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Immunephenotype of Glomerular and Interstitial Infiltrating Cells in Protocol Renal Allograft Biopsies and Histological Diagnosis
Author(s) -
Moreso F.,
Seron D.,
O'Valle F.,
Iber M.,
Gomà M.,
Hueso M.,
Cruzado J. M.,
Bestard O.,
Duarte V.,
García del Moral R.,
Grinyó J. M.
Publication year - 2007
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2007.02013.x
Subject(s) - medicine , biopsy , pathology , fibrosis , cd20 , subclinical infection , immunohistochemistry
Patients with a protocol renal allograft biopsy simultaneously displaying interstitial fibrosis/tubular atrophy (IF/TA) and subclinical rejection (SCR) have a shortened graft survival than patients with a normal biopsy, or with a biopsy only displaying IF/TA or SCR. The poor outcome of these patients could be related with a more severe inflammation. We evaluate the immunophenotype of infiltrating cells in these diagnostic categories. Nonexhausted paraffin blocks from protocol biopsies done during the first year were stained with anti‐CD45, CD3, CD20, CD68 and CD15 monoclonal antibodies. Glomerular and interstitial positive cells were counted. C4d deposition in peritubular capillaries was evaluated. Histological diagnoses were: normal (n = 80), SCR (n = 17), IF/TA (n = 42) and IF/TA + SCR (n = 17). Only interstitial CD20 positive cells were significantly increased in patients displaying IF/TA + SCR; normal (137 ± 117), SCR (202 ± 145), IF/TA (208 ± 151) and IF/TA + SCR (307 ± 180 cells/mm 2 ), p < 0.01. The proportion of biopsies displaying C4d deposition was not different among groups. The upper tertile of CD20 positive interstitial cells was associated with a decreased death‐censored graft survival (relative risk: 3.01, 95% confidence interval: 1.23–7.35; p = 0.015). These data suggest that B‐cell interstitial infiltrates are associated with histological damage and outcome, but do not distinguish whether these infiltrates were the cause or the consequence of chronic tubulo‐interstitial damage.