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Urine synaptopodin excretion is an important marker of glomerular disease progression

BACKGROUND/AIMS: Podocytes play an important role in maintaining the glomerular filtration barrier and in formation of the slit diaphragm. Podocyte loss is associated with chronic kidney disease progression, but it is not clear whether urinary podocyte proteins in urine reflect the clinical extent o...

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Autores principales: Kwon, Soon Kil, Kim, Seung Jung, Kim, Hye-Young
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Association of Internal Medicine 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5016285/
https://www.ncbi.nlm.nih.gov/pubmed/27604800
http://dx.doi.org/10.3904/kjim.2015.226
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author Kwon, Soon Kil
Kim, Seung Jung
Kim, Hye-Young
author_facet Kwon, Soon Kil
Kim, Seung Jung
Kim, Hye-Young
author_sort Kwon, Soon Kil
collection PubMed
description BACKGROUND/AIMS: Podocytes play an important role in maintaining the glomerular filtration barrier and in formation of the slit diaphragm. Podocyte loss is associated with chronic kidney disease progression, but it is not clear whether urinary podocyte proteins in urine reflect the clinical extent of glomerular damage. We investigated the correlation between the amounts of urinary podocyte proteins and renal function and albuminuria. METHODS: The study enrolled 33 patients with diabetic kidney disease or glomerular disease and measured urinary podocytes proteins using Western blotting. Urinary podocyte proteins were measured according to the density of the bands on Western blotting. We measured serum creatinine and the spot urine albumin/creatinine ratio as markers of renal damage, and compared the correlation of urinary podocyte protein in the glomerular disease patients. RESULTS: The mean patient age was 49.3 ± 16.5 years, the mean serum creatinine level was 2.30 ± 1.76 mg/dL, and the mean albumin/creatinine ratio was 4.85 ± 3.52. Among the podocyte proteins, urine synaptopodin showed strong correlation with serum creatinine by multivariate regression analysis (p < 0.001) and showed linear correlation (r = 0.429, p < 0.01). Urine podocyte proteins were increased in patients with diabetes, and synaptopodin showed the greatest significant difference (7.68 ± 5.61 vs. 2.56 ± 3.11, p < 0.001), but this might be associated with renal impairment. The urine albumin excretion did not differ between the diabetics and non-diabetics (p = 0.73). CONCLUSIONS: Urine synaptopodin is associated with serum creatinine elevation in the patients with glomerulonephritis including diabetic kidney disease regardless of urine albumin excretion. We suggest that the urine synaptopodin level can predict glomerular damage independently of the urine albumin excretion.
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spelling pubmed-50162852016-09-09 Urine synaptopodin excretion is an important marker of glomerular disease progression Kwon, Soon Kil Kim, Seung Jung Kim, Hye-Young Korean J Intern Med Original Article BACKGROUND/AIMS: Podocytes play an important role in maintaining the glomerular filtration barrier and in formation of the slit diaphragm. Podocyte loss is associated with chronic kidney disease progression, but it is not clear whether urinary podocyte proteins in urine reflect the clinical extent of glomerular damage. We investigated the correlation between the amounts of urinary podocyte proteins and renal function and albuminuria. METHODS: The study enrolled 33 patients with diabetic kidney disease or glomerular disease and measured urinary podocytes proteins using Western blotting. Urinary podocyte proteins were measured according to the density of the bands on Western blotting. We measured serum creatinine and the spot urine albumin/creatinine ratio as markers of renal damage, and compared the correlation of urinary podocyte protein in the glomerular disease patients. RESULTS: The mean patient age was 49.3 ± 16.5 years, the mean serum creatinine level was 2.30 ± 1.76 mg/dL, and the mean albumin/creatinine ratio was 4.85 ± 3.52. Among the podocyte proteins, urine synaptopodin showed strong correlation with serum creatinine by multivariate regression analysis (p < 0.001) and showed linear correlation (r = 0.429, p < 0.01). Urine podocyte proteins were increased in patients with diabetes, and synaptopodin showed the greatest significant difference (7.68 ± 5.61 vs. 2.56 ± 3.11, p < 0.001), but this might be associated with renal impairment. The urine albumin excretion did not differ between the diabetics and non-diabetics (p = 0.73). CONCLUSIONS: Urine synaptopodin is associated with serum creatinine elevation in the patients with glomerulonephritis including diabetic kidney disease regardless of urine albumin excretion. We suggest that the urine synaptopodin level can predict glomerular damage independently of the urine albumin excretion. The Korean Association of Internal Medicine 2016-09 2016-09-01 /pmc/articles/PMC5016285/ /pubmed/27604800 http://dx.doi.org/10.3904/kjim.2015.226 Text en Copyright © 2016 The Korean Association of Internal Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Kwon, Soon Kil
Kim, Seung Jung
Kim, Hye-Young
Urine synaptopodin excretion is an important marker of glomerular disease progression
title Urine synaptopodin excretion is an important marker of glomerular disease progression
title_full Urine synaptopodin excretion is an important marker of glomerular disease progression
title_fullStr Urine synaptopodin excretion is an important marker of glomerular disease progression
title_full_unstemmed Urine synaptopodin excretion is an important marker of glomerular disease progression
title_short Urine synaptopodin excretion is an important marker of glomerular disease progression
title_sort urine synaptopodin excretion is an important marker of glomerular disease progression
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5016285/
https://www.ncbi.nlm.nih.gov/pubmed/27604800
http://dx.doi.org/10.3904/kjim.2015.226
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