Background: Nephrotoxicity is a well-known effect of cyclosporine (CsA) that causes a reduction in glomerular filtration rate through vasoconstriction of the afferent glomerular arterioles and may result in acute renal failure. Isolated CsA-induced hyperkalemia occurring through different mechanisms is also common. However, there are only a few "case reports" addressing this phenomenon in allogeneic bone marrow transplantation patients. In this report, we propose mechanisms and methods of managing CsA-associated hyperkalemia in allogeneic transplantation.
Methods: We report on four allogeneic blood stem- cell transplant cases and a review of the literature.
Results: Four adult leukemia patients underwent allogeneic peripheral blood stem cell transplantation and received CsA as a part of their graft-versus-host disease prophylaxis. The patients developed hyperkalemia, despite adequate kidney function. CsA seemed to be the only pharmaceutical agent to which this electrolyte abnormality could be attributed. Renal tubule dysfunction and secondary hypoaldosteronism seemed to be the reasons for CsA-associated hyperkalemia.
Conclusion: This report of four cases demonstrates that CsA should be considered among the possible causes of hyperkalemia in bone marrow transplantation. There may be a need for urgent intervention depending on the severity of hyperkalemia. Monitoring of blood CsA level and dose adjustment are important for the prevention of this complication.