Boyce N, Holdsworth S, Atkins R, Dowling J
Clin Nephrol. 1985 Mar;23(3):148-51.
We report a case of de-novo anti-glomerular basement membrane antibody induced glomerulonephritis (anti-GBM GN) in a renal cadaveric transplant. The 52 year old male patient had developed end-stage renal failure secondary to malignant hypertension. His initial renal transplant lost function within two months because of severe allograft rejection without evidence of anti-glomerular basement membrane (anti-GBM) antibody formation. Eight months after his second cadaveric transplant he developed the nephrotic syndrome. This was followed by a rapid deterioration in graft function associated with the development of diffuse proliferative glomerulonephritis with 100% crescent formation. Linear staining of the GBM with IgG and C3 and the presence of circulating anti-GBM antibodies confirmed the anti-GBM antibody etiology of the glomerular lesion. Thus anti-GBM antibody induced glomerulonephritis can occur de-novo in a transplanted kidney despite routine immunosuppression. This represents either coincidental autoantibody production after transplantation or specific alloantibody production, stimulated by the introduction, by transplantation, of GBM neoantigens.
我们报告了一例在肾尸体移植中发生的新发抗肾小球基底膜抗体诱导的肾小球肾炎(抗GBM GN)病例。该52岁男性患者因恶性高血压继发终末期肾衰竭。他的首次肾移植由于严重的同种异体移植排斥反应在两个月内失去功能,且无抗肾小球基底膜(抗GBM)抗体形成的证据。在他进行第二次尸体移植八个月后,他出现了肾病综合征。随后移植肾功能迅速恶化,伴有弥漫性增生性肾小球肾炎伴100%新月体形成。GBM上IgG和C3的线性染色以及循环抗GBM抗体的存在证实了肾小球病变的抗GBM抗体病因。因此,尽管进行了常规免疫抑制,抗GBM抗体诱导的肾小球肾炎仍可在移植肾中新发。这代表移植后巧合的自身抗体产生或由移植引入GBM新抗原刺激产生的特异性同种抗体。