Browsing by Author "Dimkovic, Nada (6603958094)"

A 69-year-old woman presented with severe anemia, proteinuria, microscopic hematuria and rapidly progressive renal failure. She was admitted to the nephrology department due to severe deterioration of renal function with complaints of malaise, fever, dry cough and occasional epistaxis that appeared 2 months prior to admission. Histopathologic examination of a specimen from kidney biopsy and immunologic findings revealed ANCA positive pauci-immune crescentic glomerulonephritis. The patient had a history of ovarian granulosa cell tumor and lung metastases that were treated surgically with postoperative radiotherapy and chemotherapy. Thoracic computed tomography showed tissue neoplasm in the right lung and ultrasound-guided percutaneous transthoracic biopsy confirmed granulosa cell tumor. That was a relapse, thirty-nine years after initial treatment of malignant disease and twenty-four years after surgical resection of metastases from both lungs. Although the association between malignancy and vasculitis has been well known for decades, this is the first described case of ANCA vasculitis associated with any type of gynecological malignancy and glomerulonephritis. © 2023, Cent Eur J Immunol. All Rights Reserved.

Background/Aims: Compared to all other complications, literature data about vascular access aneurysm (VAA) are the scarcest. The aim of this cross-sectional study was to evaluate the prevalence of arteriovenous fistula (AVF) aneurysms and to confirm the risk factors for their appearance. Methods: The presence, number and morphological characteristics of AVF aneurysms were confirmed, and according to the score of AVF aneurysm (the sum of the length and width in cm), patients were classified into group 1 (score ≤12) and group 2 (score >12). Analysis included the last data from the medical records including vascular calcifications score. Results: Out of 181 patients, 150 with native fistula were included in this study. Aneurysmatic changes were detected in 90 (60%) patients, and the majority had two or more aneurysms. VAA were more frequent in patients with adult polycystic kidney disease (ADPKD) than in other diagnostic categories. By using forward stepwise logistic regression, we confirmed that patients on high-flux hemodialysis (HD) had 5.3-fold higher risk, and patients with diabetes mellitus had 5.8-fold less risk for developing AVF aneurysm. While vascular calcification score did not influence the incidence of VAA, higher PWV had significant negative influence on formation of AVF aneurysm (OR 1.25, 95% CI 1.003-1.56, p = 0.047). By ROC curve analysis, it was determined that patients who were longer than 5.7 years on HD had greater risk for developing VAA (area = 0.741, p = 0.000). Conclusion: This single-center study confirmed the very high prevalence of VAA (60%). Aneurysms were more frequent in patients with ADPKD and in those who had longer dialysis vintage on high-flux membranes with higher blood flow rate. © 2013 S. Karger AG, Basel.

Background: Oxidative stress in patients with end-stage renal disease (ESRD) is associated with long-term cardiovascular complications. The cytosolic family of glutathione S-transferases (GSTs) is involved in the detoxication of various toxic compounds and antioxidant protection. GST omega class members, GSTO1 and GSTO2 possess, unlike other GSTs, dehydroascorbate reductase and deglutathionylation activities. The aim of this study was to clarify the role of genetic polymorphisms of GSTO1 (rs4925) and GSTO2 (rs156697) as risk determinants for ESRD development, as well as in the survival of these patients. Methods: A total of 199 patients and 199 healthy subjects were included in the study and genotyped for both GSTO1 and GSTO2 polymorphism. Protein thiol and carbonyl groups as markers of protein oxidative damage were determined spectrophotometrically. Cox proportional hazard model and Kaplan-Meier analysis were performed to investigate the role of GSTO1 and GSTO2 genetic polymorphism on mortality of ESRD patients during the follow-up period (36 month). Results: Individuals carrying the variant GSTO2 GG genotype were at 2.45-fold higher risk of ESRD development compared to the wild type GSTO2 AA genotype (OR=2.45; 95%CI=1.18-5.07; p=0.016). The results of GSTO1/GSTO2 haplotype analysis showed that the haplotype combi - nation of GSTO1 (∗A)/GSTO2 (∗A) (GSTO1 variant/GSTO2 wild type allele) was protective for ESRD (OR=0.23 95%CI=0.12-0.44, p=0.001). Patients carrying at least one GSTO1 reference allele have shorter mean overall (Log rank=2.844, p =0.241) and cardiovascular survival probability (Log rank=4.211, p=0.122). Conclusions: GSTO polymorphisms have been shown to act as significant markers in assessing the risk of ESRD development and patients' survival. © by Tatjana Simic 2016.

