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Glomerular crescents are responsible for chronic graft dysfunction in post‐transplant IgA nephropathy
Author(s) -
Jeong Hyeon Joo,
Kim Yu Seun,
Kwon Ki Hwan,
Kim Soon Il,
Kim Myoung Soo,
Choi Kyu Hun,
Lee Ho Yung,
Han Dae Suk,
Park Kiil
Publication year - 2004
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.2004.01751.x
Subject(s) - medicine , nephropathy , creatinine , proteinuria , biopsy , renal biopsy , transplantation , pathology , gastroenterology , chronic allograft nephropathy , glomerulonephritis , kidney transplantation , urology , kidney , endocrinology , diabetes mellitus
Information is limited regarding the histological features related to chronic graft dysfunction and failure in patients with IgA nephropathy developing after renal transplantation. The prevalence and significance of glomerular crescents in post‐transplant IgAN including recurrent, de novo and transmitted forms (TxIgAN), were studied. Renal morphology was evaluated in 71 patients of TxIgAN, obtained at more than 6 months post‐transplant, and compared with regard to the presence (C‐TxIgAN) or absence (N‐TxIgAN) of glomerular crescents. Crescents were demonstrated in 12 samples of 10 patients (14.1%). The percentages of crescents were from 4.8% to 83.3% (median, 28.6%) in each sample. Ten samples of C‐TxIgAN had cellular to fibrocellular crescents, and four of these were associated with diffuse mesangial proliferation. Serum creatinine levels and the frequency of nephrotic range proteinuria at the time of biopsy and the degree of interstitial inflammation were significantly different in the two groups. Graft survival after allograft biopsies was significantly lower in C‐TxIgAN ( P = 0.0017). Chronic rejection was a major cause of graft loss in N‐TxIgAN (31.8%), whereas TxIgAN was the major cause in C‐TxIgAN (66.7%). In conclusion, the current study suggests that glomerular crescents are not rare and that they are responsible for chronic graft dysfunction in TxIgAN patients.