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Upon hospitalization with pancreatitis in the setting of growing abdominal metastases, admission serum [K+] was 3.3 mmol/L. Normalization required daily potassium supplementation, both intravenous and oral, of 60�C180 mEq (Figure?1). Nephrology consultation revealed absence of hypertension and edema. Normal serum electrolytes included [Mg2+] 0.86 mmol/L [2.1 mg/dL], [HCO3?] 29 mmol/L, and a normal anion gap. Proteinuria and glycosuria were absent, and urine pH ranged from 6 to 7.5. Twenty-four-hour urine K+ excretion ranged from 60 to 100 mmol. Serum levels of cortisol, renin and aldosterone were normal. Serum cesium concentration was 28 000 mcg/L (or 0.2 mM; normal value ankyrin normal value selleck products Serum potassium levels (light gray squares and line), potassium supplementation (black diamonds and line) and urinary potassium excretion (dark gray circles) over 12 days in hospital. After starting ... To reduce the patient's requirement for oral potassium supplementation, he was treated initially with 10 mg amiloride daily, subsequently increased to 20 mg. After 1 week of amiloride treatment, the patient no longer required extra-dietary potassium supplementation, and his urine K+ excretion decreased to 36 mmol/day. In contrast, urine cesium concentration increased to 310 000 mcg/L and serum cesium concentration remained unchanged after 4 days on amiloride. At post-discharge nephrology follow-up, the patient Selleckchem GSK3 inhibitor reported recurrence of severe pain and acknowledged continued episodic self-administration of cesium. He died 2 months later in hospice care, 18 months after initial presentation. Discussion CAH has been noted in multiple case reports (Table?1) but its prevalence cannot be reliably established in the context of cesium self-administration without prescription. Clinical data suggesting a mechanism of CAH are minimal. The current case report is the first to demonstrate inappropriate urinary potassium wasting in CAH. Amiloride, a competitive inhibitor of ENaC, the epithelial sodium channel of the connecting segment and cortical collecting duct, dramatically reduced our patient's kaliuresis and his supplemental potassium requirement. The data suggest that amiloride treatment can mitigate CAH. Table?1. Case reports documenting cesium side effects Cesium's effects on renal tubular K+ channels and transporters suggest several possible mechanisms of CAH.

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