To describe the main glycemic outcomes and the Quality of Life (QOL) observed in a cohort of people with type 1 (T1D) or type 2 (T2D) insulin-treated diabetes under dialysis who started an Automated Insulin Delivery (AID) system. This is a longitudinal retrospective pilot real-world analysis of 14 individuals with T1D and T2D undergoing dialysis who began using an AID system to optimize glycemic control. All subjects used the MiniMed™ 780G system. Glucose metrics were collected at baseline, 3, 6, and 12 months after initiating the SmartGuard™ feature. The WHOQoL-Bref questionnaire was administered at the last follow-up to evaluate the QOL. Out of the 14 people, 8 reached 1-year follow-up. Time in Range (TIR) increased from 63

Introduction: Cardiovascular morbidity and mortality (CVMM) remain highly prevalent among end-stage kidney disease (ESKD) patients undergoing chronic hemodialysis (HD). Nevertheless, risk prediction in this setting is limited by the complexity of factors involved and the individual patients’ characteristics. In this study, we evaluated whether circulating levels of Humanin, a micropeptide reflecting mitochondrial dysfunction, could refine CVMM prediction when included in established risk models for CVMM in ESKD-HD. Methods: Eighty-three chronic HD patients (mean age 67 ± 12 years; 74.7% male) were enrolled in a 24-month prospective multicenter study. CVMM (fatal or non-fatal CV events requiring hospitalization) occurred in 33 patients (39.7%). The performances of an internal prognostic model based on cohort-related risk predictors and four externally generated and validated risk scores (AROii-2, jDOPPS, You et al., and Zhang et al.) were compared before and after the inclusion of Humanin. Results: Humanin displayed a curvilinear association with CVMM, with both low (<462 pg/mL) and high (>778 pg/mL) levels linked to an increased risk. CVMM was best predicted by the internal model (AUC 0.671; R2 0.13), followed by the Zhang (0.669; 0.12), AROii-2 (0.632; 0.05), You (0.628; 0.07), and jDOPPS (0.610; 0.03) scores. All models were well calibrated. Humanin inclusion remarkably improved discrimination (ΔAUC spanning from 0.083 to 0.109), calibration, explained variance (R2 gain from 9 to 15%), and reclassification (Net Reclassification Improvement: 8–27.9%; Integrated Discrimination Index: 4.4–7.3%) of all models considered. Conclusions: Integration of Humanin significantly enhances the predictive accuracy of CVMM risk models in HD patients, supporting its potential role as an additive biomarker in this high-risk population.

Contrast-induced nephropathy (CIN), now more accurately referred to as contrast-induced acute kidney injury (CI-AKI), remains a major cause of hospital-acquired acute kidney injury (AKI) and is associated with increased morbidity and mortality, particularly in high-risk patients. This condition occurs following the intravascular administration of iodinated radiocontrast media (RCM), especially in individuals with pre-existing chronic kidney disease (CKD), diabetes mellitus, heart failure, advanced age, or exposure to high contrast volumes. The pathophysiology of CI-AKI is multifactorial and involves renal hemodynamic alterations, direct tubular toxicity, oxidative stress, inflammatory activation, and endothelial dysfunction, ultimately leading to tubular injury and reduced glomerular filtration rate (GFR). Traditional diagnostic markers such as serum creatinine (sCr) and estimated glomerular filtration rate (eGFR) are limited by low sensitivity and delayed response, prompting growing interest in novel biomarkers, including cystatin C (CysC), β-2 microglobulin (β-2M), Interleukin-18 (IL-18), Kidney Injury Molecule-1 (KIM-1), Neutrophil Gelatinase-Associated Lipocalin (NGAL), and osteopontin (OPN), which allow earlier detection and risk stratification. Preventive strategies remain the cornerstone of management and include optimizing hydration protocols, minimizing contrast dose, selecting low- or iso-osmolar agents, and individualized risk assessments. Despite extensive research into pharmacological and procedural interventions, no effective treatment for established CI-AKI exists, underscoring the critical importance of prevention and ongoing investigation into safer contrast agents and innovative prophylactic approaches.

