PERSISTENT HYPERKALEMIA AFTER KIDNEY TRANSPLANTATION: ROLE OF INTESTINAL POTASSIUM EXCRETION

Hyperkalemia is a common condition in patients with ESKD. Regaining kidney function after successful kidney transplantation (KT) generally resolves hyperkalemia. However, impaired extrarenal potassium excretion can contribute to persistent hyperkalemia after kidney transplantation. We reported a case of adult man with persistent hyperkalemia from pre- through early post-KT periods, likely from low intestinal potassium excretion.

A 57-year-old Hispanic man with ESKD presumably secondary to longstanding uncontrolled type 2 diabetes requiring hemodialysis (HD) for 6 years was admitted for an uneventful O-to-O compatible, 6-A-B-DR mismatched antigen, donation after cardiac death, deceased donor kidney transplantation. The donor was a 45-year-old man who died from anoxia with a peak and terminal serum creatinine (SCr) of 1.29 and 0.43 mg/dL, respectively. Warm ischemic time was 38 minutes. Procurement donor biopsy revealed 57 glomeruli, 11% global sclerosis, 5-25% interstitial fibrosis and tubular atrophy, and 10-25% vascular disease. Given the donor kidney histology, belatacept was used for calcineurin-inhibitor (CNI) avoidance maintenance immunosuppressive regimen. He had pre-transplant hyperkalemia with a serum potassium (K) of 5.7 mmol/L and underwent HD before KT; although, he had had HD 1 day prior as per his regular thrice-weekly HD schedule. Post-transplant course was complicated by delayed graft function (DGF) requiring HD due to hyperkalemia with a K of 6.5 mmol/L on post-operative day 2. During the 5 days of the transplant admission, K remained in high side with a range of 4.8–5.3 mmol/L despite up trending urine output (UOP) to 0.9 L/day. Work-up for hyperkalemia showed urinary potassium:creatinine (K/Cr) ratio was 64.65 mmol/g of Cr. Plasma aldosterone concentration was 4.2 ng/dL and plasma renin activity was 1 ng/mL/h. Over 3-week post-transplant follow-up clinics, his UOP increased to 2.5–3 L/day and SCr improved to 1.9 mg/dL; however, K was still elevated to 4.7–6 mmol/L.

Our patient had had persistent hyperkalemia from pre- through an early post-transplant period. DGF might explain hyperkalemia during the immediate post-transplant period given low K/Cr ratio; however, hyperkalemia during early post-transplant period despite high UOP and no CNI exposure exclude low renal potassium excretion and secretion from type 4 renal tubular acidosis as potential causes of hyperkalemia, respectively. Therefore, impaired extrarenal potassium excretion is the most likely cause of hyperkalemia from pre- through post-transplantation in this patient. Intestinal potassium excretion account for 10% of total body potassium loss. High conductance calcium-activated potassium (BK) channels are regulated by transmural conductance difference to maintain intestinal potassium excretion. Mutation of the BK channel may be at least in part of hyperkalemia in this patient.

Our case highlights a rare but critical potential cause of persistent hyperkalemia likely from dysregulation of extrarenal potassium excretion including intestinal route. This presentation likely reflects aldosterone resistance at specific target organs, potentially the colonic BK channel, and warrants consideration in the management of refractory hyperkalemia in this complex population.