Impaired renal tubular secretion of potassium, elevated sweat sodium chloride concentration and plasma inhibition of erythrocyte sodium outflux as complications of systemic lupus erythematosus

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Abstract
A 23‐year‐old male with systemic lupus erythematosus and hypocomplementemic glomerulonephritis (creatinine clearance 84 ml/min) developed severe hyperkalemia when given a normal sodium and potassium intake. Potassium excretion increased subnormally in response to ammonium chloride, sodium bicarbonate and a sodium‐retaining steroid. Renal conservation of sodium and excretion of ammonium were impaired. These observations are consistent with defects in secretion of potassium and hydrogen ion by the distal tubule. Sodium transport by sweat ducts and normal erythrocytes incubated in the patient's plasma was impaired. The several abnormalities in ion transport could have been caused by a circulating substance(s), possibly acquired as a result of systemic lupus erythematosus.