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The prevalence of heart failure (HF) with chronic kidney disease (CKD) is increasing. Both conditions are associated with poor outcomes including fluid overload causing hospitalisations and mortality. Patients with CKD are also less likely to have optimal pharmacological therapies for HF due to concerns over hyperkalaemia and declining renal function. This project aims to determine the prevalence of hyperkalaemia in CKD-HF patients and determine which factors are associated with hyperkalaemia.
Data on consecutive patients attending a CKD-HF clinic between 12th April 2019 and 11th September 2021 were retrospectively identified using electronic health records and included demographic factors (age, sex, BMI), renal function, heart function, mortality, and medications. The mean serum potassium level was measured at the beginning and end of the study period and stratified by the use of RAAS (renin-angiotensin-aldosterone system) inhibitors including ACEi (angiotensin converting enzyme inhibitors), ARB (angiotensin receptor blockers), ARNi (angiotensin receptor/neprilysin inhibitors) and MRAs (mineralocorticoid receptor antagonists). All analyses and data cleaning were performed in R version 4.2.1.
The sample of 318 patients had a mean age of 74.4 years (SD 13.3), 65.7% were male, the mean BMI was 28.4 kg/m2 (SD 7.0), 54.6% had diabetes, and 24.6% died during the study period. They had a mean estimated glomerular filtration rate (eGFR) of 28.1 (SD 12.6) and a mean ejection fraction (EF) of 41.8 (SD 13.5). The proportion of patients on beta-blockers were 79.9%, loop diuretics 73.3%, ACEi/ARB/ARNis 62.3%, MRAs 27.0%, and sodium-glucose cotransporter-2 (SGLT2) inhibitors 26.7%. Over 69% (221 of the 318 patients) were on a RAAS inhibiting medication. The mean potassium at the beginning and end of the study period were 4.58 (standard deviation (SD) 0.65) and 4.49 (SD 0.62) mmol/L, respectively. There were 34 (10.7%) and 26 (8.2%) patients who were hyperkalaemic (serum K greater that 5.4 mmol/L) at the beginning and end of the study period, respectively. Patients who were not on a RAAS inhibitor had an initial serum potassium of 4.48 (SD 0.65) mmol/L and final serum potassium of 4.42 (SD 0.61) mmol/L. Patients taking a RAAS inhibitor had an initial serum potassium of 4.62 (SD 0.65) mmol/L and a final serum potassium of 4.51 (SD 0.63) mmol/L. There were 35 patients (11%) who were ever hyperkalaemic. Compared to patients who were never hyperkalaemic, patients who experienced hyperkalaemia had a lower eGFR (26.9 vs 28.3), were more likely to be diabetic (62.9% vs 52.8%), had a lower EF (41.8 vs 42.4) and had a lower BMI (25.3 vs 29.0).
As expected, serum potassium levels were higher in the patients taking RAAS inhibitors and patients with worse kidney function. However, throughout the study period serum potassium levels decreased. This is possibly due to the use of potassium binders, such as sodium zirconium cycosilicate, which are routinely used in our clinic to lower potassium levels and allow for the use and up titration of RAAS inhibitors.