Change in renal function associated with drug treatment in heart failure: national guidance

Abstract

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.

Keywords: heart failure with preserved ejection fraction; heart failure with reduced ejection fraction; pharmacology.

Conflict of interest statement

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.

© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

Figures

Figure 1

Distribution of estimated glomerular filtration rate (eGFR) among 1216 patients with chronic stable heart failure. Data from Eur Heart J 2006;27:569–81. AKI, acute kidney injury; CKD, chronic kidney disease; HFREF, heart failure with reduced left ventricular ejection fraction; MI, myocardial infarction; RAAS, renin–angiotensin–aldosterone.

Figure 2

Relationship between change in eGFR during hospitalisation and subsequent 60-day hazard for adverse events. Data from 303 patients in the DOSE trial. J Card Fail 2016;22:753–760. DOSE, Diuretic Strategies in Patients with Acute Decompensated Heart Failure; eGFR, estimated glomerular filtration rate; ER, emergency room.

Figure 3

Management of patients with AKI or worsening renal function who are receiving RAAS inhibitor. Clinical assessment of the individual patient is key. In all cases consider original indication for RAAS inhibitor. Major prognostic benefit: HFrEF, post MI and left ventricular systolic dysfunction (LVSD), CKD and albuminuria. No/little prognostic benefit: hypertension (other drug options available) and HFpEF. Please refer to table/text box for management of moderate to severe hyperkalaemia or progressive worsening renal function  (WRF). ACEi, ACE inhibitor; AKI, acute kidney injury; ARB, angiotensin receptor blocker; BP, blood pressure; MRA, mineralocorticoid receptor antagonist; RAAS, renin–angiotensin–aldosterone.