Multiple trials have shown the benefits of blood pressure control in patients with renal disease. These benefits include slowing the progression of CKD and reducing cardiovascular outcomes and mortality. Patients with diabetic nephropathy or proteinuria particularly benefit from pharmacological blockade of the renin-angiotensin system with ACE (angiotensin-converting enzyme) inhibitors or ARBs (angiotensin receptor blockers).
These apply to all stages of CKD.
- Proteinuria low (i.e. ACR<70 or PCR<100) – Target blood pressure <140/90 (NICE suggests 120-139/ <90)
- Proteinuria high (i.e. ACR>70 or PCR>100) OR CKD and diabetes:: – Target blood pressure <130/80 (NICE suggests 120-129/<80)
Renin-angiotensin system (RAS) antagonists (e.g. ACE inhibitors or ARBs)
The co-prescription of two (or more) RAS blocking agents (e.g. an ACE inhibitor and an ARB) should generally be avoided. (see MHRA guidance)
Consider starting RAS blocking agents in patients with CKD and:
- Urinary ACR>30 or PCR>50
Exercise caution with, and potentially avoid the use of, RAS blocking agents in the following situations:
- Patients with pre-treatment potassium of >5 mmol/L
- Previous deterioration in renal function with these agents
- Known renovascular disease (this is not an absolute contraindication)
- Patients at high risk of pre-renal AKI (e.g. high output stomas, poor oral fluid intake)
- Patients co-prescribed NSAIDs
Starting and monitoring therapy with ACE inhibitors or ARBs
Check serum creatinine and potassium:
- Before starting therapy (do not routinely start if K > 5 mmol/L)
- 1-2 weeks after initiation or dose increment
If creatinine rises >30% or GFR fall >25% repeat tests, stop drug and consider other causes e.g. volume depletion, NSAID use. If no other explanation, consider investigations for renal artery stenosis.
If creatinine rises or GFR falls but by less than 30% (creatinine) or 25% (GFR) respectively repeat tests in further 1-2 weeks then action as above if criteria for drug cessation are met. Do not routinely stop or modify the renin-angiotensin system antagonists if lesser changes in renal function are observed – provided any lesser rises are stable.
If K>6 consider repeating to ensure not spurious (e.g. delayed separation), stop drugs that may be contributing, (e.g. NSAIDs, potassium-retaining diuretics, trimethoprim) and enquire about diet (especially ‘LoSalt’ which is potassium chloride). If hyperkalaemia persists the RAS blocking drug should be stopped.
Modest stable hyperkalaemia may be preferable to discontinuing a valuable therapy. This situation is most frequently encountered in patients with diabetes in whom high potassium levels are a more frequent finding and the evidence base in favour of RAS blockade is very strong. There are a number of strategies which may be employed to lower potassium in order to facilitate the continued prescription of the RAS blocking agent where it is felt imperative to do so. In selected patients, such strategies may include dietary potassium restriction, the addition of sodium bicarbonate, a diuretic and/or fludrocortisone. Before implementing any of these measures ordinarily, patients should be discussed with or referred to renal services.
It may be appropriate to stop RAS antagonists at times of high risk for acute kidney injury (e.g. acute volume depletion) and resume therapy later. Consider educating patients about these “sick day rules” when commencing these agents.
Information for patients
Blood pressure control is critically important in preventing further kidney deterioration in many patients with CKD and for protecting against damage to heart and arteries. Some of the drugs used can affect kidney function and additional monitoring may be required.