AKI Confounding Heparin-Induced Hyperkalemia

Introduction: Heparin induced hypoaldosteronism is an uncommon etiology of hyperkalemia in hospitalized patients. It poses a challenge from diagnostic and management perspectives especially when it occurs in conjunction with other causes of hyperkalemia. We present a a patient with pre-renal acute kidney injury as well as hyperkalemia where transtubular potassium gradient (TTKG) was successfully used for diagnosis and management. Case Description: A 70 year-old male with an end-ileostomy, CKD3b secondary to recurrent pre-renal acute kidney injury (AKI) from high ostomy output was admitted with atrial fibrillation with a rapid ventricular rate and hypotension. He was started on heparin infusion and cardioverted. The hospital course was complicated with pre-renal non-oliguric AKI thought to be from volume depletion from high ostomy output. Despite improving renal function (creatinine 4.3 - > 2.6 mg/dL) and with appropriate urine output (>1.3L) hyperkalemia progressively worsened (Table 1). There was no evidence of hemolysis or rhabdomyloysis. TTK calculated on day six was 3, suggestive of impaired distal tubular potassium secretion. The patient was initiated on fludrocortisone resulting in prompt improvement of hyperkalemia and increase of TTKG to 15. Discussion: Heparin induced hyperkalemia is due to decreased renal excretion secondary to decreased aldosterone activity in the distal tubule. Heparin is thought to directly interfere with production of aldosterone. TTKG can assess hypoaldosteronism (cutoff < 5-7). Increase to > 10 after fludrocortisone administration confirmatory. In above case, Fludrocortisone was shown be a successful therapy in addition other conventional treatments of such hyperkalemia. This case highlights that in non-oliguric acute kidney injury with refractory hyperkalemia, heparin must be considered as a potential culprit.