We analyzed the records of 3 patients transplanted for end-stage renal failure due to primary hyperoxaluria and evaluated on repeat biopsies the role played by oxalate deposits in the constitution of renal failure after isolated kidney graft, or combined liver and kidney transplantation. Early failure of the renal graft is frequent and often interpreted as the consequence of recurrence because of the presence of oxalate deposits on the graft biopsy. In fact, the decrease in oxalate deposits observed in our 2 cases of combined liver and kidney transplantation despite the progressive renal failure, indicates that crystal deposition is not responsible for the renal lesions. However, we cannot exclude that the oxalate molecule toxicity plays a role in the constitution of the diffuse sclerosis which occurred in these two cases after a primary renal non function, aggravating a hemodynamic process by using cyclosporin. On the other hand, as observed in our isolated kidney graft, renal crystal deposition occurring before the onset of renal failure suggests the true mechanism explaining the slow recurrence of renal oxalosis.