NOS3 Polymorphisms and Chronic Kidney Disease
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Publication Date: | 2018 |
Other Authors: | , , , , , , |
Format: | Article |
Language: | eng |
Source: | Jornal Brasileiro de Nefrologia |
Download full: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002018000300273 |
Summary: | ABSTRACT Chronic kidney disease (CKD) is a multifactorial pathophysiologic irreversible process that often leads to a terminal state in which the patient requires renal replacement therapy. Most cases of CKD are due to chronic-degenerative diseases and endothelial dysfunction is one of the factors that contribute to its pathophysiology. One of the most important mechanisms for proper functioning of the endothelium is the regulation of the synthesis of nitric oxide. This compound is synthesized by the enzyme nitric oxide synthase, which has 3 isoforms. Polymorphisms in the NOS3 gene have been implicated as factors that alter the homeostasis of this mechanism. The Glu298Asp polymorphisms 4 b/a and -786T>C of the NOS3 gene have been associated with a more rapid deterioration of kidney function in patients with CKD. These polymorphisms have been evaluated in patients with CKD of determined and undetermined etiology and related to a more rapid deterioration of kidney function. |
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NOS3 Polymorphisms and Chronic Kidney DiseaseRenal Insufficiency, ChronicNitric Oxide SynthasePolymorphism, GeneticABSTRACT Chronic kidney disease (CKD) is a multifactorial pathophysiologic irreversible process that often leads to a terminal state in which the patient requires renal replacement therapy. Most cases of CKD are due to chronic-degenerative diseases and endothelial dysfunction is one of the factors that contribute to its pathophysiology. One of the most important mechanisms for proper functioning of the endothelium is the regulation of the synthesis of nitric oxide. This compound is synthesized by the enzyme nitric oxide synthase, which has 3 isoforms. Polymorphisms in the NOS3 gene have been implicated as factors that alter the homeostasis of this mechanism. The Glu298Asp polymorphisms 4 b/a and -786T>C of the NOS3 gene have been associated with a more rapid deterioration of kidney function in patients with CKD. These polymorphisms have been evaluated in patients with CKD of determined and undetermined etiology and related to a more rapid deterioration of kidney function.Sociedade Brasileira de Nefrologia2018-09-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002018000300273Brazilian Journal of Nephrology v.40 n.3 2018reponame:Jornal Brasileiro de Nefrologiainstname:Sociedade Brasileira de Nefrologia (SBN)instacron:SBN10.1590/2175-8239-jbn-3824info:eu-repo/semantics/openAccessMedina,Alejandro MarínZubero,Eduardo EstebanJiménez,Moisés Alejandro AlatorreBarragan,Sara Anabel AlonsoGarcía,Carlos Arturo LópezRamos,José Juan GómezGutierrez,Juan Francisco SantoscoyCastillo,Zurisadai Gonzálezeng2018-11-12T00:00:00Zoai:scielo:S0101-28002018000300273Revistahttp://www.bjn.org.br/ONGhttps://old.scielo.br/oai/scielo-oai.php||jbn@sbn.org.br2175-82390101-2800opendoar:2018-11-12T00:00Jornal Brasileiro de Nefrologia - Sociedade Brasileira de Nefrologia (SBN)false |
dc.title.none.fl_str_mv |
NOS3 Polymorphisms and Chronic Kidney Disease |
title |
NOS3 Polymorphisms and Chronic Kidney Disease |
spellingShingle |
NOS3 Polymorphisms and Chronic Kidney Disease Medina,Alejandro Marín Renal Insufficiency, Chronic Nitric Oxide Synthase Polymorphism, Genetic |
title_short |
NOS3 Polymorphisms and Chronic Kidney Disease |
title_full |
NOS3 Polymorphisms and Chronic Kidney Disease |
title_fullStr |
NOS3 Polymorphisms and Chronic Kidney Disease |
title_full_unstemmed |
NOS3 Polymorphisms and Chronic Kidney Disease |
title_sort |
NOS3 Polymorphisms and Chronic Kidney Disease |
author |
Medina,Alejandro Marín |
author_facet |
Medina,Alejandro Marín Zubero,Eduardo Esteban Jiménez,Moisés Alejandro Alatorre Barragan,Sara Anabel Alonso García,Carlos Arturo López Ramos,José Juan Gómez Gutierrez,Juan Francisco Santoscoy Castillo,Zurisadai González |
author_role |
author |
author2 |
Zubero,Eduardo Esteban Jiménez,Moisés Alejandro Alatorre Barragan,Sara Anabel Alonso García,Carlos Arturo López Ramos,José Juan Gómez Gutierrez,Juan Francisco Santoscoy Castillo,Zurisadai González |
author2_role |
author author author author author author author |
dc.contributor.author.fl_str_mv |
Medina,Alejandro Marín Zubero,Eduardo Esteban Jiménez,Moisés Alejandro Alatorre Barragan,Sara Anabel Alonso García,Carlos Arturo López Ramos,José Juan Gómez Gutierrez,Juan Francisco Santoscoy Castillo,Zurisadai González |
dc.subject.por.fl_str_mv |
Renal Insufficiency, Chronic Nitric Oxide Synthase Polymorphism, Genetic |
topic |
Renal Insufficiency, Chronic Nitric Oxide Synthase Polymorphism, Genetic |
description |
ABSTRACT Chronic kidney disease (CKD) is a multifactorial pathophysiologic irreversible process that often leads to a terminal state in which the patient requires renal replacement therapy. Most cases of CKD are due to chronic-degenerative diseases and endothelial dysfunction is one of the factors that contribute to its pathophysiology. One of the most important mechanisms for proper functioning of the endothelium is the regulation of the synthesis of nitric oxide. This compound is synthesized by the enzyme nitric oxide synthase, which has 3 isoforms. Polymorphisms in the NOS3 gene have been implicated as factors that alter the homeostasis of this mechanism. The Glu298Asp polymorphisms 4 b/a and -786T>C of the NOS3 gene have been associated with a more rapid deterioration of kidney function in patients with CKD. These polymorphisms have been evaluated in patients with CKD of determined and undetermined etiology and related to a more rapid deterioration of kidney function. |
publishDate |
2018 |
dc.date.none.fl_str_mv |
2018-09-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002018000300273 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002018000300273 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/2175-8239-jbn-3824 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Nefrologia |
publisher.none.fl_str_mv |
Sociedade Brasileira de Nefrologia |
dc.source.none.fl_str_mv |
Brazilian Journal of Nephrology v.40 n.3 2018 reponame:Jornal Brasileiro de Nefrologia instname:Sociedade Brasileira de Nefrologia (SBN) instacron:SBN |
instname_str |
Sociedade Brasileira de Nefrologia (SBN) |
instacron_str |
SBN |
institution |
SBN |
reponame_str |
Jornal Brasileiro de Nefrologia |
collection |
Jornal Brasileiro de Nefrologia |
repository.name.fl_str_mv |
Jornal Brasileiro de Nefrologia - Sociedade Brasileira de Nefrologia (SBN) |
repository.mail.fl_str_mv |
||jbn@sbn.org.br |
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1752122065023926272 |