Sayin Burak, Canver Burak, Gurlek Demirci Bahar, Colak Turan, Ozdemir Binnaz Handan, Haberal Mehmet
Department of Nephrology, Baskent University Faculty of Medicine, Ankara, Turkey.
Exp Clin Transplant. 2017 Feb;15(Suppl 1):32-36. doi: 10.6002/ect.mesot2016.O19.
Chronic allograft dysfunction is a complex and multifactorial process characterized by progressive interstitial fibrosis and tubular atrophy. The finding of interstitial fibrosis and tubular atrophy is prevalent among kidney transplant patients receiving a calcineurin inhibitor-based immunosuppressive regimen and may be considered as a surrogate of allograft survival. Both immune (acute rejection episodes, sensitization, and HLA incompatibility) and nonimmune (donor age, delayed graft function, calcineurin inhibitor toxicity, infections, and hypertension) mechanisms play a role in chronic allograft dysfunction, and different causes all lead to similar histologic and clinical final pathways, with the end result of graft loss. In our study, we aimed to compare the outcomes of kidney transplant recipients with or without interstitial fibrosis and tubular atrophy in protocol biopsies to determine the conditions that may affect allograft survival.
We divided 192 kidney transplant recipients into 2 groups (96 patients with interstitial fibrosis and tubular atrophy; 96 patients without interstitial fibrosis and tubular atrophy) according to protocol biopsy at 6 months. Patient groups were compared according to their risk factors for chronic allograft dysfunction (cold ischemia time, delayed graft function, donor age, infections, mean blood calcineurin levels, and hypertension).
Cold ischemia time, delayed graft function, high 24-hour proteinuria levels, and higher mean blood calcineurin levels were found to be major risk factors for poor graft function in kidney transplant recipients with interstitial fibrosis and tubular atrophy. Renin-angiotensin system blockage with either angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was found to be preventive for interstitial fibrosis and tubular atrophy after kidney transplant.
Preventing prolongation of cold ischemia time, lowering blood cholesterol levels, angiotensin-converting enzyme inhibitors and angiotensin receptor blocker treatment even without existing proteinuria and avoiding higher doses of calcineurin inhibitors should be major approaches in kidney transplant recipients.
慢性移植肾失功是一个复杂的多因素过程，其特征为进行性间质纤维化和肾小管萎缩。间质纤维化和肾小管萎缩在接受以钙调神经磷酸酶抑制剂为基础的免疫抑制方案的肾移植患者中很常见，可被视为移植肾存活的替代指标。免疫机制（急性排斥反应、致敏和HLA不相容性）和非免疫机制（供体年龄、移植肾功能延迟恢复、钙调神经磷酸酶抑制剂毒性、感染和高血压）均在慢性移植肾失功中起作用，不同原因均导致相似的组织学和临床最终途径，最终结果是移植肾丢失。在我们的研究中，我们旨在比较在方案活检中有或无间质纤维化和肾小管萎缩的肾移植受者的结局，以确定可能影响移植肾存活的情况。
根据6个月时的方案活检，将192例肾移植受者分为2组（96例有间质纤维化和肾小管萎缩的患者；96例无间质纤维化和肾小管萎缩的患者）。根据慢性移植肾失功的危险因素（冷缺血时间、移植肾功能延迟恢复、供体年龄、感染、平均血中钙调神经磷酸酶水平和高血压）对患者组进行比较。
发现冷缺血时间、移植肾功能延迟恢复、24小时蛋白尿水平高以及平均血中钙调神经磷酸酶水平较高是有间质纤维化和肾小管萎缩的肾移植受者移植肾功能不良的主要危险因素。发现使用血管紧张素转换酶抑制剂或血管紧张素受体阻滞剂阻断肾素-血管紧张素系统对肾移植后间质纤维化和肾小管萎缩有预防作用。
预防冷缺血时间延长、降低血胆固醇水平、即使在无蛋白尿的情况下使用血管紧张素转换酶抑制剂和血管紧张素受体阻滞剂治疗以及避免使用高剂量的钙调神经磷酸酶抑制剂应是肾移植受者的主要治疗方法。