Introduction/Objectives: Sarcopenia, characterized by the progressive loss of muscle mass and strength, is highly prevalent in patients on peritoneal dialysis (PD), significantly affecting their quality of life (QoL). The SarQoL questionnaire, a newly validated tool for assessing the impact of sarcopenia on QoL, has never been evaluated in PD patients. This study aimed to explore its applicability and relevance in this population. Methods: Thirty-two adult PD patients were recruited. Sarcopenia risk was assessed using the SARC-F questionnaire, anthropometric measures (e.g., skinfold thickness, body composition), and functional tests (handgrip strength, 30 s chair-stand test). Correlations with the SarQoL score were thus explored. Results: The mean SarQoL score was 70.95 ± 15.96, indicating a low to mildly impaired QoL related to sarcopenia. Patients on automated PD (APD) scored significantly higher than those on continuous ambulatory PD (CAPD; p < 0.0001). Strong inverse relationships were observed between SarQoL and SARC-F scores (r = −0.77, p < 0.0001) and age (r = −0.50, p = 0.003). Additionally, the SarQoL score was correlated with diastolic blood pressure (r = 0.50, p = 0.003), serum albumin (r = 0.47, p = 0.006), diuresis (r = 0.46, p = 0.007), number of stands at the chair test (r = 0.46, p = 0.02), and body fat percentage (r = −0.34, p = 0.05). Conclusion: The SarQoL questionnaire may be useful for evaluating sarcopenia's impact on well-being in PD patients. Future studies are needed to confirm these findings in wider cohorts and to explore longitudinal changes in SarQoL scores in response to interventions. Resumen: Introducción/Objetivos: La sarcopenia, caracterizada por la pérdida progresiva de masa y fuerza muscular, es altamente prevalente en los pacientes en diálisis peritoneal (DP) y afecta significativamente su calidad de vida (CV). El cuestionario SarQoL, una herramienta recientemente validada para evaluar el impacto de la sarcopenia en la CV, nunca ha sido evaluado en pacientes en DP. Este estudio tuvo como objetivo explorar su aplicabilidad y relevancia en esta población. Métodos: Se reclutaron treinta y dos pacientes adultos en DP. El riesgo de sarcopenia se evaluó mediante el cuestionario SARC-F, medidas antropométricas (p. ej., pliegues cutáneos, composición corporal) y pruebas funcionales (fuerza de prensión manual, test de levantarse de la silla en 30 segundos). Se analizaron las correlaciones con la puntuación del SarQoL. Resultados: La puntuación media del SarQoL fue de 70,95 ± 15,96, lo que indica una CV relacionada con la sarcopenia de baja a levemente deteriorada. Los pacientes en DP automatizada (DPA) obtuvieron puntuaciones significativamente más altas que aquellos en DP continua ambulatoria (DPCA; p < 0,0001). Se observaron fuertes relaciones inversas entre la puntuación SarQoL y el SARC-F (r = −0,77; p < 0,0001) y la edad (r = −0,50; p = 0,003). Además, la puntuación SarQoL se correlacionó con la presión arterial diastólica (r = 0,50; p = 0,003), la albúmina sérica (r = 0,47; p = 0,006), la diuresis (r = 0,46; p = 0,007), el número de repeticiones en el test de la silla (r = 0,46; p = 0,02) y el porcentaje de grasa corporal (r = −0,34; p = 0,05). Conclusión: El cuestionario SarQoL puede ser útil para evaluar el impacto de la sarcopenia en el bienestar de los pacientes en DP. Se necesitan estudios futuros para confirmar estos hallazgos en cohortes más amplias y explorar los cambios longitudinales en la puntuación SarQoL en respuesta a intervenciones.

