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Abstract Introduction: Endothelial nitric oxide synthase (eNOS) genes have been implicated in renal hemodynamics as potent regulators of vascular tone and blood pressure. It has been linked to a reduction in plasma nitric oxide levels. Several studies have recently been conducted to investigate the role of NOS3 gene polymorphisms and end-stage renal disease (ESRD). However, the results are still unclear and the mechanisms are not fully defined. As a result, we conducted a meta-analysis to examine the relationship between NOS3 gene polymorphism and ESRD in autosomal polycystic kidney disease (ADPKD) patients. Methods: To assess the relationship between NOS3 gene polymorphism and ESRD, relevant studies published between September 2002 and December 2020 were retrieved from the PubMed (Medline), EMBASE, Google Scholar, and Web of Science databases. The pooled odds ratio (OR) and 95 % confidence interval (CI) were calculated using a fixed-effect model. To assess the heterogeneity of studies, we used Cochrane's Q test and the Higgins and Thompson I2 statistics. Results: Our meta-analysis of 13 studies showed that the presence of the two NOS3 gene polymorphisms significantly increased ESRD risk in ADPKD patients with 4a/b gene polymorphism (aa+ab vs. bb: OR=1.95, 95% CI=1.24-3.09, p=0.004). In addition, no significant association was found between the NOS3 894G>T (Glu298Asp) polymorphism and the risk of ESRD in ADPKD patients (GT+TT vs. GG: OR=1.21, 95% CI=0.93-1.58, p=0.157). There was no evidence of publication bias. Conclusions: The findings of the current meta-analysis suggest that NOS3 intron 4a/b polymorphism plays a vital role in the increasing risk of ESRD in ADPKD patients.
Resumo Introdução: Genes da óxido nítrico sintase endotelial (eNOS) têm sido implicados na hemodinâmica renal como potentes reguladores do tônus vascular e pressão arterial. Tem sido vinculado a uma redução nos níveis plasmáticos de óxido nítrico. Realizou-se recentemente vários estudos para investigar o papel de polimorfismos do gene NOS3 e doença renal em estágio terminal (DRET). Entretanto, os resultados ainda não são claros e os mecanismos não estão totalmente definidos. Como resultado, realizamos meta-análise para examinar a relação entre polimorfismo do gene NOS3 e DRET em pacientes com doença renal policística autossômica dominante (DRPAD). Métodos: Para avaliar a relação entre polimorfismo do gene NOS3 e DRET, recuperou-se estudos relevantes publicados entre Setembro-2002 e Dezembro-2020 dos bancos de dados PubMed (Medline), EMBASE, Google Scholar, Web of Science. Calculamos odds ratio (OR) e intervalo de confiança (IC) de 95% utilizando modelo de efeitos fixos. Para avaliar a heterogeneidade dos estudos, utilizamos teste Q de Cochrane e estatísticas I2 de Higgins e Thompson. Resultados: Nossa meta-análise de 13 estudos mostrou que a presença dos dois polimorfismos do gene NOS3 aumentou significativamente o risco de DRET em pacientes com DRPAD com polimorfismo do gene 4a/b (aa+ab vs. bb: OR=1,95; IC 95%=1,24-3,09; p=0,004). Ademais, não encontramos associação significativa entre polimorfismo 894G>T NOS3 (Glu298Asp) e risco de DRET em pacientes com DRPAD (GT+TT vs. GG: OR=1,21; IC 95%=0,93-1,58; p=0,157). Não houve evidência de viés de publicação. Conclusões: Achados da meta-análise atual sugerem que o polimorfismo intron 4a/b do NOS3 desempenha papel vital no aumento do risco de DRET em pacientes com DRPAD.
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The coronavirus disease 2019 (COVID-19) pandemic has emerged as a major threat to all healthcare systems across the globe, and it was declared a public health emergency of international concern by the World Health Organization (WHO). The novel coronavirus affects the respiratory system, producing symptoms such as fever, cough, dyspnea, and pneumonia. The association between COVID-19 and coagulation has been previously reported. Due to several inflammatory changes that occur in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections such as alterations in the levels of clotting factors, platelet activation leads to thrombus formation in coronary and cerebral vessels, leading to myocardial infarction and cerebrovascular accidents, respectively.Unfortunately, the progression of hypercoagulability in COVID-19 is rapid in patients with and without comorbidities. Hence, the proper monitoring of thrombotic complications in patients with COVID-19 is essential to avoid further complications. The implementation of guidelines for antithrombotic treatments based on the presentation of the disease is recommended. This review discusses the symptoms and mechanisms of upregulated coagulation in patients with COVID-19.
Реферат
The coronavirus disease 2019 (COVID-19) pandemic has emerged as a major threat to all healthcare systems across the globe, and it was declared a public health emergency of international concern by the World Health Organization (WHO). The novel coronavirus affects the respiratory system, producing symptoms such as fever, cough, dyspnea, and pneumonia. The association between COVID-19 and coagulation has been previously reported. Due to several inflammatory changes that occur in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections such as alterations in the levels of clotting factors, platelet activation leads to thrombus formation in coronary and cerebral vessels, leading to myocardial infarction and cerebrovascular accidents, respectively.Unfortunately, the progression of hypercoagulability in COVID-19 is rapid in patients with and without comorbidities. Hence, the proper monitoring of thrombotic complications in patients with COVID-19 is essential to avoid further complications. The implementation of guidelines for antithrombotic treatments based on the presentation of the disease is recommended. This review discusses the symptoms and mechanisms of upregulated coagulation in patients with COVID-19.