Search Results (3,135)

Chronic kidney disease (CKD) is a progressive disorder characterized by declining renal function and increased cardiovascular risk. Experimental models are essential for investigating these mechanisms, and the 5/6 nephrectomy (5/6 Nx) model is widely used to reproduce cardiorenal alterations observed in CKD. This review aims to critically evaluate how effectively the 5/6 Nx model reproduces vasoactive and redox mechanisms relevant for pharmacological testing. A narrative synthesis of experimental studies using the 5/6 Nx model in rodents was performed, focusing on vascular, inflammatory, and oxidative pathways. The 5/6 Nx model reproduces major CKD features, including hypertension, proteinuria, glomerulosclerosis, and cardiovascular remodeling. Early activation of the renin–angiotensin–aldosterone system, endothelin signaling, and sympathetic pathways contributes to vascular dysfunction. Sustained oxidative stress reduces nitric oxide bioavailability and promotes endothelial dysfunction. Dysregulation of natriuretic peptides and increased 20-HETE signaling further contribute to vascular imbalance and remodeling. These alterations occur in a well-defined temporal progression, supporting the use of this model for mechanistic and pharmacological studies. The 5/6 Nx model remains a robust and translationally informative platform for investigating CKD progression, provided that pathway-specific reproducibility and experimental variables are carefully considered. Full article

Epidemiological and clinical research on neurodegenerative diseases has shown that metabolic dysregulations increase the risk of developing Alzheimer’s Disease (AD). Many metabolic changes can be grouped into metabolic syndrome (MetS), which is defined as the presence of three or more risk factors, including insulin resistance, hyperglycemia, hypertension, central obesity, and dyslipidemia. These changes cause systemic effects that are crucial in triggering neuroinflammation and neurodegeneration, key factors in AD development. All these factors impair energy metabolism in peripheral tissues and the brain by decreasing glucose utilization, leading to alterations in O-GlcNAcylation, glycosylation, mitochondrial function, oxidative stress, chronic inflammation, synaptic dysfunction, autophagy impairment, and blood–brain barrier (BBB) dysfunction. However, these factors are modified and largely influenced by lifestyle choices. A newer perspective emphasizes that regular exercise is vital for maintaining brain metabolism as we age. Current evidence suggests that engaging in physical activity for individuals with metabolic syndrome reduces their risk of Alzheimer’s disease, enhances prognosis, and improves cognitive abilities. This review explores how metabolic syndrome relates to Alzheimer’s and highlights possible strategies for prevention and treatment. Full article

Background/Objectives: The objective of this study was to map and synthesize the current evidence on hemostasis in chronic and acute liver disease within the framework of Patient Blood Management (PBM). Methods: Because research in this field is heterogeneous—spanning mechanistic studies, observational data, randomized controlled trials, guidelines, and expert reviews—a scoping review was selected to comprehensively map concepts. Findings were synthesized narratively to reflect the breadth and heterogeneity of available research. Results: Hemostasis in liver disease is characterized by a fragile state of rebalanced coagulation, where parallel reductions in pro- and anticoagulant factors coexist with variable fibrinolytic disturbances and thrombocytopenia. Conventional coagulation tests (CCTs) do not accurately reflect bleeding risk, whereas viscoelastic assays and thrombomodulin-modified thrombin generation testing provide a more physiologic assessment, though with limitations. Most bleeding events arise from portal hypertension rather than coagulopathy, and the routine prophylactic correction of abnormal results of CCTs is not supported by evidence. PBM-aligned strategies—such as restrictive transfusion, targeted fibrinogen replacement, and use of thrombopoietin receptor agonists (TPO-RAs)—reduce unnecessary blood product use. Thrombosis burden is increasingly recognized in this patient population. Anticoagulation is generally safe when individualized to liver function and clinical context, however significant variability persists in clinical practice, and high-quality data remain limited for advanced disease. Conclusions: Hemostasis in liver disease reflects a dynamic and unstable equilibrium rather than a simple bleeding tendency. Diagnostic and therapeutic strategies grounded in PBM principles improve safety by avoiding unnecessary transfusion and emphasize individualized care. Despite advances in understanding rebalanced hemostasis, major gaps remain in predicting thrombotic risk, standardizing advanced coagulation testing, and defining optimal management across disease stages. Full article

