Tese
Avaliação de potenciais biomarcadores na síndrome nefrótica primária em pacientes pediátricos.
Fecha
2021-08-13Autor
Roberta da Silva Filha
Institución
Resumen
Introduction: Primary nephrotic syndrome (PNS) is a common glomerular disease in the pediatric age group, related to intrinsic changes in the glomeruli without an established cause, which leads to proteinuria, edema, hypoalbuminemia and dyslipidemia. Numerous factors have been related to the mechanisms of development and evolution of the disease, including changes in the components of the glomerular filtration barrier, alterations in the immune system and the effects of the renin angiotensin system (RAS). However, the pathophysiology of the disease remains to be elucidated and several questions regarding the most appropriate treatment persist. Objectives: To evaluate the role of RAS, inflammatory molecules, adipokines, metabolism hormones and endothelial function markers in pediatric patients with primary NS. Methods: This cross-sectional study included 33 children and adolescents with SNP in partial and complete remission. Biomarker measurements were compared between patients and healthy individuals (control group), matched for age and sex. Biomarkers were related to clinical and laboratory variables. Results: In our first original study, we found that urinary concentrations of Ang II, Ang-(1-7), ACE and MCP-1 were increased in patients with PNS compared to the control group. On the other hand, urinary ACE2 levels were significantly lower in patients with PNS and negatively correlated with proteinuria. In the second study, urinary leptin levels and plasma concentrations of resistin and ghrelin were significantly increased compared to the control group. In contrast, urinary adiponectin and PAI-1 concentrations were lower in PNS patients when compared to controls. Conclusion: RAS molecules, chemokines, adipokines, metabolism hormones and endothelial function markers were found in different concentrations in patients with PNS compared to the control group, suggesting that these molecules participate in the pathophysiology and progression of renal damage.