Volume 6 Issue 4
Jul.  2015
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Wang Guangce, Wang Suogang, Chen Zhu, et al. Study on clinicopathologic characteristics and individualized immunotherapy of antibody-mediated rejection after renal transplantation[J]. ORGAN TRANSPLANTATION, 2015, 6(4): 224-229. doi: 10.3969/j.issn.1674-7445.2015.04.004
Citation: Wang Guangce, Wang Suogang, Chen Zhu, et al. Study on clinicopathologic characteristics and individualized immunotherapy of antibody-mediated rejection after renal transplantation[J]. ORGAN TRANSPLANTATION, 2015, 6(4): 224-229. doi: 10.3969/j.issn.1674-7445.2015.04.004

Study on clinicopathologic characteristics and individualized immunotherapy of antibody-mediated rejection after renal transplantation

doi: 10.3969/j.issn.1674-7445.2015.04.004
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  • Corresponding author: Wang Guangce.Email:wgc460@medmail.com.cn
  • Received Date: 2015-04-18
    Available Online: 2021-01-19
  • Publish Date: 2015-07-15
  •   Objective  To investigate clinicopathologic characteristics, individualized immunotherapy and prognosis of antibody-mediated rejection (AMR) after renal transplantation.  Methods  Clinical data of 32 patients, who were confirmed as AMR after renal transplantation by pathology and admitted in the Department of Urology and Renal Transplantation of the First Affiliated Hospital of Henan Traditional Medical College from January 2010 to December 2013, were retrospectively studied. The corresponding immunological intervention was adopted according to the clinicopathologic characteristics of different patients. The indicators including renal function, panel reactive antibody (PRA) and serum immunoglobulin (Ig) G, IgA and IgM level before and after treatment were determined, and adverse reactions were observed.  Results  Of all 32 patients, 18 developed acute antibody-mediated rejection (AAMR) and 14 developed chronic antibody-mediated rejection (CAMR). Of 13 PRA-positive patients, 8 (62%, 8/13) cases were with donor specific antibody and 5 (38%, 5/13) cases were with non-donor specific antibody. The primary pathological manifestations of early AAMR were changes of acute tubular necrosis (ATN), peritubular capillary inflammation, glomerulitis, fibrinoid necrosis of small arteries, linear C4d deposition in peritubular capillaries (PTC) and immunoglobulin or C3 deposition in arterial wall. The pathological manifestations of CAMR were changes of glomerulopathy, splitting of PTC basement membrane, fibrous intimal thickening and diffuse C4d deposition in PTC. After treatment, the renal function of 20 (63%, 20/32) patients returned to normal, the renal function of 7 (22%, 7/32) patients were stable, the serum creatinine (Scr) of 5 (16%, 5/32) patients increased slowly. Of such 5 patients, 2 (2/5) patients continued hemodialysis, 3 (3/5) patients did not need hemodialysis and no patient died. The indicators including blood urea nitrogen (BUN), Scr, PRA and serum IgG, IgA and IgM after treatment decreased significantly when compared with those before treatment (all in P < 0.01). No serious adverse reaction was noted during the treatment.  Conclusions  AMR may manifest as AAMR or CAMR after renal transplantation. The gold standard for diagnosing AMR is pathologic biopsy of transplant kidney. To adopt effective individualized immunotherapy in time is the critical measure for treatment of AMR.

     

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