Background and Objectives: Chronic kidney disease (CKD) and end-stage kidney disease (ESKD) are characterized by persistent inflammation, malnutrition, and immune dysfunction, all of which contribute to poor outcomes in hemodialysis (HD) patients. The C-reactive protein albumin lymphocyte (CALLY) index has been proposed as a novel biomarker that integrates these mechanisms. This study aimed to evaluate the prognostic value of the CALLY index together with established markers, including the C-reactive protein-to-albumin ratio (CAR), neutrophil-to-lymphocyte ratio (NLR), and monocyte-to-lymphocyte ratio (MLR) for all-cause mortality in HD patients. Materials and Methods: This retrospective cohort study was conducted on 106 patients undergoing HD. Demographic, clinical, and laboratory parameters were obtained three months after the effects of HD initiation was reviewed. Results: During a median follow-up of 24.5 months, 29 patients (27.3 percent) died. Non-survivors were significantly older (65.3 vs. 52.5 years, p < 0.001), had a higher prevalence of coronary artery disease (31 percent vs. 2.6 percent, p < 0.001), or shorter dialysis duration (14 vs. 27 months, p < 0.001). They also showed lower hemoglobin (9.2 vs. 10.1 g/dL, p = 0.007), creatinine (5.3 vs. 6.3 mg/dL, p = 0.048), and albumin levels (28 vs. 34 g/L, p = 0.001), as well as a higher MLR (0.329 vs. 0.254, p = 0.014). In multivariate analysis, age, CAR, and NLR independently predicted mortality, explaining 83.8% of the variation. ROC analysis identified age and MLR as significant predictors, with MLR showing a high negative predictive value (83.9%). The CALLY index did not demonstrate independent prognostic value. Conclusions: Age, CAR, NLR, and MLR were independent predictors of mortality in HD patients, whereas the CALLY index was not prognostic in this cohort. Among these markers, MLR may be a practical biomarker with strong negative predictive power. Larger prospective studies are needed to validate these findings.

Multivessel coronary artery disease (MV-CAD) remains a prevalent and serious health concern despite advances in treatment. Early identification and risk stratification are crucial for optimizing treatment. The CRP-to-albumin ratio (CAR) has emerged as a promising biomarker in various inflammatory diseases. This study investigated the potential of CAR as a marker for MV-CAD. We retrospectively analyzed 1360 patients with suspected CAD. Patients were divided into three groups based on CAR tertiles. Logistic regression analyses were carried out to estimate the association between MHR and MV-CAD. Elevated CAR levels were significantly associated with an increased prevalence of CAD (p < 0.001), severe CAD (p < 0.001), and MV-CAD (p < 0.001). Patients with the highest CAR tertile had five times higher odds of MV-CAD compared to the lowest tertile (p < 0.001). CAR demonstrated moderate accuracy in predicting MV-CAD (AUC: 0.644, 95% CI: 0.615–0.674, p < 0.001). CAR holds promise as a tool for the early identification and risk stratification of multivessel CAD. Further research is warranted to validate its clinical utility and explore its potential to guide treatment decisions and improve outcomes in patients with this high-risk condition.

Background: Contrast-induced nephropathy (CIN) is one of the most important complications after invasive cardiovascular procedures. Considering the pivotal role of inflammation in CIN development, the use of peripheral blood-based indexes may be an easily available biomarker to predict CIN risk. Therefore, in the present study, we evaluated the association between the pan-immune-inflammation value (PIV) and the risk of CIN. Patients and Methods: A total of 1343 patients undergoing coronary angiography (CAG) were included. The PIV was calculated with the following equation: (neutrophil count × platelet count × monocyte count)/lymphocyte count. Multivariable regression analyses were used to determine the association between clinical and laboratory parameters and CIN development. Results: The median age of the cohort was 58 (IQR 50–67), and 48.2% of the patients were female. CIN developed in 202 patients (15%) in follow-up. In multivariate analyses, older age (OR: 1.015, 95% CI: 1.002–1.028, p = 0.020) and higher PIV levels (OR: 1.016, 95% CI: 1.004–1.028, p = 0.008) were associated with a higher CIN risk, while the use of antiplatelet agents was associated with a lower risk of CIN (OR: 0.670, 95% CI: 0.475–0.945, p = 0.022). Conclusions: We demonstrated that the risk of CIN was significantly higher in patients with higher PIV and older patients in a large cohort of patients undergoing CAG for stable ischemic heart disease. If supported with prospective evidence, PIV levels could be used as a minimally invasive reflector of CIN.