Endothelial dysfunction (ED) arises in multiple pathologies, and its severity correlates with disease progression. Common ED biomarkers could provide prognostic value for associated complications. This study aims to identify shared ED biomarkers and assess their prognostic significance. Endothelial cells in culture (human microvascular endothelial cells, HMEC-1) were exposed to sera from patients in five disease groups (n = 20 patients/group)—liver cirrhosis with portal hypertension, idiopathic pulmonary arterial hypertension, placental disorders such as intrauterine growth restriction, coronary artery disease with acute myocardial infarction, and chronic kidney disease—or matched controls, in the absence/presence of anti-inflammatory (apixaban) and antioxidant (EUK134) compounds. We explored changes in: VCAM-1, ICAM-1, eNOS, VWF, extracellular matrix thrombogenicity, and reactive oxygen species (ROS). In serum samples, proteomics and metabolomics analyses (including lipids, amino acids, and polar metabolites) were performed through an extraction protocol to identify common ED biomarkers. Expression of VCAM-1, ICAM-1, VWF, platelet adhesion, and ROS increased in most groups versus controls (p < 0.05). Both drugs decreased all biomarker levels except eNOS (n = 6 for in vitro experiments). For serum ED biomarkers, 18 metabolites and 24 proteins showed AUC-ROC and hit rates >77.5%, and six metabolites were associated with event-free survival. These diseases share ED driven by systemic inflammatory, oxidative, and metabolic stress, are partially reversible in vitro, and are linked to biomarkers associated with clinical outcomes. Overall, ED emerges as a modifiable pathological axis with potential prognostic value. Full article

Somatostatin is a potent endocrine regulator and neurotransmitter, exerting predominantly inhibitory effects in different tissues of the body, via G-protein coupled receptors. Five such specific receptors have been identified, with different effects and tissue distribution. The multifaceted actions and effects of somatostatin make it useful as a potential therapeutical means in various pathologies; however, in clinical practice, somatostatin analogues, namely octreotide, lanreotide and pasireotide, are commonly used instead, due to their increased half-life and increased receptor selectivity, with pasireotide showing a more extensive receptor binding profile and high affinity for somatotastin receptor (SSTR) 5, which may prove effective in cases of resistance to first-generation analogues. Apart from their many uses in neoplastic pathologies, somatostatin analogues represent viable treatment choices in some ocular pathologies, congenital hyperinsulinism, gastrointestinal bleedings and portal hypertension, acute pancreatitis, and dumping syndrome. They have also been used in some cases, with varying degrees of success, in patients with post-surgical gastrointestinal and lymphatic fistulas, refractory chronic diarrhoea and polycystic kidney disease; many applications in paediatric patients have also been documented. The aim of this review is to present the applications of somatostatin and its analogues as alternative or second-line therapies, along with insights into their effectiveness and future potential. Full article

Background and Objectives: Anemia is a frequent complication of chronic kidney disease (CKD), primarily attributed to erythropoietin deficiency. Interstitial fibrosis (IF), which disrupts the renal interstitium where erythropoietin-producing cells reside, may contribute to anemia independent of glomerular filtration rate (GFR). However, data in primary glomerulonephritis (PGN) are limited and conflicting. Materials and Methods: In this nationwide multicenter registry analysis (TSN-GOLD), 2794 adults with biopsy-proven PGN were included. Interstitial fibrosis was graded semi quantitatively (0–3). Anemia was defined according to KDIGO/WHO criteria. Multivariable logistic regression models were constructed to evaluate the independent association between IF severity and anemia, adjusting for age, sex, eGFR, log-transformed proteinuria, hypertension, diabetes mellitus, and biopsy diagnosis. Interaction between IF and eGFR was assessed. A predefined subgroup analysis was performed in patients with preserved renal function (eGFR ≥ 60 mL/min/1.73 m²). Results: Anemia was present in 34.4% of patients. Although moderate-to-severe IF was more frequent among anemic patients (p < 0.001), IF severity was not independently associated with anemia in multivariable analysis (p-trend = 0.72). Female sex and lower eGFR were independently associated with anemia. A statistically significant IF×eGFR interaction was observed (p = 0.0029), indicating effect modification across renal function levels. The model demonstrated moderate discrimination (AUC = 0.705). In patients with preserved renal function, IF severity was not associated with anemia. Conclusions: In this large multicenter cohort of PGN patients, interstitial fibrosis severity was not independently associated with anemia after adjustment for renal function and clinical covariates. These findings suggest that the association between interstitial fibrosis and anemia in PGN appears largely mediated by renal functional status rather than fibrosis severity alone. Full article

