Unilateral Reflux Nephropathy with Contralateral Renal Artery Stenosis Due to Fibromuscular Hyperplasia
Author(s) -
Ross R. Bailey
Publication year - 1993
Publication title -
the nephron journals/nephron journals
Language(s) - English
Resource type - Journals
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000187419
Subject(s) - medicine , renal artery obstruction , renal artery , renal artery stenosis , reflux , stenosis , nephropathy , reflux nephropathy , hyperplasia , fibromuscular dysplasia , urology , cardiology , kidney , disease , endocrinology , diabetes mellitus , vesicoureteral reflux
Dr. Ross R. Bailey Department of Nephrology, Christchurch Hospital, Christchurch (New Zealand) Dear Sir, The finding of a unilateral small kidney and a contralateral hypertrophied kidney in a patient with hypertension generally implicates the small kidney in the pathogenesis of the hypertension, whether it be of a vascular or non-vascular (parenchymal) aetiology. Recently there have been two reports [1,2] of hypertensive patients with a unilateral small kidney where the latter was thought to be the cause of the high blood pressure, but the patients were found to have a distal stenosis of the contralateral renal artery due to fibromuscular hyperplasia. We report a further such case: A 40-year-old woman was found to have persistent hypertension and was commenced on enalapril 10 mg daily. Prior to treatment the plasma creatinine was 0.08 mmol/l. Ten years previously she had suffered acute pyelonephritis, and an intravenous urogram had shown a small irregularly scarred right kidney characteristic of reflux nephropathy. The contralateral kidney showed compensatory hypertrophy. Four months after starting enalapril she presented with fever, right-loin pain, and a systemic illness and was supected of having acute pyelonephritis. She was started on antibiotics, but 2 days later was no better, and routine blood tests included a plasma creatinine level of 0.16 mmol/l. Three days later she had not improved, and the plasma creatinine had increased to 0.44 mmol/l. Enalapril was discontinued and she was hospitalized. On admission she was apyrexial, had no urinary tract symptoms, and the blood pressure was 170/114 mm Hg. Investigations: A midstream urine specimen showed 2 + protein on dipstick analysis, while on microscopy there were no cells and the specimen was sterile on culture, haemoglobin 107 g/l, plasma creatinine was confirmed at 0.44 ‘ ■■’;-■■■ •
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