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Urinary protein markers predict the severity of renal histological lesions in children with mesangial proliferative glomerulonephritis

BACKGROUND: Several renal histopathological features, including mesangial hypercellularity, glomerulosclerosis, tubular atrophy and interstitial fibrosis, are considered to be independent predictors of end-stage renal failure in patients with glomerular diseases. Mesangial proliferative glomerulonep...

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Autores principales: Li, Yanhong, Wang, Jian, Zhu, Xueming, Feng, Qihua, Li, Xiaozhong, Feng, Xing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403987/
https://www.ncbi.nlm.nih.gov/pubmed/22607047
http://dx.doi.org/10.1186/1471-2369-13-29
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author Li, Yanhong
Wang, Jian
Zhu, Xueming
Feng, Qihua
Li, Xiaozhong
Feng, Xing
author_facet Li, Yanhong
Wang, Jian
Zhu, Xueming
Feng, Qihua
Li, Xiaozhong
Feng, Xing
author_sort Li, Yanhong
collection PubMed
description BACKGROUND: Several renal histopathological features, including mesangial hypercellularity, glomerulosclerosis, tubular atrophy and interstitial fibrosis, are considered to be independent predictors of end-stage renal failure in patients with glomerular diseases. Mesangial proliferative glomerulonephritis (MesPGN) is characterized by proliferations of mesangial cells with increase in mesangial matrix and/or deposits in mesangial region. The purpose of this study is to determine the association between urinary protein markers measured at the same time as renal biopsy and the severity of renal histological lesions in children with MesPGN, and to evaluate whether these markers could serve as predictors of severe renal histological lesions in this population. METHODS: Ninety-eight children with MesPGN (40 with IgA nephropathy, 37 with IgM nephropathy, and 21 with MesPGN without IgA/IgM deposition) were enrolled. Urinary level of IgG, albumin, transferrin, α1-microglobulin, β2-microglobulin and N-acetyl-β-glucosaminidase from a morning sample before biopsy was measured. The scores of mesangial hypercellularity, glomerulosclerosis, and tubule-interstitial damage were used to semi-quantitatively evaluate renal histological lesions. RESULTS: The urine proteins, as independent factors associated with severe mesangial cellularity (> 5 mesangial cells/ mesangial area) were transferrin, albumin, α1-microglobulin, IgG and 24-hour total protein, with severe glomerulosclerosis (≥ 10 % glomeruli showing segmental adhesions or sclerosis) were transferrin and 24-hour total protein, and with severe tubule-interstitial damage (focal or diffuse tubular and interstitial lesions) were transferrin and N-acetyl-β-glucosaminidase. Urinary transferrin achieved the area under-the-receiver-operating-characteristic curve (AUC) of 0.86 and 0.82, respectively, for predicting severe mesangial cellularity and glomerulosclerosis. Urinary N-acetyl-β-glucosaminidase achieved the highest AUC of 0.82 for predicting severe tubule-interstitial damage. The combination of urinary protein markers, however, did not improve the predictability for renal histological lesions. CONCLUSIONS: Urinary protein markers are useful to predict the severity of renal histological lesions in children with MesPGN, which suggests that urinary proteins might be useful to predict the development and progression of renal histological lesions, and assist in evaluating the outcome and prognosis in children with MesPGN as non-invasive and easily repeatable indicators on the follow-up examination.
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spelling pubmed-34039872012-07-25 Urinary protein markers predict the severity of renal histological lesions in children with mesangial proliferative glomerulonephritis Li, Yanhong Wang, Jian Zhu, Xueming Feng, Qihua Li, Xiaozhong Feng, Xing BMC Nephrol Research Article BACKGROUND: Several renal histopathological features, including mesangial hypercellularity, glomerulosclerosis, tubular atrophy and interstitial fibrosis, are considered to be independent predictors of end-stage renal failure in patients with glomerular diseases. Mesangial proliferative glomerulonephritis (MesPGN) is characterized by proliferations of mesangial cells with increase in mesangial matrix and/or deposits in mesangial region. The purpose of this study is to determine the association between urinary protein markers measured at the same time as renal biopsy and the severity of renal histological lesions in children with MesPGN, and to evaluate whether these markers could serve as predictors of severe renal histological lesions in this population. METHODS: Ninety-eight children with MesPGN (40 with IgA nephropathy, 37 with IgM nephropathy, and 21 with MesPGN without IgA/IgM deposition) were enrolled. Urinary level of IgG, albumin, transferrin, α1-microglobulin, β2-microglobulin and N-acetyl-β-glucosaminidase from a morning sample before biopsy was measured. The scores of mesangial hypercellularity, glomerulosclerosis, and tubule-interstitial damage were used to semi-quantitatively evaluate renal histological lesions. RESULTS: The urine proteins, as independent factors associated with severe mesangial cellularity (> 5 mesangial cells/ mesangial area) were transferrin, albumin, α1-microglobulin, IgG and 24-hour total protein, with severe glomerulosclerosis (≥ 10 % glomeruli showing segmental adhesions or sclerosis) were transferrin and 24-hour total protein, and with severe tubule-interstitial damage (focal or diffuse tubular and interstitial lesions) were transferrin and N-acetyl-β-glucosaminidase. Urinary transferrin achieved the area under-the-receiver-operating-characteristic curve (AUC) of 0.86 and 0.82, respectively, for predicting severe mesangial cellularity and glomerulosclerosis. Urinary N-acetyl-β-glucosaminidase achieved the highest AUC of 0.82 for predicting severe tubule-interstitial damage. The combination of urinary protein markers, however, did not improve the predictability for renal histological lesions. CONCLUSIONS: Urinary protein markers are useful to predict the severity of renal histological lesions in children with MesPGN, which suggests that urinary proteins might be useful to predict the development and progression of renal histological lesions, and assist in evaluating the outcome and prognosis in children with MesPGN as non-invasive and easily repeatable indicators on the follow-up examination. BioMed Central 2012-05-20 /pmc/articles/PMC3403987/ /pubmed/22607047 http://dx.doi.org/10.1186/1471-2369-13-29 Text en Copyright ©2012 Li et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Li, Yanhong
Wang, Jian
Zhu, Xueming
Feng, Qihua
Li, Xiaozhong
Feng, Xing
Urinary protein markers predict the severity of renal histological lesions in children with mesangial proliferative glomerulonephritis
title Urinary protein markers predict the severity of renal histological lesions in children with mesangial proliferative glomerulonephritis
title_full Urinary protein markers predict the severity of renal histological lesions in children with mesangial proliferative glomerulonephritis
title_fullStr Urinary protein markers predict the severity of renal histological lesions in children with mesangial proliferative glomerulonephritis
title_full_unstemmed Urinary protein markers predict the severity of renal histological lesions in children with mesangial proliferative glomerulonephritis
title_short Urinary protein markers predict the severity of renal histological lesions in children with mesangial proliferative glomerulonephritis
title_sort urinary protein markers predict the severity of renal histological lesions in children with mesangial proliferative glomerulonephritis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403987/
https://www.ncbi.nlm.nih.gov/pubmed/22607047
http://dx.doi.org/10.1186/1471-2369-13-29
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