Introduction: Hepcidin is a regulatory protein in iron metabolism; we do not know the role in chronic kidney disease anemia. Methods: 22 patients with CKD anemia and 15 patients with CKD without anemia were investigated. CKD anemia-inclusion criteria: over 18 years, hemoglobin ≤12 g/dl for women and ≤13 g/dl for men, no treatment for anemia 6 months before enrollment, glomerular filtration rate (eGFR) <60 ml/min/1.73m² and stable creatinine three months before enrollment. Exclusion criteria: infection, bleeding, malignancy, systemic or liver disease, immunosuppression, renal replacement therapy. CKD without anemia-inclusion criteria: over 18 years, no anemia or treatment for anemia, CKD with stable creatinine values three months before enrollment. Exclusion criteria: medical conditions known to have a role in the development of polycythemia. Hepcidin-25 and ferritin were measured by ELISA method. Erythropoietin (EPO), tumor necrosis factor (TNF)-α, interleukin (IL)-6 were evaluated using chemiluminescent enzyme immunometric assays. Unpaired T test, Pearson correlation and multiple regression were used for statistical analysis. Results: Hemoglobin values were significantly lower in anemia group. There were no differences in terms of eGFR, age, body mass index, serum hepcidin, erythropoietin, fibrinogen, IL-6, and TNF-α between CKD patients with and without anemia. Serum hepcidin correlated positively with ferritin (r=0.45 p<0.05), TNF-α (r=0.54, p<0.05) and negatively with erythropoietin (r=-0.51, p<0.05). Multiple linear regression analysis demonstrated that TNF-α is an independent predictor of serum hepcidin in our patients (p=0.003, R=0.71). Conclusion: We found no differences in serum hepcidin, erythropoietin and inflammatory markers in non-dialysis CKD patients with and without anemia.

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Obesity and chronic kidney disease are epidemic size. Chronic kidney disease (CKD) appears to be more common in obese, although interrelation is not supported by all authors.Aim: The aim of the study was to investigate the effects of overweight and obesity on glomerular filtration rate (GFR) and the relationship between body mass index (BMI) and other risk factors for CKD.Methods: This is a cross-sectional study on 627 patients admitted in a Nephrology Department between January 2007 - December 2011. Patients were divided according to eGFR in a CKD group and a non-CKD group. Patients were divided based on BMI in: normal (<25 kg/m2), overweight (≥ 25 kg/m2 and ≤30 kg/m2) and obese (>30 kg/m2). Demographical, clinical and laboratory data (serum creatinine, lipid parameters, etc) were used for the statistical analysis. The relationship between BMI (as a marker of obesity and overweight), glomerular filtration rate and other possible risk factors for chronic kidney disease was studied.Results: 43.70% patients were obese and 33.17% overweight. CKD prevalence was 58.69%. Logistic regression analysis showed that systolic blood pressure was the main determinant of CKD in our patients.Conclusion: Lack of association between BMI and CKD was demonstrated in our study.

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Over the past few decades, a series of innovative medicines have been developed in order to optimize anticoagulation therapy for atrial fibrillation (AF). As a result, a number of nonvitamin K antagonist oral anticoagulants (NOAC) that directly target the enzymatic activity of factor II and factor Xa have been successfully licensed providing a more predictable effect and better safety profile compared to conventional anticoagulants (heparins and vitamin K antagonists (VKAs)). However, comparative efficacy and safety data is limited in patients with advanced chronic kidney disease (i.e., CKD stage 4/5 and end stage renal disease) because patients with estimated glomerular filtration rate (eGFR) < 30 mL/min/1.73 m2 were actively excluded from landmark trials, thus representing a major clinical limitation for the currently available agents. However, the renal function of AF patients can be altered over time. On the other hand, patients with CKD have an increased risk of developing AF. This review article will provide an overview of current concepts and recent evidence guiding the clinical use of NOACs in patients with CKD requiring chronic anticoagulation, and the associated risks and benefits of treatment in this specific patient population.

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Introduction: Chronic inflammation has a proven role in atherogenesis, lipid profile parameters being related to cytokine production. In kidney transplant recipients, interleukin 6 (IL-6) is significantly associated with graft-related outcomes and also alterations of cholesterol and triglyceride metabolism. The aim of this study was to investigate the relationship between chronic inflammation and glucidic-lipidic metabolism disorders in a group of patients with kidney transplantation as renal replacement therapy. Methods: A prospective observational study which enrolled thirtysix non-diabetic kidney transplant recipients was conducted in the Nephrology and Peritoneal Dialysis Department, County Clinic Hospital of Tirgu Mures. The study group was divided as following: recipients with serum IL-6 concentration higher than 3.8 pg/ml (group A) and IL-6 within the normal range (group B). Results: Allograft recipients with higher serum IL-6 had significant higher erytrocyte sedimentation rate(ESR, p=0.0067). Patients with over-the-range levels of IL-6 had significant higher levels of serum cholesterol and LDL-cholesterol respectively (p=0.0242 and p=0.0081). Serum Apo-B was also significant higher in Group A than Group B. Protein excretion was significant higher in patients from group A (p=0.0013). No statistical significant relationship could be proven between elevated levels of IL-6 and hbA1c, insulin and glycosuria disturbances in the two groups. Also, we found no statistical significant association between resistivity and pulsatility indices (both hilum and intragraft) or carotid intima media thickness. Conclusion: Serum interleukin 6 is related to lipid profile disorders and less to glucidic metabolism anomalies in non-diabetic kidney transplant recipients.

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