Renovascular hypertension may cause nephrotic range proteinuria and focal glomerulosclerosis in contralateral kidney.

Little attention has been paid to nephropathies and proteinuria in renovascular hypertension (RVH). Recently there has been a growing interest in the conditions induced by RVH. 10 cases of RVH were diagnosed by angiography and renin sampling from renal veins in the last 6 years in our hospital. The patients were all male and mean age was 64 +/- 8 (SD) years. Data were as follow: protein excretion was 3.8 +/- 2.2 g/day (> or = 3.5 g/day in 8 patients), sBP 202 +/- 24 mmHg, dBP 113 +/- 17 mmHg, serum renin concentration 64 +/- 45 pg/ml, and ipsilateral/contralateral renal vein renin ratio 3.3 +/- 1.0. RVH was treated by nephrectomy in 3 patients, percutaneous transluminal renal angioplasty (PTA) in 2, and angiotensin converting enzyme inhibitors (ACE-I) administration in 8. Biopsies were performed on contralateral kidney in 4 patients. Focal segmental glomerulosclerosis (FGS) was found in 3 patients, and nephrosclerosis in 1, whereas only nephrosclerosis was found in nephrectomized kidneys in all 3 patients. After nephrectomy, PTA and the treatment by ACE-I, not only blood pressure but also proteinuria was markedly reduced. These findings suggest that severe stenosis of the renal artery led to renal ischemia, which activated renin excretion, to cause glomerular hyperfiltration through vasoconstriction of the efferent arterioles in the contralateral kidney. FGS-like lesion thus induced appeared to have caused massive proteinuria.