NOS3 Polymorphisms and Chronic Kidney Disease

Author:

Medina Alejandro Marín1,Zubero Eduardo Esteban2,Jiménez Moisés Alejandro Alatorre3,Barragan Sara Anabel Alonso3,García Carlos Arturo López4,Ramos José Juan Gómez5,Gutierrez Juan Francisco Santoscoy5,Castillo Zurisadai González6

Affiliation:

1. Universidad de Guadalajara, Mexico

2. Universidad de Zaragoza, Spain

3. Asociación Mexicana de Atrofia Muscular Espinal, México; Universidad de Guadalajara, Mexico; Centro de Investigación Biomédica de Occidente, México

4. University of Texas, USA

5. Instituto Mexicano del Seguro Social, Mexico

6. Asociación Mexicana de Atrofa Muscular Espinal, México

Abstract

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.

Publisher

FapUNIFESP (SciELO)

Subject

General Medicine

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