Chronic kidney disease (CKD) and peripheral artery disease (PAD) are highly prevalent conditions associated with morbidity, mortality, and health-care costs, particularly when they coexist. Despite advances in pharmacological and interventional therapies, patients with both CKD and PAD have rapid functional decline, higher hospitalization rates, and poor cardiovascular outcomes. In populations with either CKD or PAD alone, exercise training has been shown to improve cardiorespiratory fitness, muscle strength, physical function, and quality of life and is strongly recommended in the guidelines. However, evidence for exercise training in patients with overlapping CKD and PAD remains limited with no randomized controlled trials and only a single observational cohort, suggesting potential benefits of home-based walking programs on renal and cardiovascular outcomes. This narrative review examines the potential benefits of exercise training as a nonpharmacological approach to addressing this therapeutic gap. An ongoing randomized controlled trial, EXACT-CKD-PAD, is expected to provide more definitive evidence in this high-risk population, although further studies will be required to define long-term clinical impact and optimal implementation strategies.

Vascular diseases (VD) remain a leading global cause of morbidity and mortality, often developing silently before manifesting as severe complications like stroke or ischemia. Traditional diagnostic imaging provides essential anatomical data but frequently fails to capture the dynamic molecular processes underlying vascular pathology. This narrative review summarizes current evidence regarding Extracellular Vesicles (EVs), including exosomes, microvesicles, and apoptotic bodies, as emerging biomarkers and mediators in vascular conditions. The review evaluates the biological mechanisms of EVs across several disorders, including arterial aneurysms, peripheral artery disease, carotid stenosis, and venous thromboembolism. Findings indicate that EVs concentration and molecular cargo, particularly microRNAs and proteins, reflect the physiological state of parent cells, offering a “liquid biopsy” for vascular inflammation, endothelial dysfunction, and plaque vulnerability. Furthermore, the review explores the therapeutic potential of stem cell-derived EVs in promoting angiogenesis and tissue repair in chronic vascular ulcers. Despite these advances, the review concludes that the clinical implementation of EV-based diagnostics faces significant hurdles, primarily due to the lack of standardized isolation and characterization methods. Addressing these methodological challenges is crucial for translating EV research into routine clinical practice.

Objective:Chronic kidney disease (CKD) is a global health problem with a significant impact on patients' quality of life. Haemodialysis, a common treatment for advanced CKD, can profoundly affect vestibular function, which plays a critical role in maintaining balance and spatial orientation. Methods:This prospective study was conducted over a 6-month period at the Magna Graecia University and included 18 adult patients with CKD stage 5, undergoing haemodialysis. Vestibular function was assessed using the Visual Analogue Scale (VAS) for the symptom of unsteadiness and the video Head Impulse Test (vHIT) for the vestibulo-ocular reflex (VOR) gain. Results:Our results showed a statistically significant decrease in VOR gain from 0.99 at T0 to 0.92 at T1 (T-test p = 0.034 and Welch Test p = 0.037), accompanied by an increase in VAS instability scores, after the dialysis session. These results suggest a worsening of vestibular function as a result of haemodialysis. Conclusions:These results highlight the need for early diagnosis and timely intervention, such as vestibular rehabilitation, to reduce the risk of falls and improve the quality of life in CKD patients undergoing haemodialysis. Future research should investigate the long-term effects of haemodialysis on vestibular function.