Background: Oxidative stress in patients with end-stage renal disease (ESRD) is associated with long-term cardiovascular complications. The cytosolic family of glutathione S-transferases (GSTs) is involved in the detoxication of various toxic compounds and antioxidant protection. GST omega class members, GSTO1 and GSTO2 possess, unlike other GSTs, dehydroascorbate reductase and deglutathionylation activities. The aim of this study was to clarify the role of genetic polymorphisms of GSTO1 (rs4925) and GSTO2 (rs156697) as risk determinants for ESRD development, as well as in the survival of these patients. Methods: A total of 199 patients and 199 healthy subjects were included in the study and genotyped for both GSTO1 and GSTO2 polymorphism. Protein thiol and carbonyl groups as markers of protein oxidative damage were determined spectrophotometrically. Cox proportional hazard model and Kaplan-Meier analysis were performed to investigate the role of GSTO1 and GSTO2 genetic polymorphism on mortality of ESRD patients during the follow-up period (36 month). Results: Individuals carrying the variant GSTO2 GG genotype were at 2.45-fold higher risk of ESRD development compared to the wild type GSTO2 AA genotype (OR=2.45; 95%CI=1.18-5.07; p=0.016). The results of GSTO1/GSTO2 haplotype analysis showed that the haplotype combi - nation of GSTO1 (∗A)/GSTO2 (∗A) (GSTO1 variant/GSTO2 wild type allele) was protective for ESRD (OR=0.23 95%CI=0.12-0.44, p=0.001). Patients carrying at least one GSTO1 reference allele have shorter mean overall (Log rank=2.844, p =0.241) and cardiovascular survival probability (Log rank=4.211, p=0.122). Conclusions: GSTO polymorphisms have been shown to act as significant markers in assessing the risk of ESRD development and patients' survival. © by Tatjana Simic 2016.

Background: The presence of glutathione transferase (GST) M1 null genotype (GSTM1-null) in end-stage renal disease (ESRD) patients is associated with lower overall survival rate in comparison to those with GSTM1-active variants. We examined association between GSTM1 and GSTT1 deletion polymorphisms as well as SNPs in GSTA1/rs3957357 and GSTP1/rs1695 genes with overall and cause-specific cardiovascular mortality in ESRD patients. Methods. Total of 199 patients undergoing hemodialysis were included in the study. Median value of time elapsed from dialysis initiation until the death, or the end of follow-up was 8 ± 5 years. The effect of GSTM1, GSTT1, GSTP1 and GSTA1 gene polymorphisms on predicting overall and specific cardiovascular outcomes (myocardial infarction, MI or stroke) was analyzed using Cox regression model, and differences in survival were determined by Kaplan-Meier. Results: GSTM1-null genotype in ESRD patients was found to be independent predictor of overall and cardiovascular mortality. However, after false discovery rate and Bonferroni corrections this effect was lost. The borderline effect modification by wild-type GSTA1*A/*A genotype on associations between GSTM1-null and analyzed outcomes was found only for death from stroke. Homozygous carriers of combined GSTM1*0/GSTA1*A genotype exhibited significantly shorter time to death of stroke or MI in comparison with carriers of either GSTM1-active or at least one GSTA1*B gene variant. The best survival rate regarding cardiovascular outcome was found for ESRD patients with combined GSTM1-active and mutant GSTA1*B/*B genotype. Conclusions: Combined GSTM1*0/GSTA1*A genotypes might be considered as genetic markers for cardiovascular death risk in ESRD patients, which may permit targeting of preventive and early intervention. © 2014 Suvakov et al.; licensee BioMed Central Ltd.

