This page gives advice on initiating treatment with SGLT2 inhibitors (“flozins”) in CKD. It is primarily aimed at renal physicians.
See our CKD treatment algorithms. Consider SGLT2i in ALL patients with T2DM and CKD (i.e. if eGFR < 60 or uACR > 3).
When discussion with the diabetes team is NOT required:
In patients with diabetes, use is now well-established. These drugs do not need to be prescribed or overseen by a diabetologist; they could be prescribed by a nephrologist, general physician or general practitioner.
Many patients with T2DM will be managed in primary care. Patients on diet only or diabetes drugs that are unlikely to cause hypoglycaemia in combination with SGTL2i – e.g. metformin, DPP4 inhibitors, GLP-1, pioglitazone – don’t need any extra monitoring or medication adjustment. In such patients, an SGLT2i could – and should – be initiated without any discussion with the diabetes team.
When discussion with the diabetes team would be helpful:
In short: for patients on insulin or a sulphonylurea.
Large improvements in glycaemic control can be anticipated when starting an SGLT2i in patients with good renal function (eGFR > 60). If the patient is already taking insulin or a sulphonylurea then there may be a risk of hypoglycaemia and therefore close blood glucose monitoring will be required; if control was tight prior to starting the SGLT2i then the insulin or sulphonylurea might need to be stopped before starting the SGLT2i. In such patients, blood glucose monitoring and advice on treatment of hypos would be appropriate; discussion with diabetes doctors or nurses may help, especially if the patient is already under secondary care. There may also be a risk of ketoacidosis in patients with longstanding T2DM / β-cell failure.
SGLT2i are used very infrequently in T1DM and only ever under direct specialist supervision by a diabetologist.
In non-diabetic chronic kidney disease:
Indications and contraindications:
See our CKD treatment algorithms. Consider SGLT2i in patients without diabetes if CKD and uACR > 25 mg/mmol (uPCR > 50). Such patients would usually also be prescribed maximum-dose RASi (unless contraindicated).
SGLT2i effect on blood glucose diminishes as eGFR falls but efficacy at preventing CKD progression and cardiovascular outcomes does not. Their efficacy at glucose-lowering falls off significantly at GFR < 45 ml/min. In patients already taking SGLT2i, these agents can be continued as eGFR falls below this threshold but should be discontinued at the start of dialysis therapy or time of kidney transplant. SGLT2i can be initiated for CKD at any eGFR > 15 ml/min.
Relative contraindications include immunosuppression (e.g. kidney transplant, lupus, vasculitis) and ADPKD.
How to prescribe:
The MHRA have licensed dapagliflozin (10 mg once daily) for use in CKD. The licence permits initiation in patients with eGFR 15 ml/min or above. SGLT2i are now on the NHS Lothian formulary for T2DM, HFrEF and CKD. (The East Region Formulary Committee approved Dapagliflozin for use in CKD on 25 May 2022.)
RIE pharmacy stocks empagliflozin, canagliflozin and dapagliflozin. It is highly likely that the renal and cardiovascular benefits (and side-effect profile) is similar for all SGLT2i – i.e. it is a class effect.
Do I need to monitor anything?
There is no need to routinely monitor blood glucose or eGFR after initiation. Anticipate a haemodynamic drop in eGFR – as you might get after starting an ACEi / ARB.
Counsel all patients re: risk of fungal genital infections (thrush). Warn patients with diabetes that it will lower their blood glucose levels. Some patients may experience a marked diuretic effect and therefore volume contraction / postural dizziness (especially if starting glycaemic control is poor). Here is the SGLT2i patient information leaflet used in the diabetes clinic (i.e. for patients with T2DM). Remember that the side-effect profile in patients without diabetes is likely to be different.
In patients with T2DM, many physicians advocate temporary suspension during acute illness (i.e. ‘sick day rules’) in order to avoid ketoacidosis and excessive volume contraction.
This page was drafted by Robert Hunter in March 2021 with input from Neil Turner (Nephrologist), Pauline Jones (Diabetologist) and Sarah MacInnes (Pharmacist). The date of the most recent update is given in the footer.