Clinical trials

To evaluate both sides of the common carotid artery, renal artery, and femoral artery in Hypertension patient that cause of systemic arterial hypertension and/or the effects of target organ damage, both structural and functional markers.

Clinical outcome to identify and analyze the epigenetic, phenotypic, protein variation, metabolites of CYP450 Family 11 Subfamily B, both 1 and 2, human-associated aldosterone protein release, and signaling inhibitory pathways post-aldosterone-mineralocorticoid interaction. We will include clinical studies (RCTs, cohort, case-control/series/report) from fresh human specimens. We will exclude animal studies, studies generated from cell culture, and aldosterone synthesis. To systematically review and synthesize the literature on the main 2 questions Question 1: Which environment induces CYP11B1 or CYP11B2 activation causing hyperaldosteronemia in hypertension patients? Question 2: Which intracellular signal silences aldosterone-MR activity? For Individual Participant Data Meta-analysis, data will be extracted from final analysis articles from the framework of the data selection process only; the effect measurement and multi-variable model meta-analysis will be performed. Primary Objective1: to identify CYP450 Family 11 Subfamily B and Aldosterone in hypertension patients following; By structure ● Evidence confirms Epigenetic profile of CYP450 Family 11 Subfamily B, Aldosterone, Signal in hypertension patients, both random and treated from any DNA sequencing method Protein synthesis evidence of aldosterone protein induces hypertension from Western blot or LC-MS By function Metabolomic profile: the substrate or product refers to aldosterone interaction causing end-organ cell line dysfunction or impaired structure. Inhibitory signaling profiling of hypertension patients compared to non-hypertension patients, which negatively feedback to CYP450 Family 11 Subfamily B or Aldosterone Secondary Objective 2: Sub-group analysis effect measurement following; * Proposed mechanisms, biological markers, or pathways that contribute to failure to regulate aldosteronemia * Treatment-related permanent normotensive post-hyperaldosteronemia. Primary Objective 2: Identify possible intracellular signal inhibit aldosterone action * Analyze possible mechanisms of signal that are silent aldosterone-MR activity * Differentiation of free aldosterone and attached aldosterone Secondary Objective 2: ● Sensitivity and specificity of outcomes of hypertension patients who underwent estimate substrate associated aldosterone circulation Plasma CYP450 Family 11 Subfamily B Urine CYP450 Family 11 Subfamily B Plasma Aldosterone (active form) Plasma Aldosterone (metabolite form) Urine Aldosterone