Introduction: Hyperkalemia is a recognized and potentially life threatening complication post renal transplantation. Aside from delayed graft function, the most frequent culprit identified is pharmacotherapy. Many of the medications routinely used in the post-transplant period alter renal potassium handling or impair potassium movement into cells. These include calcineurin inhibitors, sulfa based antibiotics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and beta blockers. Episodic hyperkalemia develops in 44 to 73 percent of transplant recipients on calcineurin inhibitors [1] and is associated with patient morbidity as well as increased health care costs. The aim of this chart review is to assess the prevalence of hyperkalemia in our renal transplant program, and identify any predictive factors to design preventative and therapeutic algorithms in this high risk population.
Materials and Methods: Retrospective cohort identified all adult renal transplant recipients between July 2011 and August 2017 within the University of Alberta Northern Alberta Renal Program who developed hyperkalemia (defined as serum potassium >5.0 mmol/L) within the first 6 months post-transplant. Patients with abnormal allograft function or delayed graft function were excluded (creatinine >200 umol/L). Patient characteristics, diagnoses, medications, laboratory values and outcomes were extracted from the electronic medical record. A descriptive analysis was undertaken.
Results and Discussion: Of the 505 renal transplant patients transplanted during the study period, 48 developed at least one episode of hyperkalemia. These episodes were not associated with metabolic acidosis. Most patients had a period of persistent values in the hyperkalemic range. The majority of patients were on the combination of tacrolimus and trimethoprim-sulfamethoxazole, and approximately half of the patients were on a total of 3 or more medications that could contribute to abnormal potassium handling. Elevated tacrolimus levels were only present in 10% of hyperkalemic episodes.
Conclusions: The prevalence of hyperkalemia among renal transplant recipient in our centre was lower than expected based on published data. Our findings suggest that hyperkalemia in the early post-transplant period is largely related to the additive effects of multiple therapeutic medications altering potassium homeostasis, and does not seem associated with shift due to metabolic acidosis or as a direct effect from supratherapeutic tacrolimus levels. Our recommendation is to consider alternative agents for blood pressure management and PJP prophylaxis in those patients where hyperkalemia is a recurrent issue. Further investigation into which other factors may best predict those post renal transplant patients at risk for hyperkalemia is warranted.