormal pyelogram was described as probably indicative of cicatricial calyceal changes. In the intervening years, the patient had been relatively well except for headaches. One week prior to entering the hospital, she experienced precordial pain and dyspnea, and she was admitted in a state of decompensation. Physical examination revealed bilateral crepitant râles, cardiomegaly without murmurs, venous distention, and hypertension of 210/140. The fundi showed grade I–II hypertensive retinopathy. Exclusive of diuretics, Digoxin, etc., 2.5 mg. of Serpasil was given intramuscularly in two doses two hours apart, with a resultant drop in blood pressure to 190/120 to 120/80 to 140/80. In twenty-four hours, without Serpasil, pressure returned to 210/120. In the same interval, the decompensation cleared. Laboratory studies showed hemoglobin 12.9 gm., white blood cells 10,700 with a normal differential, normal clotting time (Lee-White). Serology was normal. The specific gravity of the urine was 1.005, pH 7; albumin and sugar negative. Stools were negative for blood. Blood urea nitrogen was 15 mg. per cent. There was an initial elevated blood sugar, which could not be substantiated on follow-up studies. C02 was 24 mEq/1. Cholesterol was 264 mg. per cent. Sedimentation rate was 45 mm. in au hour. Other findings were: hematocrit, 39 per cent; serum sodium, 139 mEq/1 ; potassium, 3.5 mEq/1; protein-bound iodine, 3.5 µg. per cent; serial transaminases, 26, 26, 9, and 14 units. Urea clearance was 89 per cent of normal and standard clearance was 59 per cent of normal. Phenolsulfalein excretion was 9 per cent at fifteen minutes and 13 per cent in the second fifteen minutes. Midstream urine culture showed 1,000 colonies of proteus per cubic centimeter, which was considered to be a contaminant. Twenty-four hour aldosterone was 4 µg. in twenty-four hours (normal) ; 17 ketosteroids were 4.7 mg. in twenty-four hours. An intravenous regitine test showed a decline from the base line of 180/100 to 160/90 within three minutes after administration of 5 mg.