Angiotensina II e angiotensina-(1-7) urinárias na hipertensão gestacional e nos subtipos de pré-eclâmpsia: correlações clínicas e bioquímicas

Abstract

Background: Preeclampsia (PE) and gestational hypertension (GH) are one of the major causes of maternal and perinatal morbidity and mortality. The renin-angiotensin system (RAS) is implicated in their pathophysiology, but data on urinary angiotensin II (Ang II) and angiotensin-(1–7) [Ang-(1–7)] levels in these conditions are scarce. This study aimed to evaluate and compare urinary Ang II and Ang-(1–7) concentrations in women with PE and GH versus normotensive pregnant controls and explore their associations with clinical and biochemical parameters. Methods: A cross-sectional study was conducted involving 53 women with PE (subdivided into severe and non-severe, and early- and late-onset), 33 with GH and 53 normotensive pregnant controls. Urinary Ang II and Ang-(1–7) levels were measured using ELISA kits. Statistics included group comparisons by non-parametric tests and correlation analyses using Spearman or Pearson coefficients, with a significance level of p < 0.05. Results: No statistically significant differences between the three studies groups were found in urinary levels of Ang II, Ang-(1–7) and in the ratio Ang II/ Ang-(1-7). However, women with severe PE had significantly higher urinary Ang II levels and Ang II/Ang-(1–7) ratio compared to those with non-severe PE. In early-onset PE, urinary Ang-(1–7) levels correlated positively with creatinine and LDH, and the Ang II/Ang-(1–7) ratio correlated strongly and positively with platelet count. In late-onset PE, urinary Ang II and the Ang II/Ang-(1–7) ratio correlated positively with AST and ALT, while Ang-(1–7) correlated inversely with AST. Conclusion: While urinary angiotensin levels did not differ between hypertensive and normal gestations, increased Ang II levels and Ang II/Ang-(1–7) ratio were observed in severe PE. Distinct correlation patterns between urinary angiotensin peptides and clinical/laboratory parameters were identified in early- and late-onset PE, suggesting different pathophysiological mechanisms.