Chronic kidney disease (CKD) is an important factor that contributes to the increase of all-cause morbidity and mortality in the group of non-communicable diseases, and it is also recognized as a strong and independent risk factor that contributes to cardiovascular disease (CVD). CVDs are a consequence of the action of a large number of risk factors among which are traditional and non-traditional. These risk factors have been the subject of a large number of studies which partially explained the unfavorable cardiovascular (CV) outcome of CKD patients. Therefore, valid studies about clinical and biohumoral predictors are of particular importance, especially in the early stages of renal disease, that is, in patients with creatinine clearance below 60 ml/min/1.73 m2 when preventive measures are most effective. Among potential predictors of adverse CV outcome are biomarkers of inflammation (Interleukin-18—IL-18), oxidative stress (ischemia-modified albumin—IMA; superoxide dismutase—SOD), acute kidney injury (kidney injury molecule-1—KIM-1; neutrophil gelatinase–associated lipocalin—NGAL), and microribonucleic acids (specific microRNA-133a). In this review, we tried to confirm the relationship between risk factors of CKD and CVD and newer, less frequently examined biomarkers with the occurrence of incidental CV events in renal patients. © The Author(s) 2022.

Chronic kidney disease (CKD) is an important factor that contributes to the increase of all-cause morbidity and mortality in the group of non-communicable diseases, and it is also recognized as a strong and independent risk factor that contributes to cardiovascular disease (CVD). CVDs are a consequence of the action of a large number of risk factors among which are traditional and non-traditional. These risk factors have been the subject of a large number of studies which partially explained the unfavorable cardiovascular (CV) outcome of CKD patients. Therefore, valid studies about clinical and biohumoral predictors are of particular importance, especially in the early stages of renal disease, that is, in patients with creatinine clearance below 60 ml/min/1.73 m2 when preventive measures are most effective. Among potential predictors of adverse CV outcome are biomarkers of inflammation (Interleukin-18—IL-18), oxidative stress (ischemia-modified albumin—IMA; superoxide dismutase—SOD), acute kidney injury (kidney injury molecule-1—KIM-1; neutrophil gelatinase–associated lipocalin—NGAL), and microribonucleic acids (specific microRNA-133a). In this review, we tried to confirm the relationship between risk factors of CKD and CVD and newer, less frequently examined biomarkers with the occurrence of incidental CV events in renal patients. © The Author(s) 2022.

Purpose: Arteriovenous fistula (AVF) is the preferred vascular access for hemodialysis. The impact of vascular calcification process on AVF survival remains unclear and results of several studies about this issue are controversial. In the light of the new knowledge about the different susceptibility for calcification process in different blood vessels, the aim of our study was to analyze whether the calcification of AVF-blood vessels may have an impact on AVF longevity. Methods: The study included 90 patients, 49 males and 41 females, all of them Caucasians, with a mean age 62 ± 11 years, on regular hemodialysis for more than 1 year with patent primary AVFs. Vascular calcification in AVF-blood vessels or in the anastomotic region was detected using X-ray examination. Results: Calcification in AVF-blood vessels was found in 62% of patients. Binary logistic regression analysis demonstrated that male gender, presence of diabetes mellitus and longer duration of AVF before calcification determination were associated with calcification of AVF-blood vessels. Using a Cox proportional hazard model adjusted for these standardized predicted values revealed that patients with present AVF-blood vessels calcification had increased risk to develop AVF failure with a hazard rate of 3.42 (95% confidence interval 1.00–11.67; P = 0.049). Conclusions: Calcifications of AVF-blood vessels are found frequently among dialysis patients and may jeopardize the survival of native AVF. We suggested the local X-ray as simple and valid method for detection of patients that are at risk for AVFs failure which should be monitored more closely. © 2017, Springer Science+Business Media Dordrecht.

