MO191MANAGEMENT OF HYPERKALAEMIA TO FACILITATE RAASI THERAPY IN PATIENTS WITH HEART FAILURE IN A BESPOKE UK CLINIC

Abstract Background and Aims Best practice for treatment of patients with chronic heart failure involves beta-blockers and renin-angiotensin-aldosterone system inhibitors (RAASi) such as ACE inhibitors (ACE-i), angiotensin receptor blockers (ARB), mineralocorticoid antagonists (MRA) and neprolysin inhibitor/ARB. However, use of these agents, and optimisation of their dosage, is frequently limited by hyperkalaemia, the incidence of which is increased by the co-prevalence of chronic kidney disease (CKD). Management of patients in a bespoke Hyperkalaemia Clinic can be advantageous in facilitating optimal use of RAASi. Method A Hyperkalaemia Clinic was opened in July 2019 in this tertiary renal centre within an NHS trust that hosts 4 district hospital heart failure services. Referrals of patients with left ventricular systolic dysfunction whose RAASi could not be optimised because of hyperkalaemia were encouraged from heart failure specialist nurses and cardiologists. Management of the patients incorporated commencement of patiromer at 8.4g daily and increases in RAASi was usually devolved to the referring team. This report describes the activity and short-term outcomes of the first 17 months after opening of the clinic (follow up until 1st January 2021). Results 34 patients with systolic heart failure and problems with RAASi-associated hyperkalaemia were referred to the clinic. Mean age was 74 (range 44-88) years, 28% had stage 3a, 28% 3b and 8% stage 4 CKD. ACE-I or ARB were being used in 73% of patients at referral, 73% were using beta blockers and 50% MRA with loop diuretic use in 70%. At first visit 64% had normokalaemia, and 36% serum potassium 5.4-6.0 mmol/L. During follow-up, 6 (18%) patients discontinued patiromer due to gastrointestinal side effects, 3 no longer required the binder because of decrease in RAASi use and 2 patients died (one each from stroke and sepsis). One patient was switched to an alternative potassium binder. As of 1st January 2021, patiromer was still being administered to 22 (65%) patients, 8 of which had received this for >12 months; all patients remained normokalaemic and none of them required magnesium supplementation. An increase in RAASi therapy had occurred in only 12 (35%) patients. Conclusion Our experience demonstrates the relative simplicity of managing hyperkalaemia via a bespoke clinic in cardio-renal patients. As this was nephrology-led, optimised management was dependent upon the assertive and collaborative involvement of the referring heart failure teams who helped with biochemical monitoring and alteration of RAASi therapy. However, less than half of the patients benefitted from an increase in RAASi therapy after normalisation of serum potassium, and there was definitely scope for improving this component of the care pathway via more direct multi-disciplinary interaction with the heart failure teams.