Background/Objectives: Adults with intellectual disability are known to experience complex health needs, including an elevated presence of chronic conditions. Cardiovascular risk factors are a concern, yet the evidence base is fragmented, and the scope and focus of current research are not well understood. Methods: We conducted a scoping review to map the existing evidence on cardiovascular risk factors among adults with intellectual disability. The review included studies reporting on risk factor prevalence as well as participant characteristics (ethnicity, living arrangements, age, sex, and type of disability). Cardiovascular-related outcomes were extracted to clarify the health disparities documented in this population. Results: Searches of seven databases for studies published from 2013 onward yielded 15,598records, of which 85 met the inclusion criteria. Evidence was dominated by cross-sectional studies, with a few randomized controlled trials. Hypertension, Type 2 diabetes and obesity were commonly reported. Patterns appeared to reflect lifestyle, medication effects, genetic syndromes—particularly Down syndrome and Prader–Willi syndrome—and the severity of the disability. A notable share of the studies originated from the United Kingdom and the United States. Findings reveal a complex cardiovascular risk profile, emphasizing the need for tailored prevention and management. Conclusions: Adults with intellectual disability face a substantial burden of cardiovascular risk factors. Evidence on effective interventions remains limited, highlighting a need for targeted, evidence-informed approaches to improve cardiovascular health and long-term outcomes. Full article

The prevalence of chronic conditions such as hypertension, diabetes, and Human Immunodeficiency Virus (HIV) is rising globally, yet access to continuous care remains limited, particularly in rural low- and middle-income countries. This study evaluated the acceptability and psychosocial predictors of retention in a linkage-to-care (LTC) intervention for patients with chronic conditions in rural South Africa. We conducted a cross-sectional analytical study with a retrospective cohort component among 1673 patients diagnosed with hypertension, diabetes, and/or HIV in Limpopo Province, South Africa. Acceptability and psychosocial factors were assessed cross-sectionally using a theory-informed, interviewer-administered questionnaire between January and June 2024. Retention in care over the preceding six months (July–December 2023) was extracted from routine clinic records and classified as consistent (no gaps > 6 months between visits) or inconsistent (≥1 gap > 6 months. Logistic regression examined associations between psychosocial factors and retention outcomes, adjusting for age, gender, marital status, and diagnostic category. Overall, 25.1% of participants maintained consistent retention over six months, while 74.9% were retained inconsistently. Acceptability of the LTC intervention varied significantly by diagnosis (p < 0.001): 79.5% of participants with multimorbidity rated the intervention as acceptable compared to 54.9% with hypertension, 64.5% with diabetes, and 46.8% with HIV. However, only 12.8% of multimorbid participants agreed that intervention activities fit well with their daily lives. In adjusted analyses, participants who were not happy to participate had 85% lower odds of consistent retention (adjusted odds ratio [AOR] = 0.15, 95% CI: 0.09–0.22) and 7.2 times higher odds of inconsistent retention (AOR = 7.2, 95% CI: 4.8–10.9). Most participants supported de-identified data sharing, though privacy concerns were elevated among those with multimorbidity. Acceptability of LTC interventions differs by diagnosis, with multimorbid patients reporting poorer alignment with daily routines. Retention is strongly associated with emotional engagement and self-efficacy, suggesting that LTC interventions should integrate psychosocial support and be contextually adapted for multimorbid patients in rural settings. Full article

