Persistent hyperkalemia results from impaired urinary potassium excretion, which is mainly controlled by aldosterone. Metabolic acidosis further worsens hyperkalemia with transcellular shifts. We report a 62 yr/M, diabetic, who presented for elective cholecystectomy. His baseline serum creatinine was 1.7 mg/dL with normal acid base and electrolyte status until 5 months prior to presentation when he was started on angiotensin-converting enzyme inhibitor (ACEi) and a potassium-sparing diuretic, triamterene. Four months after ACEi initiation his renal functions were serum creatinine 1.9 mg/dL, serum K 5.1 meq/L, Na 136 meq/L, Cl 109 meq/L, and CO2 15 mmol/L. The reasons for poor follow-up or lack of interventions are unknown. Preoperatively, on this admission, his serum K 8.2 meq/L, Na 130 meq/L, Cl 107 meq/L, CO2 10 mmol/L, anion gap 13, glucose 383 mg/dL, creatinine 2.6 mg/dL, lactate 1.4 and negative serum ketones. Urinalysis: pH 5.0, no WBC/RBC, proteins and ketones negative. Random urinary potassium was 10.6 mmol/L. Arterial blood gas: pH 7.23, pCO2 32 mm Hg, pO2 99 mm Hg, HCO3 12.8 mmol/L. Hyperkalemia was treated with calcium gluconate, insulin/glucose, and bicarbonate infusions. ACEi and potassium-sparing diuretic were discontinued; loop diuretics, oral bicarbonate, and potassium binding resins were administered, which resulted in lowering of serum K and correction of his metabolic acidosis. This case report highlights Type 4 renal tubular acidosis (RTA) as an etiologic factor for severe hyperkalemia and metabolic acidosis in a diabetic. Type 4 RTA results from hyporeninemic hypoaldosteronism as seen in diabetics. Use of an ACEi contributed to the aldosterone deficiency. Insulin deficiency and hyperglycemia contributed to the hyperkalemia through transcellular shift of potassium. Multiple iatrogenic interventions without close monitoring can lead to severe and possibly life-threatening complications.
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