Introduction
Kidney transplant (KT) is an established treatment option for patients with end-stage renal disease (ESRD). Electrolyte imbalances are a common consequence of ESRD that often normalize after successful KT. However, electrolyte imbalances, including hyperkalemia, may persist after KT for various reasons including tubular dysfunction caused by acute and/or chronic rejection, direct drug-induced tubular toxicity, and drug-induced enhanced sodium delivery in the distal nephron. Moreover, KT recipients are more prone to electrolyte abnormalities compared to non-kidney transplant recipients with the same level of kidney function.[1]
The prevalence of hyperkalemia ranges from 25-44% in KT recipients on calcineurin inhibitors (CNIs). [2] The time course of hyperkalemia is not well defined after KT. In a small study, hyperkalemia occurred on an average around 100 days post-transplant. [3]
There is no consensus definition of hyperkalemia but generally potassium levels greater than 5.5 mmol/L require immediate intervention. [4 5] Hyperkalemia in the general population is usually asymptomatic but if left untreated may lead to muscle weakness or paralysis, cardiac arrhythmias, and death. [6] The exact consequences of untreated hyperkalemia after KT have not yet been established.[7] However, data from the general and chronic kidney disease (CKD) populations highlights the importance of maintaining normal serum potassium concentrations.[6 8 9] Despite the high incidence and potentially life-threatening consequences of hyperkalemia, there is a lack of consensus on the management in KT recipients. The purpose of this article is to review the pathophysiology, dietary considerations, and management of acute and chronic hyperkalemia with a focus on kidney transplant recipients.