Urinary transglutaminase 2 as a potent biomarker to predict interstitial fibrosis and tubular atrophy of kidney allograft during early posttransplant period in deceased donor kidney transplantation
Annals of Surgical Treatment and Research
; : 27-35, 2019.
Article
en En
| WPRIM
| ID: wpr-762680
Biblioteca responsable:
WPRO
ABSTRACT
PURPOSE: Transglutaminase type 2 (TG2) is an extracellular matrix crosslinking enzyme with a pivotal role in kidney fibrosis. We tested whether quantification of urinary TG2 may represent a noninvasive method to estimate the severity of kidney allograft fibrosis. METHODS: We prospectively collected urine specimens from 18 deceased donor kidney transplant recipients at 1-day, 7-day, 1-month, 3-month, and 6-month posttransplant. In addition, kidney allograft tissue specimens at 0-day and 6-month posttransplant were sampled to analyze the correlation of urinary TG2 and kidney allograft fibrosis. RESULTS: Thirteen recipients had increased interstitial fibrosis and tubular atrophy (IFTA) scores at the 6-month protocol biopsy (IFTA group). The mean level of urinary TG2 in the IFTA group was higher compared to that of 5 other recipients without IFTA (no IFTA group). Conversely, the mean level of urinary syndecan-4 in the IFTA group was lower than levels in patients without IFTA. In the IFTA group, double immunofluorescent staining revealed that TG2 intensity was significantly upregulated and colocalizations of TG2/heparin sulfate proteoglycan and nuclear syndecan-4 were prominent, usually around tubular structures. CONCLUSION: Urinary TG2 in early posttransplant periods is a potent biomarker for kidney allograft inflammation or fibrosis.
Palabras clave
Texto completo:
1
Base de datos:
WPRIM
Asunto principal:
Proteoglicanos
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Atrofia
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Donantes de Tejidos
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Biopsia
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Fibrosis
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Biomarcadores
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Estudios Prospectivos
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Trasplante de Riñón
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Matriz Extracelular
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Sindecano-4
Tipo de estudio:
Observational_studies
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Prognostic_studies
Límite:
Humans
Idioma:
En
Revista:
Annals of Surgical Treatment and Research
Año:
2019
Tipo del documento:
Article