Chronic kidney disease in the later stages poses many treatment challenges. Hyperphosphatemia is one that is well-known and is often linked to increased cardiovascular morbidity/mortality. Currently, a number of phosphate binders are available that act to conserve serum phosphate at normal or near normal levels. However, it is the overall profile of all binders that needs to be taken into account and the risks and the potential benefits associated with each agent must be balanced when selecting a particular phosphate binder. It is known that calcium-based binders, although effective phosphate binders, may lead to hypercalcemia and/or positive calcium balance and cardiovascular calcification. One, new non-calcium phosphate binder, recently approved in Europe, is colestilan. Colestilan possesses a range of properties that may afford further advantages over simply reducing serum phosphate. This review assesses the pharmacology and clinical data of colestilan used to treat hyperphosphatemia in chronic kidney disease stage 5 patients on dialysis. The article was written based on literature searches using PubMed to find articles published on phosphate binders or colestilan over the last 10 years. © 2015 Informa UK Ltd.

Objective To assess the effect of tibolone on markers of vascular risk in postmenopausal women who were receiving hemodialysis. Design One-year open-label study. Setting "Zvezdara" University Medical Center, Belgrade, Serbia. Patient(s) Twenty-eight postmenopausal women undergoing chronic hemodialysis. Intervention(s) Fifteen women received tibolone 2.5 mg three times per week; 13 other women served as controls. Main outcome measure(s) Mean arterial pressure and weight were measured at baseline and at 6 and 12 months, and blood was collected for insulin, total cholesterol, low-density lipoprotein, high-density lipoprotein, triglycerides, lipoprotein(a), high-sensitivity C-reactive protein (hs-CRP), endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), and markers of renal function. Result(s) Mean arterial pressure fell in the tibolone but not in the control group at 6 and 12 months versus baseline (mean [SD]: 93 [15] vs. 105 [11] mmHg and 94 [10] vs. 105 [11] mmHg, respectively). Weight, insulin, lipids, lipoprotein(a), hs-CRP, ET-1, VEGF, and renal function remained unchanged within each group, but high-density lipoprotein concentrations fell in the tibolone group after 12 months (1.2 [0.3] vs. 1.6 [0.6] mmol/L). Conclusion(s) The effects of tibolone on markers of vascular risk in postmenopausal women who are receiving hemodialysis and healthy women appear to differ. This should be taken into account when tailoring menopausal therapies to the specific requirements of each individual. © 2004 by American Society for Reproductive Medicine.

This prospective study was conducted with the aim of examining the efficacy of lowering dialysate calcium (dCa) in order to: (i) stimulate bone turnover in hemodialysis patients with biochemical signs of adynamic bone disease (ABD) (hypercalcemia, normal alkaline phosphatase and intact parathyroid hormone (iPTH) <150 pg/mL); and (ii) diminish hypercalcemia in patients with secondary hyperparathyroidism (sHPT) (hypercalcemia, high alkaline phosphatase and iPTH > 400 pg/mL), thus permitting the use of calcium-containing phosphorus binders and vitamin D metabolites. Patients were divided into: an ABD-treated group (24 patients), a sHPT-treated group (18 patients), an ABD-control group (12 patients) and a sHPT-control group (11 patients). For the ABD- and sHPT-treated patients, hemodialysis was conducted with dCa 1.5 mmol/L for three months and then with dCa 1.25 mmol/L for an additional three months, while in the control groups hemodialysis was conducted with dCa 1.75 mmol/L during the entire study. Reduction of dCa in patients with ABD caused a slight but insignificant decrease of Ca, but a significant and permanent increase of bone-specific alkaline phosphatase and intact parathyroid hormone level serum levels. Reduction of dCa in patients with sHPT slightly but insignificantly decreased Ca and intact parathyroid hormone level values. Nevertheless, this enabled the calcium-based phosphate binder dose to be raised and vitamin D3 metabolites to be introduced. Logistic regression analysis indicated that milder bone disease (both ABD and sHPT) was associated with more the favorable effect of dCa reduction. Thus, low dCa stimulated parathyroid glands and increased bone turnover in ABD patients, and enabled better control of mineral metabolism in sHPT patients. © 2007 International Society for Apheresis.

