Chronic kidney disease (CKD) is associated with chronic inflammation and metabolic dysregulation. While endothelin-1 (ET-1) has been extensively studied, the role of endothelin-2 (ET-2) in CKD remains poorly understood. This cross-sectional study included 76 participants, 12 healthy controls and 64 CKD patients, stratified into three groups based on estimated glomerular filtration rate (eGFR): Group 1 (eGFR ≥ 90 mL/min/1.73 m²), Group 2 (eGFR 45–89 mL/min/1.73 m²), and Group 3 (eGFR 15–44 mL/min/1.73 m²). Serum concentrations of ET-1, ET-2, ET-3, uric acid (UA), and inflammatory markers (hsCRP and IL-6) were measured. ET-2 levels were significantly higher in the advanced CKD group (median 24.49 pg/mL) compared to controls (median 19.32 pg/mL; p = 0.030). No significant differences were observed for ET-1 or ET-3 across groups. ET-2 levels positively correlated with UA (rho = 0.243, p = 0.036), hsCRP (rho = 0.241, p = 0.039), and IL-6 (rho = 0.244, p = 0.038). These findings suggest that ET-2 may represent a potential biomarker reflecting metabolic and inflammatory dysregulation in CKD and highlight its possible relevance in disease severity assessment.

Background: Chronic kidney disease (CKD) patients have an increased risk of cardiovascular disease (CVD), necessitating effective risk assessment methods. This study evaluates the calcium–phosphorus product (Ca × P) to estimated glomerular filtration rate (Ca × P/eGFR) ratio as a potential biomarker for predicting CV risk in pre-dialysis CKD patients. Methods: Eighty-four CKD patients in stages G1–G4, according to the KDIGO criteria, were classified into CVD (n = 43) and non-CVD (n = 41) groups. Biochemical parameters, including serum creatinine (SCr), blood urea nitrogen (BUN), calcium (Ca), inorganic phosphate (Pi), parathyroid hormone (PTH), alkaline phosphatase (ALP), Ca × P, eGFR, and the Ca × P/eGFR ratio, were measured and calculated. Statistical analyses were performed to identify predictors of CV risk and evaluate the diagnostic reliability of the Ca × P/eGFR ratio for predicting the risk. Results: Significant differences were observed in SCr, BUN, eGFR (p < 0.001), and the Ca × P/eGFR ratio (p = 0.007) between the groups. Regression analysis indicated the Ca × P/eGFR ratio as a significant CVD risk predictor (p = 0.012, OR = 1.206, 95% CI: 1.042–1.395). Receiver Operating Characteristic (ROC) curve analysis revealed an AUC of 0.751 (p < 0.001, 95% CI: 0.645–0.857), with a sensitivity and specificity of the method of 74.4% and 70.7%, respectively. Significant correlations were found between the Ca × P/eGFR ratio and SCr, BUN, UA, Ca, Pi, PTH, and ALP. Conclusions: The Ca × P/eGFR ratio may serve as a significant predictor of CVD risk in pre-dialysis CKD patients, suggesting that its integration into routine evaluations could enhance CV risk stratification and management.

Fibroblast growth factor 23 (FGF23) and osteocalcin are involved in mineral and bone metabolism, but their relationship in chronic kidney disease (CKD) remains insufficiently characterized. This cross-sectional study investigated the association between FGF23 and undercarboxylated osteocalcin (Glu-OC) and whether this association persisted after accounting for kidney function. The study included 80 adults: 12 healthy controls and 68 patients with non-dialysis CKD stages G1–G4. Associations were assessed using Spearman correlation, partial correlation adjusted for estimated glomerular filtration rate (eGFR), and complementary multivariable linear regression models. Among patients with CKD, FGF23 was inversely correlated with eGFR (ρ = −0.346, p = 0.004) and Glu-OC (ρ = −0.344, p = 0.004), and positively correlated with serum creatinine (ρ = 0.299, p = 0.013). The inverse association between FGF23 and Glu-OC persisted after adjustment for eGFR (partial ρ = −0.475, p < 0.001). In the multivariable regression models, Glu-OC was inversely associated with FGF23 (standardized β = −0.258, p = 0.024), whereas alkaline phosphatase was positively associated with FGF23 (β = 0.369, p = 0.001). In the model with Glu-OC as the dependent variable, FGF23 (β = −0.266, p = 0.020) and serum calcium (β = −0.366, p = 0.002) were inversely associated with Glu-OC. Significant inverse correlations between FGF23 and Glu-OC were observed in CKD stages G1–G3, but not in stage G4 or the control group. These findings support an association between FGF23 and Glu-OC in non-dialysis CKD and provide a rationale for further investigation of a potential FGF23–Glu-OC axis in CKD-associated mineral and bone disorder (CKD-MBD). Longitudinal and mechanistic studies are needed to clarify the nature and clinical relevance of this association.

