• Journal Article

Hyperkalemia in advanced diabetes: Potassium retention or cell transport adaptation? A case control study with body composition analysis

Citation

Graber, M., Shreeve, W. W., Ma, R-M., Richards, J., & Pierson, R. N. (2004). Hyperkalemia in advanced diabetes: Potassium retention or cell transport adaptation? A case control study with body composition analysis. International Journal of Body Composition Research, 2(3), 93-98.

Abstract

Hyperkalemia in diabetes is not uncommon, and has been thought to reflect renal retention of potassium. The goal of this study was to test this hypothesis by measuring total body potassium in hyperkalemic diabetic patients and normokalemic diabetic controls. We measured total body potassium (whole body counting of 40K), total body sodium, calcium, and chloride by neutron activation analysis, total body carbon by inelastic neutron scattering, and total body water from the distribution of 3H20. Measurements were made in 17 diabetic controls (mean plasma K = 4.47 mEq/l) and 14 diabetic patients with hyperkalemia (K = 5.26 mEq/l). All subjects were adult male Type II diabetic patients of comparable age, duration of disease, glycemic control, and end-organ complications. Total body potassium normalized by fat-free mass, total body water, or urinary creatinine was essentially identical (or slightly reduced) in the hyperkalemic subjects compared to controls. Additionally, the hyperkalemic diabetics were found to have significantly decreased body weight (77.2 kg hyperkalemics vs 92.9 kg control, P<0.001; BMI 26.7 vs 30.4 kg/m2, P = 0.002), and decreased fat-free mass (59.0 vs 66.2 kg, P < 0.05). It is concluded that the findings argue against the traditional belief that the hyperkalemia of advanced diabetes is solely renal in origin. We suggest that a fundamental defect in this disorder is a generalized derangement of cellular ion transport, resulting in cellular potassium depletion and a shift of potassium from the cell to the extracellular space. This elevates plasma potassium directly, and by depleting intracellular potassium contributes to decreased renal potassium secretion. In light of these findings of unchanged or reduced total body potassium in hyperkalemic diabetics, the routine use of diuretics to treat these patients may need to be re-examined. In addition, the findings demonstrate a novel observation in this syndrome, decreased fat and fat-free body mass.