Fabry disease (FD) is a progressive, multisystemic X-linked disorder caused by mutations in the GLA gene, often leading to renal failure. Although several screening programs have been conducted, the prevalence of FD in patients with chronic kidney patients who are not dependent on dialysis (NDD-CKD) is likely underestimated due to restrictive inclusion criteria and methodological shortcomings. This study aims to assess the prevalence of FD in NDD-CKD patients using an expanded screening approach. Ongoing outpatients attending Italian nephrology clinics were screened by assay of plasma α-galactosidase A (α-Gal A) activity. Genetic testing was also performed in all females and males with low α-Gal A activity. Inclusion criteria were: (1) females ≥18 years old; (2) males aged between 18 and 70 years; (3) NDD-CKD stages 1–5. Patients with histological diagnosis of glomerulonephritis or diagnosis of autosomal dominant polycystic kidney disease (ADPKD) were excluded. Demographic data and laboratory results were also collected. Among 385 NDD-CKD outpatients, 173 underwent screening. One patient with three family members carrying a novel mutation (c.320 A > G, p.Q107R); one patient with three family members carrying a silent mutation (c.48 T > G, p.L16L) and two patients with a missense mutation (c.376A > G, p.S126G), were identified. Overall, the prevalence of FD was 2.3%, increasing to 5.4% (10 in 183) with family screening. FD may be more common than previously believed, particularly within NDD-CKD populations. FD screening should be expanded to include NDD-CKD patients with known causes of CKD, such as hypertension and diabetes mellitus, and genetic testing should be routinely used for female patients.

Introduction: The Uremic Pruritus in Dialysis Patients (UP-DIAL)—14-item scale is a validated, multidimensional tool for assessing pruritus severity and clinical burden among patients with chronic kidney disease-associated pruritus (CKD-aP). While the scale has been developed in Thai and other non-Thai languages, an Italian version and cross-cultural adaptation have not been established for Italian-speaking CKD-aP populations. Aims: This study aimed to translate and validate an Italian version of the UP-Dial—14-item questionnaire for use among hemodialysis (HD) patients. Materials and Methods: Following international guidelines, a rigorous translation process was undertaken, including independent forward and backward translations to ensure linguistic and conceptual equivalence. The validation cohort comprised HD patients with CKD-aP from seven centers across Calabria, Italy. Patients and healthcare professionals reviewed the Italian version to evaluate usability, readability, and cultural adaptation. Internal consistency was assessed using Cronbach’s alpha, and test-retest reliability was evaluated with the intraclass correlation coefficient (ICC) over a 7-day interval. Results: Of 323 HD patients screened, 132 with CKD-aP were included. Both patients and professionals confirmed satisfactory face validity and adaptation. The Italian UP-DIAL—14-item demonstrated excellent internal consistency (Cronbach’s α = 0.91; 95% CI: 0.89-0.93) and reproducibility (ICC = 0.92; 95% CI: 0.90-0.94). Conclusions: The Italian version of the UP-DIAL—14-item is a valid, reliable, and reproducible instrument for assessing CKD-aP in HD patients. It is suitable as a patient-reported outcome measure for both clinical practice and research.

Background: Carotid revascularization procedures, such as carotid endarterectomy (CEA) and carotid artery stenting (CAS), can lead to restenosis. Monitoring restenosis onset through biomarkers is crucial in clinical practice. This study aimed to evaluate inflammation biomarkers in CEA and CAS to determine their predictive value for restenosis risk postprocedure. Methods: A retrospective analysis was conducted on the clinical records of patients with carotid stenosis who underwent CEA or CAS over 1 year at the vascular surgery departments of an interuniversity center. Eligible asymptomatic patients with carotid stenosis (70%-99%) underwent revascularization. Differences between preprocedural and early postprocedural inflammation indices were assessed, and restenosis risk was evaluated using receiver operating curve analysis and logistic regression. Results: The cohort comprised 100 patients, 68 undergoing CEA and 32 undergoing CAS. Significant values were observed for inflammation ratios post-CEA: neutrophils to lymphocytes ratio (NLR) (P = 0.036), platelets to lymphocytes ratio (PLR) (P = 0.009), monocytes to lymphocytes ratio (MLR) (P < 0.001), systemic inflammation index (SII) (P = 0.024), systemic immune response index (SIRI) (P = 0.003), and aggregate inflammation response index (AISI) (P < 0.001). At 12-month follow-up, 12% of patients experienced restenosis; 50% were men and 50% women. Women showed a higher restenosis rate (26.1% vs 7.8%). Preintervention NLR (odds ratio {OR} [95% confidence interval {CI}] = 13.38 [1.88 to 95.44], P = 0.010) and SIRI (OR [95% CI] = 10.22 [2.65 to 39.43], P = 0.001) remained significantly associated with restenosis after adjusting for sex and smoking. Conclusions: The study provided a predictive model for restenosis, identifying preintervention NLR and SIRI as independent predictors of restenosis at 12-month follow-up.

