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.