Introduction: Hyperphosphataemia is common in chronic kidney disease (CKD), particularly in the late stages and is associated with secondary hyperparathyroidism, abnormal bone mineralisation and increased cardiovascular morbidity/mortality. At present, there is a range of phosphate binders designed to keep serum phosphate at normal or near normal levels. Colestilan is a new binder that offers additional actions that may afford further benefits over simply lowering phosphate.Areas covered: This paper reviews the pharmacology and clinical data currently available in the use of colestilan to treat hyperphosphataemia in CKD stage 5 patients on dialysis.Expert opinion: Available phosphate binders lower serum phosphorus levels to a clinically relevant extent. The balance between the risks and the potential benefits associated with each agent must be considered when choosing a binder. Calcium-based binders can lead to hypercalcaemia and/or positive calcium balance and cardiovascular calcification. Like sevelamer, colestilan is not absorbed and there is no evidence of any risk of hypercalcaemia. In addition, a significant lowering of low-density lipoprotein-cholesterol, similar to simvastatin, a reduction in plasma uric acid and a reduction in high glycosylated haemoglobin values suggest additional beneficial actions that may convert to reductions in mortality. © 2014 Informa UK, Ltd.

Introduction: Hyperphosphataemia is common in chronic kidney disease (CKD), particularly in the late stages and is associated with secondary hyperparathyroidism, abnormal bone mineralisation and increased cardiovascular morbidity/mortality. At present, there is a range of phosphate binders designed to keep serum phosphate at normal or near normal levels. Colestilan is a new binder that offers additional actions that may afford further benefits over simply lowering phosphate.Areas covered: This paper reviews the pharmacology and clinical data currently available in the use of colestilan to treat hyperphosphataemia in CKD stage 5 patients on dialysis.Expert opinion: Available phosphate binders lower serum phosphorus levels to a clinically relevant extent. The balance between the risks and the potential benefits associated with each agent must be considered when choosing a binder. Calcium-based binders can lead to hypercalcaemia and/or positive calcium balance and cardiovascular calcification. Like sevelamer, colestilan is not absorbed and there is no evidence of any risk of hypercalcaemia. In addition, a significant lowering of low-density lipoprotein-cholesterol, similar to simvastatin, a reduction in plasma uric acid and a reduction in high glycosylated haemoglobin values suggest additional beneficial actions that may convert to reductions in mortality. © 2014 Informa UK, Ltd.

Introduction. Renal biopsy represents a diagnostic method that provides an acurrate diagnosis and adequate treatment of different renal diseases. The first biopsy in our Center was done in June 1982, but it has been performing routinely since 1984. The aim of this study was to report the histopathological features of biopsy proven kidney disease during the past 30 years. Methods. During 30 years, a total of 563 biopsies were performed, of which 530(94%) were succesfull. Data about gender, age, clinical syndrome and histopatological finding were collected from the medical records. Results. The mean age of our patients was 48±11 years, 53% were man (No=272). In the first decade (1982-1994) we performed 118(mean age 50±13), in the second (1995-2004) 208 (mean age 46±14), and in the third decade (2005-2014) 189 renal biopsies (mean age 50±16). Mean number of glomeruli per biopsy was 18±11. There were only two serious complications. The most common clinical syndromes as indication for renal biopsy were: nephrotic proteinuria (41%) followed by asymptomatic urinary abnormalities (AUA-14.8%), chronic renal failure (CRF-13.8%), acute kidney injury (AKI-12.8%), nephritic syndrome (7.6%), systemic lupus erytematosus (SLE-4.5%), isolated haematuria (2.7% of the cases) and other (2.9%). The major histological groups identified were: primary glomerulonephritis (GN) (62.3%), secondary GN (21.2%), and other (16.5% of the cases). The most common primary glomerulonephritis (PGN) were focal segmental glomerulosclerosis-FSGS (19.4%) followed by IgA nephropathy-IgAN (18.8%), membranous GNMGN (16.4%) and mesangial proliferation-MesGN (16%). Interstitial changes were present in 55% of biopsy samples in the first, in 66% in the second and in 63% in the third decade. Blood vessel changes were present in 39% of biopsy samples in the first, in 62% in the second and in 72% in the third decade. Conclusions. The most frequent finding among PGN was mesangioproliferative GN (including IgAN, alltogether 34.8%) followed by FSGS and MGN. Apart from succesful biopsies, there are several aspects to be improved in the future including expanding indications and earlier procedure during the course of chronic kidney disease-CKD.