BACKGROUND:Vascular diseases (VDs)-such as arterial aneurysms, chronic venous disease, and peripheral artery disease-are influenced by a complex interplay of genetic, biological, and social factors. Integrating the assessment of both molecular and social determinants offers a novel framework that connects factors like socioeconomic status, chronic stress, and environmental exposures to the molecular pathways that drive vascular pathophysiology. METHODS:This review was conducted searching libraries such as Web of Science, Scopus, MEDLINE, and Google Scholar. The aim was to facilitate the analytical integration of studies that highlight the relationship between social determinants of health and VDs under a biomolecular lens. RESULTS:This review explores how adverse social conditions can initiate inflammation, oxidative stress, epigenetic modifications, and dysregulation of biomarkers such as matrix metalloproteinases, thereby contributing to vascular degeneration and dysfunction. These mechanisms demonstrate how social experiences become biologically embedded, increasing susceptibility to structural vascular changes and impaired circulation. CONCLUSION:By bridging insights from molecular biology and social science, this approach provides a valuable paradigm for addressing health disparities and advancing prevention and treatment strategies for common VDs.

Background: Peripheral arterial disease (PAD) is a growing public health problem due to its high and increasing prevalence worldwide. PAD is responsible for several severe complications that affect the quality of life (QoL) of affected patients. Social determinants of health (SDHs) cover five areas: economic stability, education access, and quality, health care access and quality, neighborhood and built environment, and social and community context. This study aims to investigate SDHs-related outcomes to better understand their potential role in the lives of patients with PAD. Methods: A qualitative study has been conducted using semi-structured interviews to understand the role of SDHs in patients with PAD. Braun and Clarke’s method was used to guide the qualitative analysis of the data. Results: Twenty-seven patients were recruited to receive the interview, including twelve males (44.44%) and fifteen females (55.56%), with a mean age of 63.3 years old (a range of 50–87 years old). SDHs related to the five areas investigated significantly impacted PAD patient diagnosis and outcomes. Conclusions: Our findings suggest that physicians and vascular surgeons should consider SDHs impairments to recognize vulnerable patient populations and tailor treatment methods and follow-up protocols to their specific needs.

BackgroundChronic kidney disease (CKD) has now reached pandemic proportions but risk prediction towards end-stage kidney disease (ESKD) remains challenging. Kidney fibrosis is a key determinant in the transition from CKD to ESKD. In this prospective study, we investigated the prognostic significance of urinary Marinobufagenin (uMBG), a cardiotonic steroid with acknowledged pro-fibrotic activity, for stratifying the risk of CKD progression in individuals with non-advanced renal disease.MethodsAfter baseline uMBG measurements, 108 CKD patients (eGFR 40.54 ± 17 mL/min/1.73 m2) were prospectively followed up to 24 months. The study (renal) endpoint was a composite of serum creatinine doubling, eGFR decline >25% from baseline values, or ESKD requiring chronic renal replacement therapy.ResultsDuring follow-up (mean 21 months), 32.4% of patients had progressive CKD. These individuals displayed almost halved baseline uMBG excretion as compared to others (p < 0.0001). At ROC analysis uMBG showed a remarkable diagnostic capacity on CKD progression (AUC 0.898) and patients with uMBG ≤310 pmol/L (Best ROC-derived cut-off) had a significantly faster progression to the endpoint (Log-rank 57.9; p < 0.0001). Restricted cubic splines fitting logistic and Cox-regression analyses revealed that the risk association between uMBG and CKD progression was best described by a curvilinear, inverse J-shaped trend, the highest risk associated with very low uMBG levels. This trend remained unaffected by adjustment for age, baseline eGFR, and 24 h-proteinuria.ConclusionIn individuals with non-advanced CKD, very low urinary excretion of MBG reflects a more sustained risk of CKD progression over time. Validation studies are needed to generalize these findings in larger heterogeneous cohorts.

