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Updated: Nov 18, 2025

Digital Home-Monitoring of Patients after Kidney Transplantation: The MACCS Platform
Published on: April 12, 2021
Prevalence and clinical correlates of hyperkalemia in stable kidney transplant recipients
Elisabetta Bussalino1, Laura Panaro1, Luigina Marsano1
1Nephrology, Dialysis, and Transplantation, University of Genoa, and Policlinico San Martino, Largo R. Benzi 10, 16132, Genova, Italy.
Abstract:
Although hyperkalemia (HK) is often associated with adverse clinical outcomes in renal patients, few studies are available in the setting of kidney transplantation. Therefore, we evaluated prevalence and clinical correlates of HK in stable kidney transplant recipients (KTRs) on standard of care immunosuppressive therapy. We studied 160 stable KTRs (post-transplant vintage 46.6 ± 16.6 months), most of whom (96.2%) on calcineurin inhibitor (CNI)-based immunosuppressive therapy. HK was defined as plasma potassium levels above 5 mEq/L, confirmed in two consecutive samples. Office blood pressure was measured, and renal graft function was expressed by estimated glomerular filtration rate (eGFR), calculated according to the CKD-EPI formula. HK prevalence was 8.8%, and plasma K above 5.5 mEq/L was found in 2.5% of all KTRs. In the univariate logistic regression analysis HK was significantly associated with serum urea concentration (OR 1.03, 95% CI 1.01-1.05 for each 1 mg/dL increase), tCO2 (OR 0.77, 95% CI 0.66-0.90 for each 1 mmol/L increase), the presence of arterial hypertension (OR 4.01, 95% CI 1.3-12.64), the use of RAAS inhibitors (OR 5.26, 95% CI 1.6-17.7), and eGFR less than 30 ml/min/1.73 m2 (OR 7.51, 95% CI 2.37-23.77). By multivariable backward stepwise regression analysis, the presence of metabolic acidosis (OR 0.83, 95% CI 0.69-0.99, P = 0.04), arterial hypertension (OR 4.65 95% CI 1.01-17.46 P = 0.03), and to be administered RAAS inhibitors (OR 6.11, 95% CI 1.03-25.96 P = 0.03) remained significantly associated with HK. We conclude that in stable KTRs the prevalence of HK is about 9%, slightly lower than previously reported. Moreover, it is not associated with eGFR, but with metabolic acidosis, arterial hypertension, and the use of RAAS inhibitors.
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