BACKGROUND:Levels of zonulin, a surrogate marker of intestinal permeability, are elevated in various disorders including insulin resistance, obesity, celiac disease, and inflammatory bowel disease. We aimed to elucidate the association of zonulin levels and metabolic syndrome (MS) in renal transplant recipients.METHODS:Seventy-nine renal transplant recipients were enrolled. Diagnosis of MS was established employing the Adult Treatment Panel III (ATP III) criteria. Serum zonulin level was determined using the double antibody sandwich ELISA method.RESULTS:MS was encountered in 37 (41.6%) of the 79 patients. Serum zonulin level was significantly higher in patients with MS compared to those without MS (p < 0.001). Serum zonulin level correlated with presence of MS (r: 739, p < 0.001), abdominal obesity (r: 514, p < 0.001), fasting glucose level (r: 361, p: 0.001), presence of fasting glucose/diabetes criterion of MS (r: 316, p: 0.005), presence of low HDL criterion of MS (r: 266, p: 0.018), and BMI (r: 527, p < 0.001).CONCLUSIONS:A Zonulin-mediated increase in intestinal permeability may play a role in the pathogenesis of metabolic syndrome. We propose that zonulin may be a suitable surrogate marker of MS in renal transplant recipients.

The aim of our study was to investigate an association between E23K KCNJ11 gene polymorphism with anthropometric, biochemical, beta-cell secretion and insulin sensitivity parameters among adult ADPKD patients with normal kidney function and no diagnosis of diabetes. The comparison of genotype-phenotype associations between ADPKD and non-ADPKD subjects could reveal a hypothetical mechanism of genetic determination of diabetes speciic for ADPKD patients.

Amaç: Periferik kan lenfositlerinde mikronükleus (MN) oluşumu kanser gelişme riski için bir biyobelirteç olarak kullanılabilir. Bu çalışmada böbrek nakli hastalarında periferik lenfositlerde MN oluşumu ile malignite gelişimi arasındaki ilişkiyi değerlendirmeyi amaçladık. Hastalar ve Yöntem: Bu çalışmaya böbrek nakli sonrası malignite gelişen 10 böbrek nakli hastası alındı. Yaş ve cinsiyet uyumlu böbrek nakil sonrası malignite gelişmeyen 15 böbrek nakli hastası böbrek nakli kontrol grubu olarak çalışmaya dahil edildi. Ayrıca yaş ve cinsiyet uyumlu 12 sağlıklı gönüllü de sağlıklı kontrol grubu olarak çalışmaya dahil edildi. MN analizi sitokinez blok MN analizi ile yapıldı. Bulgular: Mononükleer hücrelerde MN sayısı malignitesi olan veya olmayan böbrek nakli hastalarında sağlıklı gönüllülerden anlamlı olarak daha yüksekti [sırasıyla 7.5 (2.0-11.0), 5.0 (0-12.0) ve 1.0 (0-9.0), p<0.001]. Benzer olarak binükleer hücrelerdeki MN sayısı malignitesi olan veya olmayan böbrek nakli hastalarında sağlıklı gönüllülerden anlamlı olarak daha yüksekti [sırasıyla 54.0 (8.0-199.0), 32.0 (0-182.0) ve 10.0 (2.00-29.00), p<0.001]. Aradaki fark istatistiksel olarak anlamlı olmamasına rağmen, hem mononükleer hücrelerde hem de binükleer hücrelerdeki MN sayısı malignitesi olan böbrek nakli hastalarında malignitesi olmayan böbrek nakli hastalarından daha yüksek saptandı. Sonuç: Binükleer ve mononükleer hücrelerdeki artmış MN sayısı böbrek naklinden sonra malignite gelişimi için umut vaat eden bir biyobelirteç olabilir.

