Urinary angiotensin II and angiotensin-(1–7) in gestational hypertension and preeclampsia subtypes: clinical and biochemical correlations

OBJECTIVE: To evaluate and compare urinary concentrations of Ang II and Ang-(1-7) among women with PE, GH, and normotensive pregnant controls, and to explore associations between these peptides and clinical/laboratory parameters in subtypes of PE. METHODS: This was a cross-sectional study involving 53 women with PE (classified as severe or non-severe and early- or late-onset), 33 with GH and 53 normotensive pregnant controls. Urinary levels of Ang II and Ang-(1-7) were measured using ELISA kits. Group comparisons were performed using non-parametric statistical tests. Correlation analyses were conducted using Spearman or Pearson coefficients, with significance set at p < 0.05. RESULTS: There were no statistically significant differences in urinary Ang II, Ang-(1-7) or their ratio when comparing PE, GH and controls. However, women with severe PE exhibited significantly higher urinary Ang II levels and Ang II/Ang-(1-7) ratios than those with non-severe PE. In early-onset PE, urinary Ang-(1-7) was positively correlated with creatinine (r = 0.62, p = 0.04) and lactate dehydrogenase levels (r = 0.67, p = 0.02) and the Ang II/Ang-(1-7) ratio correlated strongly with platelet count (r = 0.80, p < 0.001). In late-onset PE, urinary Ang II and its ratio with Ang-(1-7) correlated positively with aspartate aminotransferase (AST) and alanine transaminase, while Ang-(1-7) showed an inverse correlation with AST. CONCLUSION: Although overall urinary angiotensin levels did not differ, severe PE presented elevated Ang II and Ang II/Ang-(1-7) ratio, suggesting a local shift towards the classical Ang II-mediated pathway in the most severe disease. Furthermore, distinct correlation patterns, such as angiotensins linked to renal and hematologic markers in early-onset PE and to hepatic enzymes in late-onset PE, support different underlying pathophysiological profiles between these subtypes.