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This probably occurs by correcting diabetes\u2010linked increased clearance of thiamine, maintaining activity and expression of thiamine pyrophosphate\u2010dependent enzymes that help counter the adverse effects of high glucose concentrations\u2014particularly transketolase. Evidence from experimental and clinical studies suggests that metabolism and clearance of thiamine is disturbed in diabetes leading to tissue\u2010specific thiamine deficiency in the kidney and other sites of development of vascular complications. Thiamine supplementation prevented the development of early\u2010stage nephropathy in diabetic rats and reversed increased urinary albumin excretion in patients with type 2 diabetes and microalbuminuria in two recent clinical trials. The thiamine monophosphate prodrug, Benfotiamine, whilst preventing early\u2010stage development of diabetic nephropathy experimentally, has failed to produce similar clinical effect. The probable explanations for this are discussed. 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