Authors want to correct the list of authors by expanding the number of coauthors and by including all contributors in the Vascular Access Study Group. Vascular Access Study Group (in alphabetic order): Andric Branislav, Antic Miodrag, Aracki Snezana, Arsenovic Aleksandra, Berto Sabo Anika, Bogdanovic Jasmina, Cekovic Biljana, Cuckovic Cedomir, Cukic Zoran, Cveticanin Anica, Djordjevic Verica, Dudic Svetlana, Gajic Snezana, Gojakovic Biljana, Golubovic Predrag, Gucic Ljubinka, Hadzibulic Edvin, Hadzifejzovic Mersada, Hamzagic Nedim, Haviza-Lilic Branimir, Ilic Mira, Ilic Nasta, Jelacic Rosa, Kostic Mirjana, Kovacevic Miodrag, Lazarevic Tatjana, Markovic Rodoljub, Micunovic Vesna, Milenkovic Olgica, Milenkovic Radomir, Milenkovic Srboljub, Milicevic Biserka, Milicevic Olivera, Nikolic Zora, Obrenovic Slavica, Orescanin Mira, Pavlovic Stevan, Pesic Snezana, Petkovic Dobrila, Pilipovic Dragana, Prokopovic Miomir, Radovanovic Zoran, Rakic Nenad, Rangelov Vanja, Sefer Kornelija, Sibalic Simin Marija, Stefanovic Nikola, Stojanovic Dragoslav, Stojanovic Stanojevic Marina, Tirmenstajn Jankovic Biserka, Vasic Jovanovic Vesna, Vasilic Kokotovic Olivera, Vojinovic Goran, Vuckovic Dragana, Vukelic Vesna, Vukic Jasmina, Zagorac Nikola, Zec Nenad. © 2017, Springer Science+Business Media Dordrecht.

Background. Colestilan is a non-absorbed, non-calciumbased, phosphate binder. It also binds bile acids and reduces serum levels of low-density lipoprotein cholesterol (LDL-C). This study evaluated the efficacy of a range of fixed doses of colestilan compared with placebo for the control of serum phosphorus and LDL-C levels in patients with CKD stage 5 on dialysis. Methods. This was a multicentre, randomized, double-blind, placebo-controlled, multiple fixed-dose trial in which 642 patients with CKD stage 5 on dialysis who had both hyperphosphataemia and dyslipidaemia, were randomized to treatment with colestilan 3, 6, 9, 12 or 15 g/day or placebo for 12 weeks. The co-primary endpoints were the mean changes in serum phosphorus and the mean per cent change in LDL-C from baseline to Week 12. Results. A significantly greater mean reduction in serum phosphorus level from baseline to Week 12 than seen with placebo was seen with 9 g (-0.28 mmol/L) and pooled colestilan 12/15 g (-0.34 mmol/L). The per cent reduction in LDL-C level was significantly greater with colestilan 3, 6 and 9 g and pooled colestilan 12/15 g than with placebo (reduction ranged from 15.9 to 27.6% dependent on dose). Colestilan also reduced total cholesterol, oxidized LDL-C, HbA1c and uric acid levels, and did not increase serum calcium levels. Colestilan was generally well tolerated; the most common adverse events affected the gastrointestinal system. Conclusions. Colestilan is an effective treatment for hyperphosphataemia, and provides beneficial effects on other metabolic parameters associated with cardiovascular risk, notably LDL-C. © The Author 2013.

