The 58-year-old with a falling eGFR who wants to stop metformin
Mr Rahman, 58, attends for his quarterly diabetes review. He has had type 2 diabetes for 11 years, with hypertension and dyslipidaemia. His current prescriptions are metformin 1000 mg twice daily, gliclazide MR 60 mg each morning, ramipril 5 mg daily and atorvastatin 20 mg at night. Examination: BMI 31 kg/m², BP 148/86 mmHg, no foot ulcer, no retinopathy at last screening. HbA1c is 8.7% (71 mmol/mol). Creatinine 168 µmol/L gives an eGFR of 34 mL/min/1.73 m², down from 52 a year ago; the urine albumin-to-creatinine ratio is 68 mg/mmol. He reports two episodes of sweating and tremor in the past month, both on mornings when he skipped breakfast. He asks whether he should stop "the big white tablet" because a neighbour told him metformin destroys kidneys, and he is frightened because his mother needed dialysis at 70. The public formulary lists empagliflozin but requires prior authorisation at eGFR above 30.
1. How should the metformin be adjusted, and what is the most likely cause of his hypoglycaemia?
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Metformin is not damaging his kidneys in the way he fears, but the dose must track the eGFR. Metformin is contraindicated below an eGFR of 30 and should be dose-reduced to a maximum of 1000 mg/day at eGFR 30–45. At 34 the right action is to reduce to 500 mg twice daily, not to stop: stopping would worsen glycaemia and lose a cheap, weight-neutral agent. Give sick-day rules in writing - hold during vomiting, diarrhoea, sepsis, dehydration and around iodinated contrast - and recheck the eGFR in three months.
The hypoglycaemia is much more plausibly gliclazide than metformin, which does not cause hypoglycaemia when used alone. With an eGFR of 34, sulfonylurea metabolites accumulate and the risk rises with missed meals. Reduce gliclazide MR to 30 mg or stop it, and relax his HbA1c target to roughly 7.5–8.0% because advanced CKD and hypoglycaemia both change the risk-benefit balance; 8.7% with recurrent hypoglycaemia is worse than 8.0% without.
Empagliflozin is a reasonable add-on: it slows eGFR decline and reduces cardiovascular events, can be initiated down to an eGFR of 20, and his value of 34 satisfies the formulary threshold of above 30. Counsel on genital mycotic infection, volume depletion, euglycaemic ketoacidosis and sick-day interruption. Explain the lactic acidosis risk honestly: it is low at this eGFR and rises mainly with hypoxia, sepsis, liver disease and alcohol excess.
2. What will you do to slow the decline in kidney function, and does he meet criteria for nephrology referral?
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Three things drive the plan: blood pressure, albuminuria and glycaemia. Titrate ramipril from 5 mg towards the maximum tolerated dose, with potassium and creatinine checked 1–2 weeks later; a creatinine rise of up to 30% is expected and is not a reason to withhold or stop the drug. Target BP below 130/80 mmHg. Add empagliflozin - the ACE inhibitor plus SGLT2 inhibitor combination has the strongest evidence for slowing progression. Increase atorvastatin to 40 mg, since an eGFR below 60 is itself a risk-enhancing factor. Review every drug he takes, including over-the-counter analgesics: stop NSAIDs, discourage herbal remedies, and flag contrast exposure.
Look for a non-diabetic contributor, because an 18 mL/min/1.73 m² fall in one year is faster than typical diabetic decline. Check urine dipstick for blood and protein, arrange a renal ultrasound if not recently done, and request calcium, phosphate, PTH and haemoglobin.
He does meet referral criteria - but on the rate of decline (KDIGO refers at more than 5 mL/min/1.73 m² per year) and an ACR approaching 70 mg/mmol, not on the eGFR of 34 alone. Refer with a written summary of the trend, current drugs and BP. Finish the annual foot and retinal checks at this visit rather than deferring them.