Aim: We aimed to single out admission predictors of acute respiratory distress syndrome (ARDS) in hospitalized COVID-19 patients and investigate the role of bioelectrical impedance (BIA) measurements in ARDS development. Method: An observational, prospective cohort study was conducted on 407 consecutive COVID-19 patients hospitalized at the University Clinical Center Kragujevac between September 2021 and March 2022. Patients were followed during the hospitalization, and ARDS was observed as a primary endpoint. Body composition was assessed using the BMI, body fat percentage (BF%), and visceral fat (VF) via BIA. Within 24 h of admission, patients were sampled for blood gas and laboratory analysis. Results: Patients with BMI above 30 kg/m², very high BF%, and/or very high VF levels were at a significantly higher risk of developing ARDS compared to nonobese patients (OR: 4.568, 8.892, and 2.448, respectively). In addition, after performing multiple regression analysis, six admission predictors of ARDS were singled out: (1) very high BF (aOR 8.059), (2) SaO₂ < 87.5 (aOR 5.120), (3) IL-6 > 59.75 (aOR 4.089), (4) low lymphocyte count (aOR 2.880), (5) female sex (aOR 2.290), and (6) age < 68.5 (aOR 1.976). Conclusion: Obesity is an important risk factor for the clinical deterioration of hospitalized COVID-19 patients. BF%, assessed through BIA measuring, was the strongest independent predictor of ARDS in hospitalized COVID-19 patients.

Background: An implantable loop recorder (ILR) represents the gold standard in the diagnosis of cardiac arrhythmias in patients with neurological or cardiac symptoms. Our study aimed to determine the real-world diagnostic effectiveness of ILRs in detecting arrhythmias requiring permanent pacemaker implantation. Methods: The study enrolled and followed up for two years 62 ILR recipients from the Cardiology Clinic of the Clinical Center Kragujevac, Serbia. Results: The most common indication for pacemaker implantation was pauses in cardiac activity (83%). The use of oral anticoagulants (OR: 11.80; 95% CI: 1.76, 79.4), ACE inhibitors or AT receptor blockers (OR: 3.87; 95% CI: 1.21, 12.35), and diuretics (OR: 5.29; 95% CI: 1.55, 18.04) had a statistically significant impact on the detection of pacemaker-requiring arrhythmias by an ILR. After adjustment for other factors of influence, oral anticoagulants (OR: 7.82; 95% CI: 1.08, 56.9) and diuretics (OR: 3.68; 95% CI: 1.04, 13.00) remained significant in predicting pacemaker requirement in ILR recipients. Conclusions: An ILR represents an effective diagnostic approach in detecting cardiac arrhythmias requiring permanent pacemaker implantation, especially in patients treated with oral anticoagulants or diuretics.

Background/Objectives: Impaired quality of life (QoL) represents one of the most important clinical determinants in heart failure with preserved ejection fraction (HFpEF). This study aimed to evaluate the incremental explanatory value of functional performance and inflammatory biomarkers for QoL in a clinically stable HFpEF cohort. Methods: A single-center observational study enrolled 110 consecutive patients with stable HFpEF. Functional capacity was assessed using the six-minute walk test (6MWT), expressed mainly as percentage of predicted distance. Health-related QoL was measured using the EQ-5D-5L utility index (primary outcome). Circulating IL-6, CRP, and NT-proBNP were obtained from peripheral blood. Hierarchical multivariable linear regression was applied to quantify the incremental contribution of clinical variables, functional capacity, and biomarkers. Results: The median age was 72 years, and 52.7% of the participants were women. The median 6MWT distance was 340 m (75.9% of predicted), and the median EQ-5D index was 0.76. The baseline clinical regression model (age, sex, atrial fibrillation, and glomerular filtration rate) explained 23.5% of EQ-5D variance. The addition of functional capacity increased explained variance to 45.2% (ΔR² = +0.217). The inclusion of IL-6 and NT-proBNP provided a modest additional increase (R² = 0.468; ΔR² = +0.042 in addition to Model 2). In the fully adjusted model, functional capacity (β = 0.376, p < 0.001) and IL-6 (β = −0.185, p < 0.05) remained independent predictors, whereas NT-proBNP lost significance. Conclusions: In stable HFpEF, objective functional capacity represents the dominant determinant of QoL, while inflammatory activation provides an independent but smaller contribution. Functional assessment may therefore be central to patient-centered phenotyping and therapeutic targeting.

