Impaired Potassium and Magnesium Homeostasis in Acute Tubulo-Interstitial Nephritis

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Abstract
Although acute tubulo-interstitial nephritis is increasingly recognized as a cause of acute renal failure, little is known about renal tubular function in this disease. We report on two patients with acute tubulo-interstitial nephritis who demonstrated abnormalities in proximal and distal tubular fraction. The first patient developed hyperkalemia presumably from a potassium secretory defect in the distal nephron. The second patient developed an incomplete Fanconi''s syndrome with glycosuria and aminoaciduria and two heretofore unreported complications of acute interstitial nephritis: hypokalemia and hypomagnesemia secondary to urinary losses of these cations. Careful monitoring of renal tubular function is indicated in patients with acute tubulo-interstitial nephritis.

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