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Introduction: The prevalence of cardiovascular (CV) comorbidity in patients with chronic kidney disease (CKD) is high, particularly in end‑stage renal disease (ESRD). There is an ongoing search for novel biomarkers of CV disease in this population., Objectives: We aimed to investigate the associations of matrix proteoglycans (PGs) and glycosaminoglycans (GAGs), collagen, and arterial calcifications with selected serum and plasma markers of endothelial dysfunction, inflammation, oxidative stress, and bone turnover in patients with ESRD., Patients and Methods: We enrolled 47 adult patients (32 men) with stage 5 CKD. The following parameters were investigated: fibrinogen, soluble thrombomodulin (sTM), plasminogen activator inhibitor 1 (PAI‑1), stromal cell‑derived factor 1α (SDF‑1α), calcium (Ca), phosphate (Pi), intact parathormone, interleukin 6, high‑sensitivity C‑reactive protein (hs‑CRP), ferric reducing ability of plasma, 2,2‑diphenyl‑1‑picrylhydrazyl scavenging, ferric reducing ability of ascorbate in plasma, fetuin‑A, fibroblast growth factor 23, osteopontin, osteoprotegerin, osteocalcin, transforming growth factor β (TGF‑β), hepatocyte growth factor, secreted protein acidic and rich in cysteine, as well as matrix metalloproteinase 2. Radial artery specimens were stained with alizarin red for calcifications, alcian blue for PGs and GAGs, and sirius red for collagen., Results: We observed positive correlations between PG and GAG, collagen, and calcification staining. The most intense (grade 3) alcian blue staining was significantly correlated with diabetes as well as higher levels of Ca × Pi product, hs‑CRP, fibrinogen, SDF‑1α, PAI‑1, and sTM. However, PAI‑1 was the only significant predictor of grade 3 alcian blue staining in a multiple logistic regression model adjusted for hemodialysis, Ca× Pi product, and hs‑CRP levels., Conclusions: Coagulation disorders and endothelial dysfunction are the hallmarks of ESRD. The levels of SDF‑1α, PAI‑1, sTM, and fibrinogen may be novel predictors of early vascular wall alterations and may serve as CV risk markers.

INTRODUCTION Urinary uromodulin excretion has been associated with kidney diseases. However, serum uromodulin concentrations have not been extensively studied in patients with chronic kidney disease (CKD), and the results of published studies are inconsistent. OBJECTIVES The aims of the study were to evaluate serum uromodulin concentrations in patients with CKD and to assess the utility of serum uromodulin measurements for diagnosing CKD stages. PATIENTS AND METHODS This observational study included 170 patients with CKD stages 1 to 5, not treated by renal replacement therapy, and 30 healthy individuals. The serum levels of creatinine, cystatin C, and uromodulin were measured, and estimated glomerular filtration rate (eGFR) was calculated according to the 2012 CKD Epidemiology Collaboration cystatin‑creatinine equation. RESULTS Among patients with CKD, serum uromodulin concentrations were significantly lower than in controls, and were strongly negatively correlated with renal retention markers (ie, serum creatinine and cystatin C) and strongly positively correlated with eGFR. An inverse, hyperbolic relationship between serum creatinine and uromodulin levels was analogous to the well‑known association between serum creatinine concentrations and eGFR. A receiver‑operating characteristic curve analysis showed a high diagnostic accuracy of the measurement of serum uromodulin concentrations in the assessment of CKD stages. CONCLUSIONS Serum uromodulin concentrations are closely correlated with eGFR, which is the recommended measure of renal function. As uromodulin is produced exclusively by renal tubular cells, the assessment of uromodulin levels in patients with CKD may be an alternative method for evaluating the number of functioning nephrons.

Introduction: Family history of premature coronary artery disease (CAD) is a risk factor of atherogenesis and adverse coronary events., Objectives: The aim of the study was to establish whether asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide formation, might be elevated in the asymptomatic offspring of patients with early‑onset CAD and whether it might contribute to subclinical atherosclerosis., Patients and Methods: We studied 20 healthy subjects (10 men and 10 women) aged from 19 to 30 years with a parental history of documented CAD before 60 years of age, and 20 controls with no evidence of parental CAD. ADMA and its isomer, symmetric dimethylarginine (SDMA), were determined by enzyme‑linked immunosorbent assays. Mean intima‑media thickness (IMT) of the common carotid arteries was assessed by B‑mode ultrasound., Results: Characteristics of the 2 groups were similar, except for insignificant tendencies towards higher low‑density lipoprotein (LDL) cholesterol (P = 0.07) and estimated glomerular filtration rate (eGFR) (P = 0.06) in the group with a positive family history. Compared with controls, subjects with a parental history of premature CAD had increased IMT (0.54 ±0.05 vs. 0.48 ±0.05 mm; P <0.001) and similar levels of ADMA (0.66 ±0.17 vs. 0.74 ±0.15 μmol/l; P = 0.14) and SDMA (0.49 ±0.07 vs. 0.50 ±0.07 μmol/l; P = 0.61). The results did not change substantially on adjustment for LDL cholesterol and eGFR. In a multivariate analysis, parental CAD (P = 0.005) and LDL cholesterol (P = 0.06), but not ADMA, were independent positive IMT predictors., Conclusions: Our preliminary data suggest that elevated ADMA is not a part of the proatherogenic risk profile in the young adult offspring of patients with premature CAD.