Diagnostic approach to hypokalemia: hypokalemia due to renal losses with normal acid-base status or metabolic acidosis. Hypokalemia is occasionally observed during the diuretic recovery phase of acute tubular necrosis (ATN) or after relief of acute obstructive uropathy, presumably secondary to increased delivery of sodium and water to the distal nephrons. Patients with acute monocytic and myelomonocytic leukemias occasionally excrete large amounts of lysozyme in their urine. Lysozyme appears to have a direct kaliuretic effect on the kidneys (by an undefined mechanism). Penicillin in large doses acts as a poorly reabsorbable anion, resulting in obligate renal potassium wasting. Mechanisms for renal potassium wasting associated with aminoglycosides and cisplatin are ill-defined. Hypokalemia in type I renal tubular acidosis is due in part to secondary hyperaldosteronism, whereas type II renal tubular acidosis can result in a defect in potassium reabsorption in the proximal nephrons. Carbonic anhydrase inhibitors result in an acquired form of renal tubular acidosis. Ureterosigmoidostomy results in hypokalemia in 10% to 35% of patients, owing to the sigmoid colon's capacity for net potassium secretion. The osmotic diuresis associated with diabetic ketoacidosis results in potassium depletion, although patients may initially present with a normal serum potassium value, owing to altered transcellular potassium distribution.

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