Renal Tubular Dysfunction as the Driving Force Behind Refractory Hypokalemia in Ogilvie Syndrome

Introduction: Ogilvie's syndrome typically arises in postoperative or critically ill patients, but its development in hematologic malignancies—particularly those requiring nephrotoxic chemotherapy—remains poorly understood. This report details the case of a 57-year-old male with IgG kappa multiple myeloma undergoing treatment with daratumumab, lenalidomide, and dexamethasone (DRd) who developed severe Ogilvie's syndrome complicated by refractory hypokalemia (K ≤3.1 mEq/L despite aggressive IV repletion). The case illustrates how chemotherapy-induced distal renal tubular acidosis (dRTA), compounded by chronic alcohol-related hyperaldosteronism, led to profound renal potassium wasting, exacerbating colonic dysmotility. By exploring the interplay between tubular dysfunction, electrolyte imbalances, and pseudo-obstruction, this report provides a framework for nephrologists managing similar cases. Case Description: A 57-year-old male with IgG kappa multiple myeloma on daratumumab-lenalidomide-dexamethasone developed Ogilvie's syndrome with refractory hypokalemia (K 2.4-3.1 mEq/L) despite 120 mEq/day IV supplementation. Nephrology evaluation revealed renal potassium wasting (TTKG 6.2, 24h urine K 45 mEq), hypomagnesemia (1.4 mg/dL, FE Mg 8.2%), and metabolic alkalosis (pH 7.48). Urine beta-2-microglobulin was elevated (4,200 μg/L), suggesting proximal tubular injury. Treatment included IV magnesium (2g/day), transition to KHCO3, and amiloride (5mg BID). Serum K normalized by Day 3, with colonic diameter improving from 11cm to 7cm by Day 5. Discussion: This case highlights chemotherapy-induced tubular dysfunction as a key driver of refractory hypokalemia in Ogilvie's syndrome. The patient exhibited a unique lenalidomide-associated distal nephron defect featuring metabolic alkalosis with preserved ammonium excretion, suggesting voltage-dependent potassium secretion rather than classic dRTA. The "magnesium-potassium clamp" phenomenon was evident - hypomagnesemia exacerbated potassium wasting through ROMK channel dysregulation and impaired Na/K-ATPase activity. The 48-hour lag between potassium normalization (Day 3) and colonic recovery (Day 5) demonstrates that electrolyte correction must precede functional GI improvement. Amiloride's effectiveness supports ENaC blockade as superior to mineralocorticoid antagonism in chemotherapy-induced tubular disorders.