Association of angiotensinogen gene polymorphisms (M235T and T174M) with preeclampsia among Pakistani women

Background Preeclampsia (PE) is a progressive, gestational condition marked by physiological and metabolic manifestations. Significant research on the underlying genetic factors is underway; however, the role of renin-angiotensin system (RAS)-associated angiotensinogen protein (AGT), which is a major checkpoint for hypertensive disorders, has produced heterogeneous outcomes with varying geographical and ethnic data especially within Pakistani population. Thus necessitating the need to explore the understudy group. Methods and results The study focused on the contribution of two prominent single nucleotide polymorphisms (SNPs) of AGT gene (M235T and T174M ) with the incidence and/or risk of PE among the Pakistani population. A total of 150 participants were divided into two groups: 100 cases and 50 controls. Allele-specific polymerase chain reaction (AS-PCR) was performed. The results statistically suggested a significant correlation between the polymorphism and elevated disease risk with the C allele in case of M235T and T allele with T174M indicating the influence of genetic variation on disease pathophysiology. Furthermore, an increased likelihood was observed for the M235T variant (CT vs. TT = OR: 3.3, CI 1.3–8.8) (CC vs. TT = OR: 16.3, CI 3.0–88.9); conversely, for the second variant, T174M was also observed to be associated with the disease, thus favoring the outcome (CT vs. CC = OR: 4.6, CI 1.5–14.2) and adjusted odds ratio (CT vs. CC = AOR: 8.2, CI 2.5–27.2). Conclusion The study highlights a prospective chance of disease occurrence among subjects with C allele in case of M235T as opposed to the T allele in T124M variant; though the preliminary findings seem promising, the limited sample size restricts their generalizability. Further validation of the results with larger cohort and diverse populations is essential in strengthening the statistical power and enable more definitive conclusions regarding the polymorphism's role in disease development.