Hyperglycemia-induced hyperkalemia is a common and underappreciated problem in diabetes [2,3]. This is related to the hyperosmolar effect of hyperglycemia and to insulin deficiency. It often occurs in patients who are otherwise predisposed to hyperkalemia because of renal insufficiency, hypoaldosteronism, medications, volume depletion, or other causes. It is rapidly responsive to the administration of insulin.
The pathogenesis of this disorder is as follows. Hyperosmolality causes translocation of potassium from the intracellular fluid to the extracellular fluid, raising the circulating potassium level. In diabetic patients with nephropathy, insulin and aldosterone are often both deficient. Insulin promotes entry of potassium into cells in the liver and other organs. It is part of the body's hormonal defenses against hyperkalemia, along with aldosterone [3]. When insulin and aldosterone are both deficient, the patient is unable to defend against the hyperkalemia induced by hyperglycemia and its attendant hyperosmolality.
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