Acute interstitial nephritis induced by glucosamine

Dual blockade of the renin angiotensin system versus maximal dose of ACE-inhibition in diabetic nephropathy. Acute interstitial nephritis induced by glucosamine Sir, Acute tubulointerstitial nephritis (TIN) is an important cause of acute renal dysfunction resulting from immune-mediated tubulointerstitial injury. The commonest causes of TIN include drugs and infection. Acute interstitial nephritis accounts for up to 15% of patients hospitalized for acute renal dysfunction. Glucosamine is a relatively new alternative therapy for the treatment of osteoarthritis (OA). We present a case of possible glucosamine-induced TIN. A 75-year-old man was admitted with a history of difficulty in passing urine, urgency, nocturia and hesitancy. There was no history of fever, rash or arthralgia. Past history was uneventful; he denied known drug allergy and the only medication he had been exposed to had been glucosamine (2–3 months) used for treatment of his osteoarthritis. General and systemic examination was unremarkable except for dehydration. Investigation revealed haemoglobin 10.3 g/dl; white cell count 15.1Â10 9 /(neutrophils 13.98, eosinophils 0.02), platelets 179Â10 9 /l, sodium 140 mmol/l, potassium 4.3 mmol/l, urea 45.8 mmol/l, creatinine 97 mmol/l, bicarbon-ate 19 mmol/l, bilirubin 2 mmol/l, alanine transferase 36 IU/l, alkaline phosphatase 183 IU/l, albumin 26 g/l and CRP 221 mg/l. He was initially fluid-resuscitated aggressively and catheterized, draining approximately 2000 ml of urine. Despite the above, his renal functions deteriorated. During the same period, he also had a series of blood tests which included normal complement and negative serum electrophoresis, auto-immune screen, ANCA and anti-GBM. Ultrasound demonstrated normal sized kidneys with good cortical thickness and a simple cyst in the left kidney. Prostatic volume was mildly increased at 48 cm 3 and prostatic specific antigen was within normal limits. Renal biopsy demonstrated a heavy mixed inflammatory cell infiltrate within the interstitium, suggestive of acute TIN. A minor degree of age-related atherosclerosis, involving the small and slightly larger blood vessels, was also noted. Glucosamine was discontinued and the patient received haemodialysis along with a short course of steroids. His symptoms improved significantly and he was dialysis-independent on discharge. Drug-induced acute TIN is an inflammatory process involving the tubules and the space between the tubules and the glomeruli. It is mediated by T cell hypersensitivity reaction and cytotoxic T cell injury. Renal biopsy is the gold standard for diagnosis. Stopping the suspected medication forms the main component of treatment, with most patients recovering rapidly on withdrawal of the offending drug. Corticosteroid and immunosuppressants, …