Fludrocortisone for Calcineurin Inhibitor–Associated Hyperkalemia After Solid Organ Transplantation

Background Hyperkalemia is a frequent post-transplant complication commonly associated with calcineurin inhibitor (CNI) therapy. Fludrocortisone may improve potassium balance through mineralocorticoid activity, but comparative data in solid organ transplant recipients are limited. Methods We conducted a single-center retrospective cohort study of adult solid organ transplant recipients who developed hyperkalemia during their post-transplant hospitalization. Patients treated with fludrocortisone for suspected CNI-associated hyperkalemia were compared with those receiving standard care. Serum potassium trajectories over 15 days were evaluated using linear mixed-effects models adjusted for serum creatinine, age, sex, APACHE II score, and transplanted organ. Results Overall, 958 patients had post-transplant hyperkalemia: 38 received fludrocortisone and 920 received standard care. The adjusted complete-case analysis included 755 patients (9,196 potassium measurements). At baseline, the fludrocortisone group had a higher adjusted serum potassium level (+0.20 mEq/L; 95% CI, 0.01–0.39; p=0.038). Serum potassium declined in both groups. Although fludrocortisone showed a more pronounced early reduction, the treatment-by-time interaction was not statistically significant (p=0.058). Notably, no fludrocortisone-treated patient required CNI withdrawal due to persistent hyperkalemia. Conclusions Fludrocortisone was associated with serum potassium reduction in suspected CNI-induced hyperkalemia, but overall trajectories did not significantly differ from standard care. These short-term findings remain exploratory and do not establish comparative efficacy or long-term safety.