Background: Migration from low- and middle-income to high-income settings is often accompanied by dietary and lifestyle changes that may increase long-term risk of non-communicable diseases. African migrants represent a growing but under-studied population in Australia, with limited evidence on post-migration nutrition transitions and associated chronic disease risk. This study examined changes in diet and lifestyle among Nigerian-born adults before and after migration to Australia and explored any association with chronic diseases. Methods: A pilot cross-sectional study was conducted among adults who migrated from Nigeria to New South Wales, Australia, between 1992 and 2019. Data were collected via a culturally adapted, self-administered online questionnaire assessing socio-demographic characteristics, dietary intake, lifestyle behaviours, and self-reported chronic conditions in the 12 months immediately before and after migration. Descriptive statistics (frequencies and proportions) and inferential analyses (Chi-square tests, McNemar test, and the Bowker test) were used to compare pre- and post-migration behaviours and examine associations with chronic disease outcomes. Results: Ninety-three participants completed the survey (mean age 37.0 ± 7.2 years; 50.5% male). Post-migration, regular breakfast consumption declined (−24.3%), while irregular eating (low and moderate) patterns increased (+7.6% and +16.7%). Regular vegetable intake improved (+5.4%), whereas fruit intake remained low (13.0%). Regular consumption of Nigerian local foods decreased markedly (−53.7%), while regular intake of meat (+18.5%), dairy foods, fats (+14.3%), and non-alcoholic beverages increased (+22.8%). Salt use shifted away from the highest-risk category (−22.2%), and smoking and alcohol consumption remained low and stable. Self-reported chronic conditions were uncommon; hypertension (6.5%) and obesity (5.4%) were the most frequently reported. Conclusions: Nigerian migrants in Australia experience substantial post-migration dietary and lifestyle transitions that may elevate long-term chronic disease risk despite a currently low reported disease burden. Early, culturally responsive nutrition and lifestyle interventions are needed to support healthy adaptation and prevent the progression of cardiometabolic conditions in this growing migrant population. Full article

Background/Objectives: Candidates with cardiometabolic risk are considered for living kidney donation more frequently because of the global organ shortage. The 2017 Kidney Disease: Improving Global Outcomes (KDIGO) guidelines introduced individualized risk assessment based on composite donor profiles rather than categorical exclusion, but the long-term implications of accepting donors with potential risk factors require careful evaluation. This review synthesizes current evidence on outcomes of living kidney donors with obesity, prediabetes, hypertension, and smoking. Methods: A literature search was conducted in PubMed/MEDLINE for studies published between 1 January 2000 and 28 February 2026, including cohort studies, registry analyses, meta-analyses, and clinical guidelines evaluating living kidney donors with obesity, smoking, prediabetes, or hypertension. Priority was given to large cohorts with long-term follow-up. Over 70 publications were included in the final synthesis. Findings were synthesized narratively by risk factors and outcomes. Results: Obesity was associated with an 86% increased end-stage kidney disease (ESKD) risk and 32% increased 20-year mortality. Central adiposity measures outperformed body mass index (BMI) for predicting estimated glomerular filtration rate (eGFR) decline. Post-donation weight gain increased the risk for developing hypertension and diabetes. Smoking conferred a 7.5-fold chronic kidney disease (CKD) risk, with impaired compensatory renal adaptation after donation. Prediabetic donors showed comparable outcomes to normoglycemic donors, with 57.8% reverting to normoglycemia at 10 years. Pre-donation hypertension increased 15-year ESKD risk 3-fold, but absolute risk remained low. At 15 years post-donation, over 50% of the donors developed hypertension. Glucagon-like peptide-1 (GLP-1) receptor agonists reduce diabetes progression by 73–94% in at-risk populations, but prospective studies in donors are lacking. Conclusions: Each risk factor carries quantifiable risks for individualized stratification. These risk factors usually coexist and interact. Refinement of risk prediction models, strategies for metabolic optimization and prospective evaluation of emerging pharmacologic therapies are key priorities. Full article

Pulmonary hypertension (PH) can be defined as a mean pulmonary artery pressure (mPAP) greater than 20 mm Hg at rest during right heart catheterization (RHC). The reported prevalence of PH throughout the globe has been estimated to impact approximately 1% of the total population, with a majority of those afflicted being women more than men. Numerous etiologies give rise to the pathophysiology of PH, including heart disease (i.e., left-sided heart failure), lung diseases, and other unclear causes related to chronic stages and complications surrounding long-standing pulmonary thromboembolisms, side effects of certain medications, and genetic and environmental factors. Untreated PH can lead to severe morbidities such as cardio-renal syndrome and congestive hepatopathy (cardiac cirrhosis). Management of PH focuses on decreasing pulmonary pressures by using vasodilators such as prostanoids, and phosphodiesterase type 5 (PDE-5) inhibitors, as well as newer treatments such as sotatercept, which inhibits activin signaling, thereby inhibiting excessive cell growth in the pulmonary artery vasculature and down-regulating the pro-proliferative pathways. Full article

