In type II diabetes treated with metformin, lactic acidosis is a rare but severe complication. Commonly patients with lactic acidosis show signs of shock, tissue hypoxia, acute hepatic or renal failure and the link between metformin therapy and lactic acidosis may be coincidental, associated or causal. Excessive plasma metformin concentrations show that lactic acidosis is due to a toxicological mechanism. The case of a 65-year-old woman with type II diabetes, in whom severe type B2 lactic acidosis secondary to metformin was precipitated by acute renal failure, is presented. The association of diuretics with non-steroidal anti-inflammatory drugs and colchicine was responsible for a volume depletion and an acute renal failure. Initial serum creatinine was 643 micromol x l(-1) and arterial blood gas analysis revealed a pH of 7.01. Aggressive volume expansion and correction of the acidosis with intravenous bicarbonate therapy failed. At the intensive care unit, calculated anion gap was 35 mmol x l(-1) (normal range 10-18) and lactate concentration was 12.4 mmol x l(-1), liver profile was normal. Prolonged haemodialysis using bicarbonate dialysate resulted in a favourable outcome. Toxicology confirmed retrospectively the presence of a plasma concentration of metformine of 20 mg x l(-1) (normal <2). One month after this episode she has made a recovery of tubular necrosis, although no longer prescribed metformin. Metformin should be temporally stopped when acute renal failure occurs or is anticipated; patient with acute renal failure and high calculated anion gap should benefit from lactate measurements. Early bicarbonate haemodialysis is an adequate treatment of lactic acidosis caused by accumulation of metformin associated with acute renal failure