This guidance has been recently written by the British Renal Association and British Heart Failure Society, and is an excellent summary of how to respond to renal issues in heart failure patients. Clark AL, Kalra PR, Petrie MC, et al Change in renal function associated with drug treatment in heart failure: national guidance. Heart 2019;105:904-910. For those with less time, I will summarise it below.
- Renin–angiotensin–aldosterone system (RAAS) blockers such as ACE inhibitors (ACEi), Angiotensin Receptor Blockers (ARB), and Angiotensin-Neprilysin inhibitors (ARNI; sacubital/valsartan trade name Entresto) have a major prognostic benefit in patients with heart failure with a reduced ejection fraction (HF-REF). They have no benefit in patients with heart failure with a preserved EF (HFPEF)
- Accordingly in HF-REF all efforts should be made to continue RAAS blockers
- In HF-PEF there is no prognostic or symptomatic benefit of RAAS blockers for the heart failure, and so they can be stopped if clinically indicated with minimal concern. They may still be indicated for other reasons such as hypertension, renal protection etc.
Management of RAAS inhibitors in response to change in renal function
Taken from the above document.
- Make a 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 for the patient (low BP does not necessarily mean patient needs fluid). Reduce RAASI only if symptomatic hypotension; try and reduce rather than stop.
- 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 serum creatinine compared with baseline||What to do in HF with a reduced EF|
|Increase <30%||Continue ACEI/ARB/ARNI/MRA unless symptomatic hypotension.|
|Increase 30%–50%||Consider reducing dose or temporary withdrawal.*|
|Increase >50%||Temporarily stop RAAS inhibitor.*|
|Severe, eg eGFR <20||Stop RAAS inhibitor if symptomatic uraemia irrespective of baseline function.|
*Reinitiate and/or retitrate when renal function improved in patients with HFrEF.
During intercurrent illness (NOT including worsening heart failure), consider stopping RAAS inhibitors if creatinine rises more than 30% from baseline
In HF PEF no prognostic or symptomatic benefit has been shown from ACE/ARB. Hence if if creatinine rises more than 30% it is suggested to stop these agents.
Patients with worsening heart failure
- In patients with congestion (the most common presentation with heart failure) the most common issues worsening renal function are
- Renal venous hypertension / congestion
- Increased intra-abdominal pressure due to ascites or oedema
- These respond to diuretics: ie increasing or giving diuretics will improve renal function
- In a small subset of patients with shock (ie BP lower than usual for them; please note many HF patients have low BP all the time), the predominant problem is poor renal perfusion and they will not respond to diuretics. Clinical assessment is key, as well as involving a HF specialist early