Reduction of erythrocyte (Na +-K +)ATPase activities in non-insulin-dependent diabetic patients with hyperkalemia

Abstract

To elucidate the mechanism of hyperkalemia in diabetic patients without renal failure, we investigated (Na +-K +) adenosine triphosphatase (ATPase) activity in erythrocyte membrane, erythrocyte Na + and K + content, and plasma endogenous digitalis-like substance in control subjects (n = 16) and non-insulin-dependent diabetes mellitus (NIDDM) patients (n = 62). NIDDM patients were divided into normokalemic patients (NKDM, n = 48) and hyperkalemic patients (HKDM, n = 14). There was no difference in plasma glucose or hemoglobin A 1c (HbA 1c) levels, plasma renin activity (PRA), and plasma aldosterone concentrations (PAC) between NKDM and HKDM patients. (Na +-K +)ATPase activities in NIDDM patients were significantly reduced compared with those in control subjects (0.336 ± 0.016 μmol-inorganic phosphate [Pi]/mg protein/h, mean ± SEM, P < .05), and (Na +-K +)ATPase activities in HKDM patients (0.243 ± 0.015 μmol Pi/mg protein/h) were significantly reduced compared with those in NKDM patients (0.295 ± 0.008 μmol Pi/mg protein/h, P < .01). Plasma K + content had a significant negative correlation with (Na +-K +)ATPase activity in diabetic patients ( r = −.365, P < .01). Erythrocyte Na + content had a significant negative correlation with (Na +-K +)ATPase activity in control subjects ( r = −.619, P < .05). There was no difference in plasma endogenous digitalis-like substance among the three groups. (Na +-K +)ATPase activity was not significantly correlated with plasma endogenous digitalis-like substance in control subjects and diabetic patients. These findings suggest that the reduction of (Na +-K +)ATPase activity, which was not related to plasma digitalis-like substance, may be partly responsible for hyperkalemia in diabetic patients.