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Impaired Renal Tubular Potassium Secretion in Systemic Lupus Erythematosus
- RALPH A. DeFRONZO, M.D.;
- C. ROBERT COOKE, M.D., F.A.C.P.;
- MARTIN GOLDBERG, M.D., F.A.C.P.;
- MALCOLM COX, M.D.;
- ALLEN R. MYERS, M.D., F.A.C.P.; and
- ZALMAN S. AGUS, M.D.
Abstract
Two patients with long-standing systemic lupus erythematosus were found to have persistent hyperkalemia. The hyperkalemia could not be explained by renal insufficiency, oliguria, diminished distal sodium delivery, acidemia, or hemolysis. After sodium depletion, urinary aldosterone excretion and plasma aldosterone concentration rose appropriately. No increase in urinary potassium excretion or decrease in serum potassium concentration was noted after fludrocortisone acetate, furosemide, or acetazolamide plus sodium bicarbonate. We conclude that these patients have a primary defect in renal tubular potassium secretion that may be related to an immune complex interstitial nephritis.
Article and Author Information
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▸From the Renal-Electrolyte and Arthritis-Rheumatology Sections, Department of Medicine, Hospital of the University of Pennsylvania and Veterans Administration Hospital; Philadelphia, Pennsylvania; and the Renal Section, Department of Medicine, The Johns Hopkins University School of Medicine; Baltimore, Maryland.
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Grant support: by a research grant from the National Heart and Lung Institute, HL-0034, and by a training grant from the National Institute of Arthritis, Metabolism, and Digestive Diseases, AM 05634. Dr. Agus is a Clinical Investigator of the Veterans Administration.
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▸Requests for reprints should be addressed to Zalman S. Agus, M.D.; Renal-Electrolyte Section, 860 Gates Pavilion, Hospital of the University of Pennsylvania, 3400 Spruce St.; Philadelphia, PA 19104.
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- Received June 15, 1976.
- Accepted December 9, 1976.
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