Incidence of hyperkalemic RTA in pediatric post‐renal transplant patients and the role of fludrocortisone

Abstract

Background One of the most common forms of post‐transplant tubulopathy is hyperkalemic (RTA). The true incidence of hyperkalemic RTA in pediatric patients has not yet been studied. (CNIs) remain mostly blamed. Most cases are managed with sodium bicarbonate and potassium binding resins. Few studies have addressed the role of fludrocortisone in managing such patients. This study aimed to assess the efficacy and safety of fludrocortisone in the treatment of post‐transplant hyperkalemic RTA. Method This is a retrospective cohort study of all pediatric (aged ≤16 years) post‐kidney transplant patients who were followed up in KFSH‐D, Saudi Arabia from January 2015 until September 2019. A total of 136 pediatric post‐renal transplant patients were reviewed, of these, 39 patients who were commenced on fludrocortisone post‐transplant treatment and were followed up for at least 6 months after fludrocortisone initiation were included in this study. Results The incidence of hyperkalemic RTA in our center was 60.6%. The medication requirements decreased significantly after fludrocortisone initiation. The median sodium bicarbonate dose decreased from 1.2 mEq/kg/day (range, 0.0–4.7) prior to fludrocortisone treatment to 0.0 mEq/kg/day (range, 0.0–4.3) at 6‐month follow‐up (p < .001). Similarly, the median (SPS) dose decreased from 1.2 g/kg/day (range, 0.0–4.0) before fludrocortisone treatment to 0.0 g/kg/day (range, 0.0–3.6) (p < .001) at 6‐month follow‐up. The initial mean potassium level 5.17 mmol/L ± 0.61SD dropped to 4.60 mmol/L ± 0.46SD at 6‐month follow‐up (p < .001). The initial mean serum bicarbonate level 22.31 mmol/L ± 3.67SD increased to 24.5 mmol/L ± 2.8SD at 6‐month follow‐up (p < .01). No effect on systolic and diastolic blood pressure was observed during follow‐up. Conclusion Hyperkalemic RTA incidence was high in our cohort. Fludrocortisone is safe and effective drug in the treatment of post‐kidney transplant hyperkalemic RTA.

Calcineurin inhibitor‐related hyperkalemia is caused by hyporeninemic hypoaldosteronism and fludrocortisone is an effective treatment: Report of a case series and review of the literature

“…However, more recent papers, like ours, denote a higher likelihood of hyperkalemia with higher doses of CNI. 17 As observed in our cases, multiple studies reported a similar trend toward more severe hyponatremia and hyperkalemia in tacrolimus-treated patients than in CsA. 3,6,18 CNI is fundamental for graft survival and graft versus host disease management in pediatric transplantation.…”

“…16 In pediatric studies, hyperkalemia and hyponatremia in renal transplant recipients using CNI were reported to be as high as 10%-60.6%. 2,17 In this study, CNI-related hyperkalemia was detected relatively early in case 1, who had HSCT (22 days), than in the second and third cases, who had kidney transplantation (24 and 30 months post-transplantation, respectively). Alabdulqader et al…”

“…hyperkalemia is yet to be delineated. 17,18 Therefore, enlightening the pathogenesis of CNI-related hyperkalemia and treating it accordingly is crucial. A recent study investigated the potential nephrotoxic effects of CNI in mice, focusing on its in-vivo and real-time effect on the renin system.…”

“…24 Unfortunately, renin and aldosterone were not measured in the latter three studies. 17,23,24 Despite these limitations of current literature regarding laboratory findings, it was deduced in some of these studies that the underlying pathophysiologic mechanism of CNI-related hyperkalemia is aldosterone resistance.…”

“…reported 39 pediatric renal transplant recipients with CNI-related hyperkalemia where median time from renal transplantation to detection of hyperkalemia was 8 weeks. 17 in renal transplant recipients. Previously, it was suggested that the severity of hyperkalemia is not associated with CNI dose.…”