Inhibitors of the renin–angiotensin–aldosterone (RAAS) system are cornerstones of the management of patients with heart failure with reduced left ventricular ejection fraction (HFrEF). However, RAAS inhibitors may cause decline in renal function and/or hyperkalaemia, particularly during initiation and titration, intercurrent illness and during worsening of heart failure. There is very little evidence from clinical trials to guide the management of renal dysfunction. The Renal Association and British Society for Heart Failure have collaborated to describe the interactions between heart failure, RAAS inhibitors and renal dysfunction and give clear guidance on the use of RAAS inhibitors in patients with HFrEF. During initiation and titration of RAAS inhibitors, testing renal function is mandatory; a decline in renal function of 30% or more can be acceptable. During intercurrent illness, there is no evidence that stopping RAAS inhibitor is beneficial, but if potassium rises above 6.0 mmol/L, or creatinine rises more than 30%, RAAS inhibitors should be temporarily withheld. In patients with fluid retention, high doses of diuretic are needed and a decline in renal function is not an indication to reduce diuretic dose: if the patient remains congested, more diuretics are required. If a patient is hypovolaemic, diuretics should be stopped or withheld temporarily. Towards end of life, consider stopping RAAS inhibitors. RAAS inhibition has no known prognostic benefit in heart failure with preserved ejection fraction. Efforts should be made to initiate, titrate and maintain patients with HFrEF on RAAS inhibitor treatment, whether during intercurrent illness or worsening heart failure.
- heart failure with reduced ejection fraction
- heart failure with preserved ejection fraction
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Contributors Each author was involved in the conception and planning of the article. Each author was the primary writer of one of the sections of the document, but each section has in turn been edited and approved by all the other authors. ALC and CT are responsible for the overall content as guarantors on behalf of, respectively, the British Society for Heart Failure and the Renal Association.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests MCP has received support from Boehringer Ingelheim, Novartis and AstraZeneca. PK has received speaker and advisory board fees from: Astrazeneca, Novartis and Vifor Pharma. MCP has received speaker and advisory board fees from: Vifor Pharma, AstraZeneca and Novartis. ALC has received speaker and advisory board fees from: Novartis. LT and CT have no conflicts of interest to declare.
Provenance and peer review Not commissioned; externally peer reviewed.
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