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移植后肾小球病的重叠发病机制:慢性体液性排斥反应、丙型肝炎感染和血栓性微血管病。

Overlapping pathways to transplant glomerulopathy: chronic humoral rejection, hepatitis C infection, and thrombotic microangiopathy.

机构信息

Department of Nephrology and Medical Intensive Care, Campus Virchow Clinic, Charite Universitatsmedizin Berlin, Berlin, Germany.

出版信息

Kidney Int. 2011 Oct;80(8):879-85. doi: 10.1038/ki.2011.194. Epub 2011 Jun 22.

DOI:10.1038/ki.2011.194
PMID:21697808
Abstract

Transplant glomerulopathy (TG) has received much attention in recent years as a symptom of chronic humoral rejection; however, many cases lack C4d deposition and/or circulating donor-specific antibodies (DSAs). To determine the contribution of other causes, we studied 209 consecutive renal allograft indication biopsies for chronic allograft dysfunction, of which 25 met the pathological criteria of TG. Three partially overlapping etiologies accounted for 21 (84%) cases: C4d-positive (48%), hepatitis C-positive (36%), and thrombotic microangiopathy (TMA)-positive (32%) TG. The majority of patients with confirmed TMA were also hepatitis C positive, and the majority of hepatitis C-positive patients had TMA. DSAs were significantly associated with C4d-positive but not with hepatitis C-positive TG. The prevalence of hepatitis C was significantly higher in the TG group than in 29 control patients. Within the TG cohort, those who were hepatitis C-positive developed allograft failure significantly earlier than hepatitis C-negative patients. Thus, TG is not a specific diagnosis but a pattern of pathological injury involving three major overlapping pathways. It is important to distinguish these mechanisms, as they may have different prognostic and therapeutic implications.

摘要

移植肾小球病 (TG) 近年来作为慢性体液性排斥反应的一种症状受到广泛关注;然而,许多病例缺乏 C4d 沉积和/或循环供体特异性抗体 (DSA)。为了确定其他原因的贡献,我们研究了 209 例连续的肾移植指征活检,这些活检均为慢性移植物功能障碍,其中 25 例符合 TG 的病理标准。三种部分重叠的病因占 21 例(84%):C4d 阳性(48%)、丙型肝炎阳性(36%)和血栓性微血管病 (TMA) 阳性(32%)TG。大多数确诊为 TMA 的患者也患有丙型肝炎,大多数丙型肝炎阳性患者存在 TMA。DSA 与 C4d 阳性显著相关,但与丙型肝炎阳性 TG 无关。在 TG 组中,丙型肝炎的患病率明显高于 29 例对照患者。在 TG 队列中,丙型肝炎阳性患者的移植物衰竭发生明显早于丙型肝炎阴性患者。因此,TG 不是一种特异性诊断,而是一种涉及三种主要重叠途径的病理损伤模式。区分这些机制很重要,因为它们可能具有不同的预后和治疗意义。

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