Background: Chronic venous disease (CVD) substantially influences workers' comfort, productivity, and capacity to remain employed, yet many occupational settings complicate the implementation of effective symptom management strategies. Temperature fluctuations, in particular, influence daily functioning: heat often worsens swelling, heaviness, pain, and fatigue, while cold may offer partial relief. This study examines how workplace thermal and organizational conditions affect adults with CVD, paying attention to the challenges they face in applying clinical recommendations. Methods: Fifty adults with CEAP C1-C6 disease were interviewed and observed in clinical settings. A qualitative descriptive approach was adopted to capture workers' accounts rather than generate a new theory. Data were analyzed using Braun and Clarke's reflexive thematic analysis within a qualitative descriptive framework. Results: Heat exposure consistently aggravated swelling, pain, and fatigue, whereas moderate cold often improved comfort and functional capacity. Participants highlighted numerous workplace barriers, including rigid schedules, restrictive uniforms, and difficulties maintaining compression in hot environments. Supportive supervisors, micro-breaks, access to hydration, and flexibility in posture facilitated better symptom control. Workers frequently described tensions between clinical advice and job demands, noting that instructions such as leg elevation or frequent breaks were often unrealistic in their occupational context. Conclusions: Aligning clinical guidance with workplace realities is essential for the well-being and long-term employability of individuals with CVD. Climate-sensitive and ergonomic job design represents an important strategy for supporting employees' ability to manage symptoms and sustain productivity amid increasing thermal variability.

BACKGROUND:This study aimed to investigate the relationship between work activities and chronic venous disease of the lower limbs. METHODS:Patients referred to our clinical units of Interuniversity Center of Phlebolymphology for chronic venous disease (CVD) assessment between January 2019 and December 2023 were retrospectively enrolled in the study. Inclusion criteria were (a) CVD status confirmed by office visit and Duplex ultrasound, (b) not having any other vascular disease of the lower limbs (such as arterial or lymphatic problems), (c) work activities of at least 1-year duration, in the medical records. RESULTS:A total of 948 patients (642 females and 306 males) were retrospectively enrolled. Of these, 613 patients (431 females and 182 males) were affected by CVD and 335 patients (211 females and 124 males) were not affected by CVD and served as controls. Sedentary jobs and jobs where the ambient work temperature ambient is hot have been associated with CVD. Other types of work with no sedentary activities or with a cool ambient work temperature were not associated with CVD. CONCLUSIONS:Work activity and the occupational environment may be tightly related to the onset and progression of CVD. Forced postures, excessive standing or sitting, and high ambient temperatures can reduce lower limb venous function at work and cause CVD.

Hemodialysis is the primary treatment for patients with total loss of renal function and is performed through a vascular access called an arteriovenous fistula (AVF). AVF can be associated with several complications, such as stenosis, thrombosis, and aneurysms. While digital subtraction angiography (DSA) is the gold standard for AVF monitoring, its limited availability, invasiveness, and harmfulness has enabled Doppler ultrasound (DUS) as alternative technique. Herein, the development of a portable device based on a triboelectric sensor for AVF monitoring that exploits the concept of impedance cardiography (ICG) is presented. The triboelectric sensor consists of a thin polyvinylidene fluoride (PVDF) layer placed close to the AVF to evaluate the triboelectric ICG signal (T-ICG), thus avoiding the need for standard multiple-electrode equipment. Electrocardiographic (ECG) dry electrodes based on a composite of polydimethylsiloxane (PDMS) and multi-walled carbon nanotubes (MWCNTs) were fabricated. Concept validation was performed in a cohort of hemodialysis patients with and without AVF stenosis. The results demonstrated a linear dependence between blood flow and the maximum deviation (dZ/dtmax) of the T-ICG pattern. Patients with stenosis showed a statistically significant change in morphology at the B-point. The extent of stenosis was evaluated by analyzing the temporal slope of the ICG pattern in the B- and C-point regions, evidencing a linear trend for stenosis from 20 % up to 60 %. The proposed device represents an innovative approach compared with the gold clinical standards for the continuous monitoring of AVF in hemodialysis patients.

