Ordaya-Gonzales, Karina

Resistant hypertension (RH) is a high-risk phenotype characterized by blood pressure readings ≥130/80 mmHg despite maximally tolerated therapy with three antihypertensive agents, including a diuretic, or controlled blood pressure requiring four or more medications. The diagnosis of RH requires a structured evaluation that confirms accurate blood pressure measurement, excludes pseudoresistance—particularly nonadherence and white coat hypertension—and identifies secondary causes such as obstructive sleep apnea, primary aldosteronism, renovascular disease, pheochromocytoma, and Cushing syndrome. RH arises from overlapping mechanisms, including activation of the renin–angiotensin–aldosterone system (RAAS), sympathetic overactivity, arterial stiffness, volume expansion, and immune-mediated pathways. Management begins with lifestyle modification and optimized triple therapy, followed by mineralocorticoid receptor antagonists as the preferred fourth-line treatment. Emerging pharmacological options, such as sodium–glucose cotransporter-2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, endothelin receptor antagonists, aldosterone synthase inhibitors, and angiotensin receptor and neprilysin inhibitors (ARNIs), offer additional therapeutic potential; meanwhile, device-based interventions, including renal denervation and baroreflex activation therapy, have shown sustained blood pressure reductions in selected patients. Future directions highlight precision medicine, digital health technologies, and artificial intelligence as methods to improve diagnosis, guide individualized therapy, and enhance long-term blood pressure control.

Abstract Background: Chronic kidney disease (CKD) has been associated with higher risk of gastrointestinal disorders, particularly Gastroesophageal reflux disease (GERD). However, the magnitude of this association and the underlying mechanisms remains unclear. Methods: A systematic search was conducted across major databases from inception to November 2024. We included cross-sectional and case-control studies evaluating the relationship between CKD and GERD. Data were extracted and analyzed using a random-effects model to calculate pooled odds ratios (ORs) and prevalence rates. Study quality was assessed using the Newcastle-Ottawa Scale, and heterogeneity was evaluated using the Cochran’s Q test and I² statistic. Results: Nine studies involving 4,650,709 participants were included. The pooled prevalence of GERD among CKD patients was 18% (95% CI: 0.10–0.26, I² =93.64%). The pooled crude OR for the association between CKD and GERD was 2.53 (95% CI: 1.30–4.92) and adjusted OR was 1.48 (95% CI: 1.05–2.08). Conclusion: This meta-analysis reveals a marginally significant association between CKD and GERD, highlighting higher prevalence of GERD among individuals with CKD. Furthers studies are needed to elucidate the underlying pathophysiological mechanisms and potential clinical implications.