Mechanisms of hyperkalemia in systemic lupus erythematosus.

We found that nearly 10% of 142 patients with systemic lupus erythematosus (SLE) had persistent, unexplained hyperkalemia. Renal mineralocorticoid resistance has been suggested to account for the hyperkalemia in SLE. We studied the renin-aldosterone response to intravenous furosemide (60 mg) and upright posture and the renin response to converting enzyme inhibition (captopril, 50 mg) and upright posture in five patients with SLE and hyperkalemia (group 1) and five normokalemic patients with SLE (group 2). Renal function was comparable. Plasma chloride level was higher and bicarbonate level slightly lower in group 1 than in group 2. Plasma cortisol level was normal in all patients. None of the patients was receiving nonsteroidal anti-inflammatory drugs or corticosteroids at the time of study. Basal plasma renin concentration and plasma aldosterone level were not significantly different between the two groups, although both tended to be higher in group 2. However, four of the five patients in group 1 had significantly blunted renin response to captopril compared with group 2. The same four patients also had blunted renin and aldosterone responses to furosemide. Thus, the majority of hyperkalemic patients with SLE had an impaired renin and aldosterone response to stimulation. We conclude that hyporeninemic hypoaldosteronism plays a key role in the pathogenesis of hyperkalemia in SLE.