Table 1.

Management of RAAS inhibitors in response to change in renal function

Clinical assessment: Compare with baseline renal function (review series of results). Assess fluid status: if intravascularly depleted (jugular venous pulse not visible, postural drop in BP and no oedema), consider cautious intravenous fluids. Interpret BP in the context of usual values (low BP does not necessarily mean patient needs fluid). Reduce/withdraw RAASI if symptomatic hypotension. Repeated clinical and biochemical assessment is vital. Presence of moderate or severe hyperkalaemia may override recommendations based on change in renal function. In severe renal dysfunction assess for symptoms or uraemia.
Change in renal function compared with baseline	Recommendations for RAAS inhibitors
	HFpEF (assuming no other prognostic indication).	HFREF.
Increase in serum creatinine by <30%	Consider stop ACEI/ARB/ARNI Review MRA according to fluid status.	Continue unless symptomatic hypotension.
Increase in serum creatinine 30%–50%	Stop RAAS inhibitor.	Consider reducing dose or temporary withdrawal.*
Increase in serum creatinine >50%	Stop RAAS inhibitor.	Temporarily stop RAAS inhibitor.*
Severe renal dysfunction, for example, eGFR <20	Stop RAAS inhibitor.	Stop RAAS inhibitor if symptomatic uraemia irrespective of baseline function.

*Reinitiate and/or retitrate when renal function improved in patients with HFrEF.

ACEI, ACE inhibitor; ARB, angiotensin receptor blocker; BP, blood pressure; eGFR, estimated glomerular filtration rate; HFrEF, heart failure with reduced left ventricular ejection fraction; HFpEF, heart failure with preserved left ventricular ejection fraction; MRA, mineralocorticoid receptor antagonists; RAAS, renin–angiotensin–aldosterone.