Resistant hypertension (RH) is disproportionately prevalent in patients with chronic kidney disease (CKD) and is strongly associated with accelerated cardiovascular morbidity and CKD progression. Emerging evidence suggests that gastrointestinal dysbiosis may represent a modifiable contributor to RH through multiple converging mechanisms, including accumulation of protein-bound uremic toxins, impaired short-chain fatty acid signaling, heightened systemic inflammation and oxidative stress, sympathetic activation, altered bile acid metabolism, increased intestinal permeability, and microbe–drug interactions that attenuate antihypertensive efficacy. This review synthesizes mechanistic, clinical, and translational evidence linking gut dysbiosis to RH in CKD, with a focus on therapeutic strategies and unmet needs. Finally, critical research gaps were outlined and a pragmatic agenda was proposed for translational studies and precision microbiome-guided interventions aimed at improving blood pressure control and cardiovascular-renal outcomes. Cite this article as: Ćićarić N, Đukić V. Gastrointestinal dysbiosis and resistant hypertension in chronic kidney disease: mechanisms, clinical evidence, and therapeutic perspectives. Turk J Nephrol. Published online May 22, 2026. doi: 10.5152/turkjnephrol.2025.251200.

Despite the availability of antihypertensive drugs, many patients worldwide have uncontrolled hypertension (1,2). In this regard, the term „resistant hypertension“ was introduced, with a prevalence of 10%-20% in hypertensive patients (3). According to the current guidelines of the European Association of Cardiology, hypertension is defined as resistant when the treatment strategy, which includes appropriate lifestyle measures and treatment with maximum or maximally tolerated doses of diuretics (thiazides and thiazide-like diuretics), blockers of the renin-angiotension-aldosterone system (RAAS) and calcium channel blockers, fails to lower systolic arterial pressure <140 mm Hg and/or diastolic arterial pressure <90 mm Hg (4). Compared to patients who achieve adequate blood pressure control with antihypertensives, patients with resistant hypertension have a worse prognosis and consequently a higher risk of myocardial infarction, stroke and end-stage renal disease, with two to six times higher mortality (5,6). The cause of uncontrolled hypertension is usually identified in secondary hypertension), with a prevalence of up to 30% among patients with resistant hypertension (7,8). In addition to secondary hypertension, it is important to rule out pseudoresistant hypertension, including that caused by non-adherence to treatment (4). In this regard, large observational studies have found that within one year, approximately 50% of patients stop taking antihypertensive medications for various reasons, such as inadequacy, adverse drug reactions, and socioeconomic variables (9). Uncontrolled hypertension is significantly associated with increased sympathetic activity, which can be caused by afferent signals originating from the kidneys and the influence of sympathetic tone by stimulating hypothalamic centers (10). Chronic activation of renal sympathetic nerves is key in the pathogenesis of hypertension through various mechanisms (reabsorption of salt and water in renal tubules, reduction of renal perfusion and consequently glomerular filtration rate, activation of the RAAS cascade) (9). Consequently, renal denervation (RDN) has emerged as a therapeutic option in conditions of overactive central sympathetic nervous system (10). This chapter explores the role of SGLT2i in the treatment of hypertension, with a focus on their mechanisms of action, recent clinical evidence, and future implications. The introduction of this drug class may represent a paradigm shift in the management of UAH, offering new opportunities for more effective and individualized therapeutic strategies.

Background/Objectives: Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome characterized by systemic inflammation and impaired functional capacity. Interleukin-6 (IL-6) is implicated in HFpEF pathophysiology, but the influence of IL6 genetic variability on its clinical impact remains unclear. This study investigated the associations of circulating IL-6, IL6 polymorphisms, and functional severity in HFpEF. Methods: This single-center observational study included 110 clinically stable HFpEF patients. Clinical, laboratory, and functional data, including C-reactive protein (CRP), IL-6 serum levels were collected. The neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio were calculated from complete blood count, while IL6 polymorphisms rs1800795 and rs1818879 were genotyped using TaqMan assays. Functional status was assessed using NYHA classification, the six-minute walk test (6MWT), and the Borg dyspnea scale. Results: Among carriers of the rs1800795 G/C+C/C genotype, elevated IL-6 was associated with higher odds of advanced symptoms (NYHA III; OR = 6.08, 95% CI 1.45–25.45, p = 0.014) and reduced exercise capacity (6MWT; OR = 6.55, 95% CI 1.60–26.72, p = 0.009). The combined effect of elevated IL-6 levels and the rs1800795 genotype was also associated with greater dyspnea burden, as assessed by the Borg scale (OR = 1.17, 95% CI 1.02–1.34, p = 0.029). In multivariable analysis, the NYHA and 6MWT models additionally retained NLR as an independent predictor, while the Borg model included advanced age, pulmonary hypertension, and the combined effect of elevated IL-6 levels and the rs1800795 genotype. Conclusions: The observed combined effect of elevated IL-6 levels and the rs1800795 genotype on symptom burden and functional impairment suggests that combined inflammatory and genetic profiling may improve severity assessment in HFpEF.