The gut microbiota plays a fundamental role in the host’s energy metabolism and the development of metabolic diseases such as arterial hypertension, insulin resistance, and atherosclerosis. Our study aimed to investigate the potential role of the gut microbiota in arterial hypertension among individuals of the Kazakh population without insulin resistance. 16S rRNA gene sequencing of faecal samples from 197 Kazakh subjects was performed. Preliminary binary comparisons of the faecal microbiota composition depending on the presence of arterial hypertension and insulin resistance revealed statistically significant differences in the abundance of the phylum Firmicutes. Logistic regression analysis showed that only the phylum Firmicutes influenced hypertension risk in individuals without insulin resistance after adjusting for age, sex, BMI, fasting glucose, triglycerides, and triglyceride–glucose index. The higher the abundance of the phylum Firmicutes in faeces, the greater the risk of arterial hypertension (OR = 1.064 [95% CI 1.005–1.125]). Correlation analysis revealed a negative association between the abundance of the phylum Firmicutes and the triglyceride–glucose index, primarily driven by triglyceride levels. These findings suggest the potential role of the gut microbiota, especially the phylum Firmicutes, in the development of hypertension in individuals without insulin resistance.

Introduction: Idiopathic pulmonary arterial hypertension (IPAH) is a progressive and fatal disease. The aim of this study was to evaluate the association of polymorphism of the type 2 bone morphogenetic protein receptor gene (BMPR2) with the risk of IPAH development in an ethnic group of Kazakhs. We also describe the clinical and hemodynamic characteristics and outcomes of patients with and without carriers of BMPR2 gene mutations in IPAH. No available research highlights this problem in an ethnic group of Kazakhs. Materials and methods: A total of 53 patients of only Kazakh nationality with IPAH participated in the study. Clinical, functional, and hemodynamic characteristics, as well as the outcome of the disease, were compared among carriers and non-carriers of the BMPR2 mutation. Results: When receiving IPAH diagnosis, the average age of patients was 40.0 (32.0–48.0) years. Women predominated among the patients (86.8%). Of these, 17 (32.0%) were carriers of the gene mutation, and 36 (68.0%) did not have this mutation. The results of our research demonstrate that the Rs17199249 variant in BMPR2 contributed to increased susceptibility to IPAH. The T allele was associated with an increased risk of IPAH, with T = 75 (70.75%), G = 31 (29.24%), MAF—0.2925, x²—0.001, and HWE p—0.975. Carriers of the BMPR2 mutation were predominantly women (80.0%), and they had higher pulmonary vascular resistance (8.7–14.9 vs. 5.9–12.6 WU; p = 0.038), a low cardiac index (1.9–2.6 vs. 2.3–3.1 L/min per m²; p = 0.027), and a shorter time to death (p = 0.022). Conclusions: This is the first study of the genetic causes of IPAH that demonstrates the genetic polymorphism of BMPR2 is associated with an increased risk of IPAH developing with worse hemodynamic parameters and clinical outcomes.