Noel C, Pruvot F R, Talaska A, Gosselin B, Houdret P, Declerck N, Brevet E, Lelièvre G
Service de Néphrologie A, Hôpital Calmette, CHRU, Lille.
Presse Med. 1992 Dec 2;21(41):1997-8.
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.
我们分析了3例因原发性高草酸尿症导致终末期肾衰竭而接受移植患者的记录，并通过重复活检评估了草酸盐沉积在单纯肾移植或肝肾联合移植后肾衰竭构成中所起的作用。肾移植早期失败很常见，且由于移植活检中存在草酸盐沉积，常被解释为复发的结果。事实上，在我们的2例肝肾联合移植病例中，尽管肾衰竭在进展，但草酸盐沉积减少，这表明晶体沉积并非肾损伤的原因。然而，我们不能排除草酸盐分子毒性在这两例原发性肾功能丧失后发生的弥漫性硬化形成中起作用，环孢素通过加剧血流动力学过程而加重了这种毒性作用。另一方面，正如在我们的单纯肾移植病例中所观察到的，肾衰竭发作前出现的肾晶体沉积提示了真正解释肾草酸沉积缓慢复发的机制。