Background: Stretching exercises are strongly recommended as part of exercise training programs; however, their effects on blood pressure (BP) and other related cardiovascular parameters in adult individuals with elevated BP (pre-hypertension) or hypertension remain unclear. Methods: A systematic search was conducted in PubMed and databases accessed via the EBSCO platform up to 30 September 2025, following the PRISMA guidelines. An additional search of Scopus was performed on 8 April 2026. Studies eligible for inclusion were randomized controlled trials, randomized crossover trials, non-randomized clinical trials and single-arm trials investigating stretching interventions in adults with pre-hypertension and or hypertension. Risk of bias assessment was performed using RoB 2 for randomized trials and ROBINS-I for the non-randomized trials. A random-effect meta-analysis was performed when at least two studies reported sufficiently comparable BP outcomes. The quantitative synthesis was considered exploratory. Results: Eleven records published between 2014 and 2025 met the eligibility criteria and were included. All protocols used static stretching, although only a small number were clearly described as active stretching. The results were heterogeneous across the design, duration of intervention and outcomes. Chronic interventions more often reported favorable changes in indices of arterial stiffness, whereas acute interventions demonstrated more variable immediate BP responses. In the exploratory meta-analysis, the pooled estimate suggested a reduction in systolic blood pressure (SBP) in favor of stretching; however, this effect did not reach statistical significance (mean difference (MD) = −5.39 mmHg, 95% confidence interval (CI): −11.32 to 0.53; I² = 0%). For diastolic blood pressure (DBP), the pooled estimate favored stretching and reached statistical significance (MD = −3.93 mmHg, 95% CI: −7.25 to −0.60; I² = 0%). In sensitivity analyses including a third study, the pooled effects remained in favor of stretching for systolic BP (MD = −6.6 mmHg, 95% CI: −12.2 to −1.0; I² = 56%) and diastolic BP (MD = −5.4 mmHg, 95% CI: −7.1 to −3.7; I² = 8%). These pooled estimates should be interpreted with caution due to the small number of studies, heterogeneity in study design and participant characteristics, and overall limitations in methodological quality. Secondary findings suggested possible improvements in selected vascular parameters, including brachial–ankle pulse wave velocity, augmentation index, and cardio–ankle vascular index, whereas acute responses were more variable and protocol-dependent. Overall, the level of evidence was limited, with most randomized trials judged as having some concerns and non-randomized studies judged as having a critical risk of bias. Conclusions: Stretching interventions may improve BP and selected vascular parameters in adults with pre-hypertension and hypertension and may represent a practical adjunct within the non-pharmacological management of BP. However, the current evidence is limited by methodological heterogeneity, risk of bias, and the small number of studies available for quantitative synthesis. Therefore, the pooled findings should be considered exploratory and hypothesis-generating rather than definitive. Further high-quality randomized controlled trials are required to determine the optimal type, dose, and long-term clinical relevance of stretching interventions in this population. Full article

Background and Objectives: Acute kidney injury (AKI) is a frequent and life-threatening complication in patients with liver cirrhosis (LC). Nephrotic-range proteinuria may reflect underlying structural renal vulnerability; however, its association with AKI severity in cirrhosis remains unclear. Materials and Methods: We conducted a retrospective cohort study of 408 adults with LC admitted to a tertiary referral hospital between January 2016 and December 2025. Nephrotic-range proteinuria was defined as a urine protein-to-creatinine ratio (UPCR) ≥3.5 g/g measured within 7 days before or at admission. AKI was staged using serum creatinine-based Kidney Disease: Improving Global Outcomes criteria. Baseline creatinine was defined as the lowest value within 7 days before admission; if unavailable, the lowest stable value within the preceding 3 months was used. Severe AKI was defined as KDIGO stage 2–3. Multivariable logistic regression was performed to evaluate the association between nephrotic-range proteinuria and severe AKI after adjustment for age, sex, diabetes mellitus, hypertension, chronic kidney disease (CKD), sepsis, ICU admission, and Child–Pugh class. Results: Of the 408 patients, 56 (13.7%) had nephrotic-range proteinuria. Severe AKI occurred more frequently in patients with nephrotic-range proteinuria than in those without (39.3% vs. 21.9%), corresponding to an absolute risk difference of 17.4 percentage points (p = 0.008). In the adjusted model, nephrotic-range proteinuria was associated with a higher likelihood of severe AKI (adjusted odds ratio [OR], 2.27; 95% confidence interval [CI], 1.17–4.41; p = 0.015). CKD (adjusted OR, 2.26; 95% CI, 1.33–3.81; p = 0.002), ICU admission (adjusted OR, 2.03; 95% CI, 1.22–3.39; p = 0.007), and Child–Pugh class C versus A (adjusted OR, 3.50; 95% CI, 1.37–8.93; p = 0.009) were also significantly associated with severe AKI. Conclusions: Among hospitalized patients with LC, nephrotic-range proteinuria was associated with a higher likelihood of severe AKI. Quantitative proteinuria assessment may help identify patients at increased risk of advanced renal dysfunction, although causal inference is limited by the retrospective observational design. Full article