Chronic kidney disease (CKD) has now reached pandemic proportions but risk prediction towards end-stage kidney disease (ESKD) remains challenging. Kidney fibrosis is a key determinant in the transition from CKD to ESKD. In this prospective study, we investigated the prognostic significance of urinary Marinobufagenin (uMBG), a cardiotonic steroid with acknowledged pro-fibrotic activity, for stratifying the risk of CKD progression in individuals with non-advanced renal disease. After baseline uMBG measurements, 108 CKD patients (eGFR 40.54 ± 17 mL/min/1.73 m²) were prospectively followed up to 24 months. The study (renal) endpoint was a composite of serum creatinine doubling, eGFR decline >25% from baseline values, or ESKD requiring chronic renal replacement therapy. During follow-up (mean 21 months), 32.4% of patients had progressive CKD. These individuals displayed almost halved baseline uMBG excretion as compared to others (P < 0.0001). At ROC analysis uMBG showed a remarkable diagnostic capacity on CKD progression (AUC 0.898) and patients with uMBG ≤310 pmol/L (Best ROC-derived cut-off) had a significantly faster progression to the endpoint (Log-rank 57.9; P < 0.0001). Restricted cubic splines fitting Cox-regression analyses (Fig. 1) revealed that the risk association between uMBG and CKD progression was best described by a curvilinear, inverse J-shaped trend, the highest risk associated with very low uMBG levels. This trend remained unaffected by adjustment for age, baseline eGFR, and 24 h-proteinuria. Low urinary excretion of MBG is an independent prognostic factor for CKD progression in patients with non-advanced CKD. These findings suggest that uMBG may serve as a valuable biomarker for early risk stratification in CKD. Further validation in larger cohorts is needed to confirm its role in clinical practice.

BACKGROUND:Arterial diseases like coronary artery disease (CAD), carotid stenosis (CS), peripheral artery disease (PAD), and abdominal aortic aneurysm (AAA) have high morbidity and mortality, making them key research areas. Their multifactorial nature complicates patient treatment and prevention. Biomarkers offer insights into the biochemical and molecular processes, while social factors also significantly impact patients' health and quality of life. This scoping review aims to search the literature for studies that have linked the biological mechanisms of arterial diseases through biomarkers with social issues and to analyze them, supporting the interdependence of biological and social sciences. METHODS:After a rigorous selection process, adhering to the Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines for Scoping Reviews, 30 articles were identified through Scopus, Web of Science, and PubMed. Inclusion and exclusion criteria were based on the population, intervention, comparator, outcome, time, and setting framework. Inclusion criteria were studies involving human subjects that explored the relationships among arterial diseases, biomarkers, and psychosocial factors, with no restrictions on publication date. Nonhuman studies, purely biological or medical analyses without psychosocial dimensions, and non-English publications were excluded. Eligible study types included experimental, observational, and review articles published in peer-reviewed journals. Data extraction focused on study characteristics, such as authors, publication year, country, methods, population, and findings. Results were synthesized narratively, as this format was deemed the most suitable for summarizing diverse findings. The quality or methodological rigor of the included studies was not formally assessed, consistent with the scoping review methodology. RESULTS:In CAD, biomarkers such as high-sensitivity C-reactive protein are strongly associated with psychological stress, whereas lipoprotein (a) and the apolipoprotein B/apolipoprotein A1 ratio reflect lipid profiles that are influenced by socioeconomic factors and ethnicity. In CS, increased carotid intima-media thickness is linked to psychiatric conditions like attention deficit/hyperactivity disorder, and heat shock protein-70 levels are associated with socioeconomic status and gender. In PAD, inflammatory markers, including interleukin-6, intracellular adhesion molecule-1, and high-sensitivity C-reactive protein, mediate the connection between depression and disease severity, with gender and ethnicity influencing the expression of biomarkers and clinical outcomes. In AAA, factors like smoking and exposure to air pollution have increased matrix metalloproteinase levels and other inflammatory markers. Additionally, estradiol provides partial protection in women, underscoring the role of hormones and environmental influences in disease progression. Social determinants such as socioeconomic status, healthcare access, and ethnicity significantly affect biomarker levels and arterial disease progression. CONCLUSIONS:These findings are crucial for the assumption that social determinants of health modulate the levels of inflammatory biomarkers involved in the progression of arterial diseases such as CAD, CS, PAD, and AAA. This highlights the need to integrate highly predictive mathematical systems into clinical practice, combining biological sciences with social sciences to achieve advanced standards in precision medicine. However, further studies are needed to validate these approaches fully.

