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Recurrent hypoglycaemia in a diabetic patient as a result of unexpected renal failure
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     1 Department of Internal Medicine, Timmins and District Hospital, Timmins, ON, Canada P4N 8R1

    Correspondence to: M S Parmar, Suite 108, 707 Ross Avenue East, Timmins, ON, Canada P4N 8R1 atbeat@ntl.sympatico.ca

    Introduction

    A 64 year old man with a 15 year history of type 2 diabetes mellitus presented with a third episode of hypoglycaemia in two weeks. His diabetes was well controlled with 35 units of insulin a day, and he had had no hypoglycaemic episodes in the past two years. He had no history of hypertension, retinopathy, or nephropathy. He was compliant with his diet, insulin therapy, and exercise programme. At a regular check up two months previously, his blood pressure had been 116/70 mm Hg and his HbA1c level 0.07 (normal 0.050 to 0.064), with home blood glucose readings of 5.0-8.0 mmol/l during the previous month. The ratio of urine microalbumin concentration to creatinine concentration was 2.0 (< 2.5), and serum creatinine concentration was 104 μmol/l (44-106 μmol/l).

    He had started to experience low back pain a month before presentation with his third episode of hypoglycaemia and saw his family doctor, who prescribed diclofenac 50 mg twice daily; his back pain then improved. Two weeks later, he started to experience headache and irritability with periods of sweating. His wife brought him to the emergency department on three occasions—16, 19, and 23 days after starting diclofenac—and he was noted to be hypoglycaemic with blood glucose concentrations of 1.2-2.5 mmol/l. At each visit his symptoms responded to intravenous glucose and feeding. No investigations were done at his first two visits to the emergency department.

    At his third visit, his blood glucose concentration was 1.2 mmol/l. A history taken at this visit after correction of hypoglycaemia was unremarkable. The patient reported no decrease in his appetite or increase in physical activity in the past month and no decrease in urine output. Physical examination was unremarkable, with a blood pressure of 150/90 mm Hg. There was no peripheral oedema. Investigations showed a raised serum creatinine concentration of 440 μmol/l and a raised serum urea concentration of 14.6 mmol/l (1.7-8.3 mmol/l); serum potassium concentration was 4.8 mmol/l (3.5-5.0 mmol/l).

    Since starting to take the non-steroidal anti-inflammatory drug diclofenac, the patient had developed a decline in renal function with a fourfold increase in serum creatinine. Diclofenac was immediately stopped and his insulin dosage was decreased. Two weeks later, his serum creatinine concentration returned to baseline and he resumed his usual insulin dosage, with no further episodes of hypoglycaemia and with reasonable glucose control.

    Discussion

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