Abstract
A 16-year-old girl with recent onset of idiopathic nephrotic syndrome (INS) developed severe hypertension and sustained acute renal insufficiency (ARI) despite minimal lesion histology, treatment with albumin infusions, and absence of renal vein thrombosis. The nephrotic syndrome failed to respond to oral prednisone administration, “pulse” methylprednisoione, and cytotoxic agents. Peak BUN was 128 mg/dl; peak serum creatinine, 5.5 mg/dl. Plasma renin activity (PRA) was 49 ng/ml/hr. Plasma volume was 70% of normal. Elevated PRA was partially suppressed by albumin infusion. Azotemia persisted for 3 months. BUN declined to 18 mg/dl and serum creatinine to 1.8 mg/dl concurrent with tapering of prednisone dosage. We speculate that this oatient had incipient vasomotor nephropathy due to angiotensin-mediated renal vasoconstriction consequent to multiple factors: 1. corticosteroid-induced vascular sensitization to angiotensin (Am. J. Med. 58:216,1975): 2. hypovolemia; and 3. treatment with renin-raising drugs (hydralazine, furosemide). We suggest that patients with INS and ARI may benefit from treatment with an angiotensin-antagonist.
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Kallen, R., Ooi, Y., Calabrese, K. et al. HYPERRENINEMIC ACUTE RENAL INSUFFICIENCY AND HYPERTENSION IN MINIMAL-LESION NEPHROTIC SYNDROME. Pediatr Res 11, 553 (1977). https://doi.org/10.1203/00006450-197704000-01098
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DOI: https://doi.org/10.1203/00006450-197704000-01098