Background: Chronic kidney disease (CKD) elevates the risk of cardiovascular disease (CVD) and mortality. Uremic cardiomyopathy, frequently observed in CKD and end-stage renal disease (ESRD), involves alterations in cardiac structure and function, which may reverse post-kidney transplantation, although data remain controversial. This study examines the relationship between graft function and changes in cardiac parameters pre- and post-transplantation in kidney transplant recipients. Methods: A total of 145 pediatric and adult recipients of living or deceased donor kidney transplants were enrolled at Gazi Yaşargil Training and Research Hospital. This cohort study utilized transthoracic echocardiographic (TTE) imaging pre-transplant and at least two years post-transplant. Echocardiographic parameters were analyzed using standard techniques. Results: The mean age of the participants was 35 years, with 60% male. The average dialysis duration prior to transplantation was 27 months. Most recipients (83.4%) received kidneys from living donors. Left ventricular diastolic dysfunction increased significantly post-transplant (p < 0.05), while other cardiac dimensions and functions, such as ejection fraction and pulmonary artery pressure, showed no significant change (p > 0.05). Notably, diastolic dysfunction worsened in patients with dysfunctional grafts (GFR < 45), correlating with increased pulmonary artery pressure post-transplant. The rate of antihypertensive drug use and the prevalence of diabetes mellitus increased significantly post-transplant (p < 0.05). Conclusions: This study demonstrates that left ventricular diastolic dysfunction present before kidney transplantation continues to persist post-transplantation in patients with end-stage renal disease undergoing chronic kidney disease treatment. Furthermore, it shows an increased rate of pulmonary artery pressure and pericardial effusion in patients with dysfunctional grafts after transplantation. Further research is required to explore strategies to reverse uremic cardiomyopathy and reduce cardiovascular risk in these patients.

Background: This study aimed to investigate the relationships of AHA/ACC blood pressure stages and circadian blood pressure patterns with clinical, metabolic, inflammatory, and structural echocardiographic parameters in newly diagnosed hypertensive (HT) patients, and to identify independent predictors of high-risk circadian disruptions. Methods: A total of 539 patients undergoing 24 h Ambulatory Blood Pressure Monitoring (ABPM) between 2022 and 2024 were retrospectively analyzed. Patients were grouped by nocturnal blood pressure dipping percentages and HT stages; laboratory markers (TyG index (Triglyceride–Glucose İndex), AIP (Atherogenic İndex of Plasma), SII (Systemic Immune-Inflammation Index), AISI (Aggregate Index of Systemic Inflammation), NLR (Neutrophil-to-Lymphocyte Ratio)) and echocardiographic data were evaluated via multivariable logistic regression. Results: The mean cohort age was 46.49 ± 13.98 years. Progressing HT stages were associated with significant increases in metabolic risk indicators: TyG index (p = 0.002) and AIP (p = 0.004). The prevalence of left ventricular hypertrophy (LVH) increased significantly from 7.3% in the normal group to 34.5% in Stage 2 HT (p < 0.001). The highest-risk “reverse-dipper” group had a significantly higher mean age (50.32 ± 14.55 years) than other groups (p < 0.001). In multivariable logistic regression, left atrial diameter (LAd) was the only common independent structural predictor of circadian disruption across all models (Extreme-Dipper OR: 1.19, p = 0.003; Non-Dipper OR: 1.11, p = 0.001). In the Reverse-Dipper model score analysis, both LAd (p < 0.001) and LVH (p = 0.001) demonstrated strong independent predictive potential. Inflammatory indices (SII, AISI, NLR) showed no independent predictive value (p > 0.05). Conclusions: Advanced HT stages and disrupted circadian rhythms are strongly associated with metabolic impairment, left atrial dilatation, and LVH. In older hypertensive patients presenting with left atrial enlargement and LVH, echocardiographic screening and close ABPM are crucial for early “reverse-dipper” pattern detection.