BACKGROUND:Aortic aneurysms (AAs), characterized by localized dilation of the aorta, represent a life-threatening condition often progressing asymptomatically until rupture. This review explores the multifactorial pathogenesis of aortic wall degeneration, integrating molecular, cellular, and structural perspectives. METHODS:A focused search of international bibliographic sources was conducted using WoS, PubMed, and Scopus databases, Google Scholar was used as an additional source. The aim was to facilitate the analytical integration of studies that highlight the relationship between pathological features and molecular pathways involved in AA development and progression. RESULTS:The review synthesizes findings from 78 studies spanning diverse disciplines, emphasizing the dynamic interplay between genetic predispositions and environmental factors in aneurysm development. Key pathological mechanisms include extracellular matrix degradation mediated by upregulated matrix metalloproteinases, chronic inflammation with immune cell infiltration, vascular smooth muscle cell apoptosis and phenotypic switching, oxidative stress, and dysregulated transforming growth factor-beta signaling. Emerging roles of ADAM/ADAMTS proteases, noncoding RNAs, and epigenetic modifications are highlighted, alongside novel contributions from intraluminal thrombus and perivascular adipose tissue, which foster hypoxia and inflammation. CONCLUSION:Understanding these interwoven mechanisms is crucial for the development of effective diagnostic tools and personalized treatments aimed at halting aneurysm progression and rupture.

Chronic kidney disease (CKD) is a disorder that causes changes in both the structure and function of the kidneys, causing complications such as hypertension, edema, and oliguria. Renal fibrosis is also a common pathological feature of CKD. Matrix metalloproteinases (MMPs) are endopeptidases that degrade extracellular matrix (ECM) proteins. The proteinase domain consists of a zinc ion in the active site, which contributes to its stabilization with another zinc and three calcium structural ions. Many cellular processes are controlled by MMPs, such as cell–cell interactions and various signaling pathways, while they are also involved in degrading substrates on cell surfaces. Tissue inhibitors of metalloproteinases (TIMPs) are key regulators of metalloproteinases, and both are involved in regulating cell turnover, the regulation, and the progression of fibrosis and apoptosis in the tissue. MMPs play a role in renal fibrosis, such as the tubular cell epithelial–mesenchymal transition (TEM), activation of resident fibroblasts, endothelial–mesenchymal transition (EndoMT), and pericyte–myofibroblast transdifferentiation. This review aims to show the mechanisms through which MMPs contribute to renal fibrosis, paying particular attention to MMP-9 and the epithelial–mesenchymal transition.