Massive Proteinuria due to Renal Artery Stenosis
Author(s) -
Hirofumi Sato,
Takao Saito,
Yutaka Kasai,
K. Abe,
KAORU YOSHINAGA
Publication year - 1989
Publication title -
the nephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000185275
Subject(s) - icon , medicine , citation , library science , computer science , programming language
Hiroshi Sato, MD, The second Department of Internal Medicine, Tohoku University School of Medicine, 1-1, Seiryo-cho, Sendai, 980 (Japan) Dear Sir, Nephrotic-range proteinuria associated with renal artery stenosis has been reported by several authors [1–4]. Hyperreninemia secondary to renal artery stenosis was proposed as a possible cause of protein leak [2]. In this article, we present a case of renovascular hypertension exhibiting hyperreninemia with massive proteinuria. Renal biopsy showed no significant glomerular abnormalities on light microscopy, immunofluorescence study, and electron-microscopic examination. Following radical surgery, both proteinuria and hyperreninemia were dramatically improved. Case Report A 56-year-old man was referred to our hospital for evaluation of hypertension. His brachial blood pressure was 210/120 mm Hg. Peripheral pulses were symmetric and not weakened. Abdominal bruit was not audible. There was slight pitting edema in the legs. The electrocardiogram and chest X-ray were normal. Urinalysis showed massive proteinuria (4–7 g/day) with normal sediment. BUN was 26 mg/dl, serum creatinine 2.2 mg/dl, creatinine clearance 37 ml/min, and serum total protein 6.0 g/dl. Serum sodium was 142 mEq/1, potassium 4.0 mEq/1, and chloride 109 mEq/1. Serum cholesterol was 288 mg/dl. Antistreptolysin O titer and serum level of C3, C4, and CH50 were within the normal range. Antinuclear antibodies were absent. Plasma renin activity (PRA) was over 100 ng/ml/6 h (normal range 5–30), and plasma aldosterone concentration 15.6 ng/ml (normal range 2–12). Renal scintigram and renogram exhibited marked reduction in the size and perfusion of the left kidney. Abdominal arteriogram showed diffuse atherosclerosis of the aorta with severe stenosis of the left renal artery (approximately 75% stenosis). The right renal artery was almost intact. From these clinical data, he was diagnosed as having renovascular hypertension due to left renal artery stenosis, and underwent a bypass surgery that reconstructed the left renal artery by autovein grafting (the femoral vein was used). Following surgery, the blood pressure and PRA returned to normal, and proteinuria decreased to 0.5 g/day. Renal biopsy, performed at the operation, revealed no significant abnormalities on light microscopy and immunofluorescence
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom