Significance of Multinucleated Polyploidization of Tubular Epithelial Cells in Kidney Allografts.


Journal

Nephron
ISSN: 2235-3186
Titre abrégé: Nephron
Pays: Switzerland
ID NLM: 0331777

Informations de publication

Date de publication:
2023
Historique:
received: 25 11 2022
accepted: 21 02 2023
medline: 15 11 2023
pubmed: 27 3 2023
entrez: 26 3 2023
Statut: ppublish

Résumé

Multinucleated polyploidization (MNP) of tubular epithelial cells is occasionally observed in kidney allografts. The present study aimed to clarify the clinical and pathological significance of MNP of tubular epithelial cells in kidney allografts. Fifty-eight 1-year biopsies from 58 patients who underwent kidney transplantation at our hospital from January 2016 to December 2017 were included. MNP was counted in each specimen, and the specimens were divided into two groups by the median value. The differences in clinical and pathological characteristics were compared. Ki67-positive cells were counted among tubular epithelial cells to explore the association between cell cycle and MNP. In an additional cohort, MNP was compared between biopsies after precedent T-cell-mediated rejection and precedent medullary ray injury. The 58 cases were divided into two groups by the median total amount of MNP: group A (MNP > 3) and group B (MNP ≤ 3). Maximum t-score before the 1-year biopsy was significantly higher in group A compared with group B. Other clinical or histological characteristics did not differ significantly. Total amount of Ki67-positive tubular epithelial cells was significantly correlated with total amount of MNP. Significantly higher amount of MNP was observed in cases with precedent T-cell-mediated rejection compared with precedent medullary ray injury. On receiver operating characteristic curve analysis, the cut-off value of MNP to predict precedent T-cell-mediated rejection was 8.5. MNP in tubular epithelial cells reflects prior tubular inflammation in kidney allografts. High amount of MNP indicates precedent T-cell-mediated rejection rather than precedent medullary ray injury caused by nonimmune etiologies.

Identifiants

pubmed: 36966529
pii: 000530339
doi: 10.1159/000530339
pmc: PMC10652653
doi:

Substances chimiques

Ki-67 Antigen 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

28-34

Informations de copyright

© 2023 The Author(s). Published by S. Karger AG, Basel.

Références

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Auteurs

Noriyuki Kounoue (N)

Department of Nephrology, Toho University Faculty of Medicine, Tokyo, Japan.
Department of Nephrology, Toho University Graduate School of Medicine, Tokyo, Japan.

Hideyo Oguchi (H)

Department of Nephrology, Toho University Faculty of Medicine, Tokyo, Japan.

Naobumi Tochigi (N)

Department of Surgical Pathology, Toho University Faculty of Medicine, Tokyo, Japan.

Tetuo Mikami (T)

Department of Pathology, Toho University Faculty of Medicine, Tokyo, Japan.

Yutaka Yamaguchi (Y)

Yamaguchi's Pathology Laboratory, Chiba, Japan.

Kazuho Honda (K)

Department of Anatomy, Showa University School of Medicine, Tokyo, Japan.

Takashi Yonekura (T)

Department of Nephrology, Toho University Faculty of Medicine, Tokyo, Japan.

Masaki Muramatsu (M)

Department of Nephrology, Toho University Faculty of Medicine, Tokyo, Japan.

Yoshihiro Itabashi (Y)

Department of Nephrology, Toho University Faculty of Medicine, Tokyo, Japan.

Ken Sakai (K)

Department of Nephrology, Toho University Faculty of Medicine, Tokyo, Japan.

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Classifications MeSH