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A 55-year-old woman presented with recurrent episodes of hypoglycaemia over 4 weeks. She had had type 1 diabetes mellitus (DM) for 35 years, managed by an insulin basal bolus regime. Her comorbidities included retinopathy, chronic renal failure, (presumed to be on the basis of diabetic nephropathy), hypertension, obesity, gout and an ischaemic stroke 15 years earlier. Over 5 years of follow-up, her renal function showed a stable decline of 3ml/min/year, with a creatinine of 141mmol/l and estimated glomerular filtration rate (eGFR) of 66ml/min/1.73m 5 months before presentation (Figure 1). She self-regulated an insulin basal bolus regime and hypoglycaemic episodes had been rare. Her other medication included a statin, six anti-hypertensive agents, warfarin and orlistat. Orlistat had been commenced 5 months previously with a subsequent 12 kg weight reduction. There had been no other new medication. Clinical examination was unremarkable other than a body mass index (BMI) of 35 kg/m and a blood pressure of 176/86mmHg. Initial investigations revealed advanced renal failure with a serum creatinine of 626 mmol/l, eGFR 12ml/ min/1.73m, metabolic acidosis and hyperkalaemia (potassium 6.8mmol/l). Urinalysis revealed only proteinuria. An ultrasound scan showed that both kidneys were non-obstructed and anatomically normal. The bladder was empty. Her inflammatory markers were normal. Immunological investigations were negative. Despite preservation of urine output, there was no improvement in renal function, and persistent hyperkalaemia necessitated haemodialysis. After reversal of anticoagulation, renal biopsy showed diabetic nephropathy with moderate interstitial scarring and widespread glomerulosclerosis. Additionally there was extensive, superimposed, intra-tubular deposition of calcium oxalate crystals in the kidney, with mild to moderate tubulo-interstitial inflammation (Figure 2). There was no personal or family history of renal stone disease or traditional risk factors for calcium oxalate crystallization. A 2-week course of oral steroid therapy was initiated to reduce the inflammatory component of the renal disease, without objective improvement. There was no recovery of renal function and 24 months later she remains dialysis-dependent.

Rapidly progressive renal failure associated with successful pharmacotherapy for obesity