Background: Chronic kidney disease (CKD) patients have an increased risk of cardiovascular disease (CVD), necessitating effective risk assessment methods. This study evaluates the calcium-phosphorus product (Ca×P) to estimated glomerular filtration rate (Ca×P/eGFR) ratio as a potential biomarker for predicting CV risk in pre-dialysis CKD patients. Methods: Eighty-four CKD patients in stages G1 - G4, according to the KDIGO criteria, were classified into CVD (n = 43) and non-CVD (n = 41) groups. Biochemical parameters, including serum creatinine (SCr), blood urea nitrogen (BUN), calcium (Ca), inorganic phosphate (Pi), parathyroid hormone (PTH), alkaline phosphatase (ALP), Ca×P, eGFR, and the Ca×P/eGFR ratio, were measured and calculated. Statistical analyses were performed to identify predictors of CV risk and evaluate the diagnostic reliability of the Ca×P/eGFR ratio for predicting the risk. Results: Significant differences were observed in SCr, BUN, eGFR (p < 0.001) and the Ca×P/eGFR ratio (p = 0.007) between the groups. Regression analysis indicated the Ca×P/eGFR ratio as a significant CVD risk predictor (p = 0.012, OR = 1.206, 95% CI: 1.042-1.395). Receiver Operating Characteristic (ROC) curve analysis revealed an AUC of 0.751 (p < 0.001, 95% CI: 0.645–0.857), with sensitivity and specificity of the method 74.4% and 70.7%, respectively. Significant correlations were found between the Ca×P/eGFR ratio and SCr, BUN, UA, Ca, Pi, PTH, and ALP. Conclusions: The Ca×P/eGFR ratio is a significant predictor of CVD risk in pre-dialysis CKD patients, suggesting its integration into routine evaluations could improve CV risk stratification and management.

Introduction: FGF23 and osteocalcin are important regulators of mineral and bone metabolism. The association between FGF23 and undercarboxylated osteocalcin (Glu-OC) in chronic kidney disease (CKD) remains insufficiently understood. This study aimed to investigate the association between FGF23 and Glu-OC and assess whether it is independent of kidney function. Methods: This cross-sectional study included 80 adults: 12 healthy controls and 68 patients with non-dialysis CKD stages G1–G4. FGF23, Glu-OC, calcium, phosphate, PTH, and bone metabolism markers were measured. Associations were assessed using Spearman correlation, partial Spearman correlation adjusted for eGFR, and multivariable linear regression. Results: FGF23 was inversely correlated with eGFR (ρ = −0.346; p = 0.004) and positively correlated with creatinine (ρ = 0.299; p = 0.013). FGF23 was inversely associated with Glu-OC (ρ = −0.344; p = 0.004), with the association becoming stronger after adjustment for eGFR (partial ρ = -0.477; p < 0.001). In complementary multivariable models, the inverse association between FGF23 and Glu-OC persisted: Glu-OC was associated with FGF23 (β = −0.258; p = 0.024), along with ALP (β = 0.369; p = 0.001), while FGF23 was associated with Glu-OC (β = −0.266; p = 0.020), along with calcium (β = −0.366; p = 0.002). Conclusion: FGF23 is independently and inversely associated with Glu-OC in non-dialysis CKD, and this relationship persists after adjustment for kidney function. These findings support an association between FGF23 and Glu-OC in CKD–mineral and bone disorder (CKD-MBD).

Background: The identification of reliable biomarkers for early diagnosis and monitoring of chronic kidney disease (CKD) progression is crucial for improving prognosis and treatment. Neutrophil gelatinase-associated lipocalin (NGAL) is a promising candidate, already validated as a marker for acute kidney injury. This study evaluates NGAL's potential as a biomarker for early diagnosis and monitoring the progression of CKD. Seventy-one patients at CKD stages G1–G4 according to the KDIGO criteria were divided into three groups: Group 1 (eGFR ≥90 mL/min/1.73m²), Group 2 (eGFR 45–89 mL/min/1.73m²), and Group 3 (eGFR 15–44 mL/min/1.73m²). Blood samples were collected and analyzed via standard biochemical and immunological techniques. Serum NGAL levels were measured using ELISA. Results: NGAL levels increased significantly with disease progression and strongly correlated with declining eGFR. Higher NGAL levels were linked to elevated serum creatinine and inflammatory markers, indicating progressive damage to the kidney tissue against the backdrop of persistent systemic inflammation. Conclusions: NGAL demonstrates considerable potential as a biomarker for early detection and monitoring of kidney damage progression. Its use in clinical practice could enrich the traditional methods of diagnosis and monitoring of patients with CKD.