The twinkling artifact is a very useful color Doppler ultrasound tool for the detection of small urinary stones. We suggest the routine use of color Doppler in all suspicious cases in order to avoid unnecessary irradiating and expensive radiological methods.

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.

Objective: The aim of this study was to assess the serum levels of Lipoprotein(a) [Lp(a)] in subjects with thyroid disorders, as well as to investigate their relationship with lipid profile and the markers of thyroid function and autoimmunity, admitting that elevated Lp(a) levels and dyslipidemia caused by thyroid disorders synergistically increased the atherogenic process. Methods: This study enrolled 38 subjects with hypothyroidism, 30 with hyperthyroidism and 55 with euthyroidism. The following parameters were measured: Lp(a), apolipoprotein AI (apo AI), apolipoprotein B (apo B), total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), very-low-density lipoprotein (VLDL), thyroid stimulating hormone (TSH), free thyroxine (FT4), triiodothyronine (T3), thyroid-peroxidase antibody (TPO-Ab). Results: Lp(a) was found with increased mean serum levels in hypothyroid subjects (483.28 ± 281.55 mg/L). Hyperthyroid subjects showed normal levels (253.13 ± 94.29 mg/L) of Lp(a), but significantly lower than those with hypothyroidism and slightly increased levels in the euthyroid subjects (305 ± 100.44 mg/L). In hypothyroidism a significant positive correlation between Lp(a) and TSH, apo B, TC, TG, TC/HDL, VLDL levels and a negative correlation with FT4, T3 and apo AI/B (p < 0.05) was observed. No correlations were found between serum Lp(a) levels, lipids profile and thyroid function parameters in hyperthyroid subjects, neither with TPO-Ab. Conclusions: The association of hypothyroidism with increased levels of Lp(a) seems to increase the already high cardiovascular risk in the hypothyroid subjects, while increased levels of Lp(a) represents independently a relevant cardiovascular risk factor.

Introduction. Cardiovascular risk factors, pre-existing comorbidities, molecular factors, and the direct effects of second- and third-generation BCR-ABL1 tyrosine kinase inhibitors on the vascular endothelium contribute to the progression of cardiovascular (CV) events, especially atherothrombotic conditions. The study objective was to evaluate comorbidities, the cardiovascular risk profile, and events throughout the chronic myeloid leukaemia disease course. Methods. Retrospective data from adults who experienced haematology treatment at a single centre were continuously updated and followed throughout the disease course. A total of 43 subjects conforming with the inclusion and exclusion criteria of the study protocol were finally recruited. The median disease course was 77.0 ± 17.5 months. Statistical analyses were performed. Results. More than three CV risk factors were identified in 41.9% of cases. Almost half of the cases had relevant comorbidities (Charlson Comorbidity Index (CCI) ≥ 4), and no statistically significant comorbidities were found when comparing the tyrosine kinase inhibitor (TKI) treatment subgroups (p = 0.53). The patients at high and very high CV risk, according to Systematic Coronary Risk Evaluation (SCORE) risk classification, had 75.0% CV events (12/22 patients), p = 0.45. Throughout the disease course, 19 cardiovascular events were reported in 37.2% patients (13 males/3 females, p < 0.03). Conclusion. To the best of our knowledge, this is the first study exploring cardiovascular risk factors in Romanian chronic myeloid leukaemia patients. This study reinforces the need for close long-term follow-up that should be performed by a multidisciplinary team. The target should be not only the disease and specific drug-related toxicities but, also, the identification of cardiovascular and metabolic risk factors before the commencement of and throughout TKI therapy.

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.

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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