Rivolta E, Ponticelli C, Imbasciati E, Vegeto A
Transplantation. 1983 Apr;35(4):328-31. doi: 10.1097/00007890-198304000-00013.
A patient with end-stage renal failure caused by bilateral kidney stones received a kidney transplant from his identical twin. No immunosuppressive therapy was given. After a few days he developed a urinary fistula from a polar artery section, which spontaneously healed. Renal function remained subnormal, blood pressure and urinalysis were normal. After one year proteinuria appeared, and after about four years it entered a nephrotic range. Renal biopsy showed focal glomerular sclerosis (FGS). In the following years progressive renal insufficiency and arterial hypertension developed, and the patient had to be submitted to regular dialysis about 9 years after transplantation. As far as we know this is the first case of late renal failure in an isograft related to the development of de novo FGS. It is suggested that de novo FGS in this isotransplant was related to the partial loss of renal mass caused by polar necrosis, which caused glomerular hyperfiltration. Another possible contributing factor may be kidney denervation, which removes an important mechanism for adjustment of renal arterial flow.
一名因双侧肾结石导致终末期肾衰竭的患者接受了来自其同卵双胞胎的肾脏移植。未给予免疫抑制治疗。几天后，他出现了来自肾极动脉断面的尿瘘，该尿瘘自行愈合。肾功能仍未恢复正常，血压和尿液分析正常。一年后出现蛋白尿，约四年后进入肾病范围。肾活检显示局灶性节段性肾小球硬化（FGS）。在接下来的几年里，逐渐出现肾功能不全和动脉高血压，患者在移植后约9年不得不接受定期透析。据我们所知，这是首例与新发FGS相关的同基因移植晚期肾衰竭病例。提示该同基因移植中的新发FGS与肾极坏死导致的肾实质部分丧失有关，这导致了肾小球高滤过。另一个可能的促成因素可能是肾脏去神经支配，它消除了调节肾动脉血流的重要机制。
