Hyperkalemia and coma associated with renal tubular acidosis in an old patient with refractory edema due to the nephrotic syndrome: furosemide-bicarbonate therapy.

Abstract

ABSTRACT:In a 70‐year‐old man, renal tubular acidosis and hyperkalemia occurred together with the nephrotic syndrome and stable chronic renal failure associated with diuretic‐refractory edema. Apparently an extreme medullary hyaline sclerosis accompanying nephroarteriosclerosis was the anatomical basis of the insufficiency of distal potassium and hydrogen‐ion secretion. The patient was refractory even to excessive doses of exogenous aldosterone. Therefore the edema was attributed exclusively to an increase of proximal tubular sodium reabsorption. The renal tubular acidosis was predominantly of the distal type, but the high daily bicarbonate requirement indicated also the presence of a proximal component. Hyperkalemia presumably was caused by the lack of aldosterone effect, but excessive proximal tubular sodium reabsorption also may have played a part. With or without the influence of diuretics, a definite correlation could be demonstrated between the osmolal clearance and the potassium clearance.The decrease of hyperkalemia caused by furosemide, ethacrynic acid and hydrochlorothiazide was attributed to an enhanced sodium‐for‐potassium exchange in the distal tubules due to the increased sodium load induced by these drugs. The “refractory edema” could be drained off by high doses of furosemide (1600 mg a day) even in the presence of progressive impairment of renal function. By the intravenous infusion of high doses of furosemide and bicarbonate, the acidotic and hyperkalemic coma of this patient with “refractory edema” was successfully combatted several times.