Reversal of glucose-induced hyperkalemia by sodium restriction in normaldosteronemic diabetes: evidence for elevated mineralocorticoid threshold.

Abstract

Acute glucose loading studies were performed on seven diabetic patients and 18 control subjects. In two normaldosteronemic insulin-dependent diabetic patients during high sodium intake and insulin withdrawal infusion of hypertonic glucose induced a paradoxical elevation of serum potassium levels, while no such abnormalities were found in two other diabetics despite of lower plasma aldosterone levels. Paradoxical glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained l glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained l glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained also by sodium restriction or by administering a large intravenous dose of desoxycorticosterone. These findings suggested an elevated mineralocorticoid threshold level for the normal cellular regulation of potassium distribution in normaldosteronemic diabetics with PGIH.