BackgroundIncreased oxidative stress is a hallmark of end-stage renal disease (ESRD). Glutathione S-transferases (GST) are involved in the detoxification of xenobiotics and protection of oxidative damage. We hypothesized that genetic polymorphism in antioxidant enzymes GSTA1, GSTM1, GSTP1 and GSTT1 is more frequent in ESRD and modulates the degree of oxidative stress in these patients.MethodsGSTA1, GSTM1, GSTP1 and GSTT1 genotypes were determined in 199 ESRD patients and 199 age-and gender-matched controls. Markers of protein and lipid oxidative damage [thiol groups, carbonyl groups, advanced oxidative protein products, nitrotyrosine, malondialdehyde (MDA) and MDA adducts], together with total oxidant status and pro-oxidant-antioxidant balance were determined. Results Individual GST polymorphisms influence vulnerability to both protein and lipid oxidation, with GSTM1-null gene variant having the most pronounced effect. Furthermore, a strong combined effect of null/low-activity GSTM1, GSTT1, GSTA1 and GSTP1 genotypes in terms of susceptibility towards oxidative and carbonyl stress was found in ESRD patients. When patients were stratified according to GSTM1 and GSTT1, the highest oxidant damage was noted in those with the GSTM1-null/GSTT1-null genotype. The observed effect was even stronger in patients with the third low-activity GSTP1 or GSTA1 genotype. Finally, the level of oxidative and carbonyl stress was most pronounced in the subgroup of patients with all four null or low-activity GSTM1, GSTT1, GSTP1 and GSTA1 genotypes.ConclusionsAccording to the GST genotype, ESRD patients may be stratified in terms of the level of oxidative and carbonyl stress that might influence cardiovascular prognosis, but could also improve efforts towards individualization of antioxidant treatment. © 2013 The Author.

[No abstract available]

For adequate hemodialysis, functional vascular access is obligatory. Neointimal hyperplasia (NIH) has a central role in stenosis and thrombosis development, which represent the most frequent causes of vascular access failure. Polymorphism of different genes that have a significant role in endothelial function may have an impact on NIH development. Therefore, the aim of our study is to determine the effect of angiotensin-converting enzyme (ACE) I/D and matrix metalloproteinase-3 (MMP3) 5A/6A polymorphism on risk for developing vascular access failure in hemodialysis patients. The study included 200 patients on regular hemodialysis at Nephrology Department, University Medical Center Zvezdara. Retrospective analysis included a collection of general and vascular access data from medical records. Genetic analysis was performed by using polymerase chain reaction-restriction fragment length polymorphism method (PCR-RFLP). Patients were divided into two groups: Group 1 - patients who have never experienced vascular access failure and Group 2 - patients who have at least one spontaneous vascular access failure. There was no difference in age, gender, hemodialysis vintage, main diagnosis, presence of hypertension, and diabetes mellitus between the two groups. There were no statistically significant differences in the frequencies of ACE and MMP3 genotypes between the two groups. Without statistical significance, it was found that homozygotes for I allele had two times higher risk for developing vascular access failure than homozygotes for D allele (OR 2.00; 95%CI: 0.727-5.503; P = 0.180). In addition, patients with 5A allele have 1.7 times higher risk for developing vascular access failure compared with patients without this allele (OR 1.745; 95% CI: 0.868-3.507; P = 0.118). Patients with vascular access failure do not have different genotype distribution regarding ACE gene and MMP3 gene polymorphism as compared with patients without vascular access failure. Still, homozygotes for I allele and homozygotes for 5A allele have higher risk for developing vascular access failure compared with other patients. © 2019 Wolters Kluwer Medknow Publications. All rights reserved.

Background: This study investigated in a North American patient population the longer-term treatment effects of the phosphate binder, colestilan, in patients with CKD Stage 5D and hyperphosphataemia. Methods: One hundred and sixteen CKD Stage 5D patients with hyperphosphataemia were entered into a multi-centre, open-label study where they received flexible dose colestilan (6-15 g/day) to maintain serum phosphorus levels between 3.5 and 5.5 mg/dl. The primary endpoint was safety, assessed by treatment-emergent adverse events. Efficacy was assessed by changes in serum phosphorus, mineral metabolism, lipids, HbA1c, uric acid and bone markers. Results: Serum phosphorus was significantly reduced by 1.18 mg/dl (p < 0.001), from 6.99 mg/dl at baseline to 5.80 mg/dl at week 52. LDL-cholesterol was also significantly reduced as well as uric acid. Significant change was observed only for one bone marker - PINP. Most adverse events were of mild or moderate intensity. Nausea (22.4%), vomiting (21.6%), and diarrhoea (19.8%) were most commonly reported. Conclusions: Long-term flexible dosing with colestilan reduces serum phosphorus and demonstrates an acceptable safety and tolerability profile. © 2015 S. Karger AG, Basel. Copyright: All rights reserved.