Progression of renal failure without proteinuria in a patient with type 1 diabetes.

A.Z. is a 42-year-old Caucasian male who has had type 1 diabetes since the age of 19. He was referred to a nephrologist from an internal medicine ward because of a moderate renal dysfunction (serum creatinine 1.7–2mg/dl up from 1.1mg/dl; creatinine clearance 55–69ml/min), which developed over a few months. Further tests revealed microalbuminuria (0.159 g/24 h), with a few red cells in the urinary sediment, and moderate anaemia (haemoglobin 11.1 g/dl), with glycated haemoglobin at 8.8%. Ultrasonography demonstrated kidneys of normal shape and echogeneicity; renal scintigraphy produced normal curves, with fine nonhomogeneities, minor signs of urostasis and modest pelvic distension. At his clinic visit, A.Z. was a sporty, well nourished person, in good clinical condition (weight 75.3 kg, height 180 cm, body mass index 23), and normotensive (blood pressure 110/75mmHg; heart rate 64 beats/ min). The only pathological finding was modest ankle oedema. His clinical history, beside poorly controlled diabetes and his report of occasional hand and foot swelling, was unremarkable. He denied alcohol or drug abuse, as well as any self-prescribed medications. His therapy consisted only of injections of insulin, four times daily. He recently had developed severe depression after the death of one of his two daughters, which he reported to have been due to a congenital neuromuscular problem, though he was not able to recall the diagnosis precisely. According to his wife, he recently had lost interest in living, changed his habits, stopped playing sport and gained weight. In the same 6–8 month period, his hypoglycaemic crises changed in pattern: he reported being disoriented in space and time, and becoming aggressive, before losing consciousness (blood glucose 20–30mg/dl). Tests for diabetic end-organ damage revealed: background retinopathy; neuropathy with reduction of vibratory sensibility; no sign of vasculopathy; and normotension. Under the working diagnosis of a non-diabetic renal disease, the patient was hospitalized for a renal biopsy. During hospitalization, he suffered a severe hypoglycaemic episode preceded by aggressive behaviour (blood glucose <30mg/dl). The neurologist suggested a functional component to account for his mild ideomotor slowing and his aggressive behaviour. Electroencephalography revealed non-specific metabolic alterations. After the hypoglycaemic episode, he reported muscular aches, which he admitted had been present for a few months, but were acutely exacerbated. Suspecting a link with the unspecified problem of his daughter, muscle enzymes were tested. His creatinine phosphokinase and lactic dehydrogenase levels were high (CPK 1960U/l and LDH 1018 IU/l).