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 baselineRecommendations 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 <20Stop 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.