Background and Objectives: To identify predictors of pulmonary infection in critically ill patients after abdominal surgery and to develop an early postoperative risk stratification model. Materials and Methods: Medical records of ICU patients after abdominal surgery (January 2016–June 2024) with Acute Physiology and Chronic Health Evaluation II (APACHE II) scores ≥10 were retrospectively analyzed. Patients were categorized according to the presence or absence of pulmonary infection. Candidate variables were screened using LASSO regression, followed by multivariate logistic regression to identify independent predictors. A nomogram-based prediction model was constructed and internally validated. Results: Among 4852 patients, 390 (8.0%) developed pulmonary infections. Overall, 8 independent predictors were identified: Male sex (vs. female) (OR 1.509, 95% CI: 1.091–2.087, p = 0.013), chronic obstructive pulmonary disease (OR 4.139, 95% CI: 2.872–5.966, p < 0.001), atrial fibrillation (OR 2.320, 95% CI: 1.366–3.939, p = 0.002), hypertension (OR 1.869, 95% CI: 1.372–2.539, p < 0.001), chronic renal insufficiency (OR 2.412, 95% CI: 1.143–5.091, p = 0.021), preoperative total bilirubin (OR 1.003, 95% CI: 1.001–1.004, p = 0.002), rectal surgery (OR 0.354, 95% CI: 0.151–0.830, p = 0.017), and invasive mechanical ventilation duration > 6 h (OR 2.206, 95% CI: 1.628–2.990, p < 0.001). The nomogram demonstrated good discrimination (AUC: 0.734 95% CI: 0.698–0.770) and calibration. Conclusions: This study identified 8 independent predictors of pulmonary infection and developed an internally validated early postoperative risk stratification model with satisfactory performance. The model may assist clinicians in identifying high-risk patients and guiding timely preventive strategies in ICU practice. Full article

Background/Objectives: Cardiovascular disease (CVD) in chronic kidney disease (CKD) arises from a multifaceted interplay of pathophysiological processes, including chronic inflammation, oxidative stress (OS), and accelerated vascular calcification (VC). Red blood cell distribution width (RDW) and the neutrophil-to-lymphocyte ratio (NLR) have emerged as simple, inexpensive, and readily available hematological indices that may capture these underlying disturbances. As such, they hold promise as accessible biomarkers for stratifying cardiovascular risk in patients with CKD. Methods: This cross-sectional study enrolled 497 patients, comprising 477 with CKD across all stages and 20 controls. We evaluated the associations of RDW and NLR with both traditional and non-traditional cardiovascular risk factors, as well as with serum calcification propensity (T50). Spearman’s correlation and multivariable regression analysis were used to assess these relationships. Results: Both RDW and NLR were significantly elevated in patients with established CVD (p < 0.001 for both) and demonstrated a progressive increase across advancing CKD stages (p < 0.001). RDW and NLR showed positive correlations with age, CVD duration, urea, phosphorus, parathormone, CRP, FG23, and mean carotid intima–media thickness (cIMT), while exhibiting inverse correlations with eGFR, serum albumin, hemoglobin, lipids, antioxidants such as superoxide dismutase, fetuin-A, and T50. Additionally, NLR correlated positively with the duration of hypertension and diabetes, as well as with albuminuria. Quartile analysis revealed a stepwise decline in T50 across increasing categories of RDW and NLR, supporting the link with impaired calcification defense. In multivariable analysis, T50 independently predicted NLR (β = −0.013; p = 0.018), whereas total cholesterol (β = −0.011; p = 0.019) and cIMT (β = 0.38; p = 0.018) emerged as independent determinants of RDW. Conclusions: RDW and NLR strongly reflect the burden of inflammation, metabolic disturbance, and vascular dysfunction in patients across the CKD spectrum. The consistent associations with impaired calcification defense and with established cardiovascular risk markers underscore the potential value as accessible indicators of cardiovascular vulnerability in CKD. These findings support incorporating RDW and NLR into routine risk assessment and highlight T50 as a mechanistically relevant determinant of hematologic inflammation profiles. Full article