Background. The pathogenesis of post -transplantation erythrocytosis (PTE) is not well understood and appears to be multifactorial. Our hypothesis in this study was that several factors, including toxicity of calcineurin inhibitor, immunologic factors, and chronic allograft nephropathy, can trigger local tissue hypoxia in peritubular interstitium, which is where production of erythropoietin (EPO) takes place. This local interstitial tissue hypoxia can cause an increase in renal EPO production, which induces the development of PTE. Methods. This cross-sectional study included 15 renal transplant recipients, in whom polycythemia developed after kidney transplantation, with elevated hematocrit level to >51%. Forty-eight age- and gender-matched renal transplant recipients with normal hematocrit level were included as the renal transplant control group. In addition, 13 age- and gender-matched healthy subjects were also included as the healthy control group. We used urine hypoxia-inducible factor-2 alpha (HIF-2 alpha) levels to evaluate whether there is local tissue hypoxia in renal allograft. HIF-2 alpha levels were measured by double antibody sandwich enzyme-linked immunosorbent assay (ELISA). Serum EPO and insulin-like growth factor-1 (IGF-1) levels were also measured. Results. HIF-2 alpha levels were significantly lower in the polycythemia group than the other two groups, but there was no significant difference between the healthy control group and the renal transplant control group with regard to HIF-2 alpha levels. There was no significant difference among the 3 study groups in terms of levels of serum EPO and IGF-1. Conclusion. Local tissue hypoxia in renal allograft does not seem to play an important role in the development of PTE.

OBJECTIVE: In this study, we aimed to investigate whether serum GGT levels are associated with microalbuminuria in patients with diabetes mellitus. MATERIAL and METHODS: The study included 107 diabetic patients. Albuminuria was assessed using urinary albumin creatinine ratio (UACR). Normoalbuminuria and microalbuminuria were defined as UACR <0.030 and UACR of 0.030-0.300, respectively. RESULTS: Fifty-six (52.3%) of the 107 patients had microalbuminuria, whereas 51 (47.7%) patients were normoalbuminuric. Serum GGT levels were significantly higher in patients with microalbuminuria than in those with normoalbuminuria [27 (4-315) IU/L vs. 21 (8-77) IU/L, p: 0.011; respectively]. Serum GGT values were divided as high or low according to the median value. High serum GGT levels were more frequent in patients with microalbuminuria than in those with normoalbuminuria [35 (62.5%) vs. 17 (33.3%), p: 0.002]. UACR value s were positively correlated with the serum GGT level (r: 0.331, p: <0.001), age (r: 0.195, p: 0.044), and duration of diabetes mellitus (r: 0.202, p: 0.037), and negatively correlated with estimated glomerular filtration rate (eGFR) (r: -0.441, p: <0.001). In the multivariate analysis (binary logistic regression analysis), eGFR and GGT status were found to be independent risk factors for microalbuminuria. CONCLUSION: Serum GGT levels were significantly higher in microalbuminuric diabetic patients. The underlying cause of this finding should be elucidated.

Autosomal-dominant polycystic kidney disease (ADPKD) is associated with oxidative stress and hypertension development before renal function decline and cardiovascular disease development. Oxidative stress-responsive kinase-1 (OSR-1) participates in the signaling regulating Na+ transport during oxidative stress and also plays a role in the regulation of cell volume and blood pressure. Therefore, we aimed to investigate the potential role of OSR-1 in ADPKD patients. Eighty ADPKD patients, 80 healthy controls, and 80 non-ADPKD patients with hypertension were enrolled in this cross-sectional study. Twenty-four-hour ambulatory blood pressure monitoring was conducted in all participants. Blood samples were taken after 12-h fasting for the measurement of biochemical parameters and OSR-1 gene expression. Vascular dysfunction was assessed using ischemia-induced forearm flow-mediated vasodilation (FMD). Briefly, of the 80 ADPKD patients, 41(51%) were male, and 53(66%) of them were hypertensive. The mean age of the 80 controls was 35.3 +/- 12.6 years, and 37(46%) of them were male. The mean age of the 80 non-ADPKD patients with hypertension was 44.6 +/- 11.9 years, and 38(47.5) of them were male. There were significant differences in serum OSR-1 gene expression between the ADPKD patients and the control subjects. Serum OSR-1 gene expression was also significantly increased in hypertensive ADPKD patients in comparison with both normotensive ADPKD counterparts and non-ADPKD hypertensive subjects. Serum OSR-1 gene expression was increased in patients with ADPKD than healthy subjects. Low estimated glomerular filtration rate (eGFR), OSR-1 gene expression, total kidney volume (TKV), and high-density lipoprotein (HDL) were also independently associated with hypertension in ADPKD patients.

A 28-year-old female patient, who had been undergoing continuous ambulatory peritoneal dialysis (CAPD) because of end-stage renal disease of unknown origin, presented with secondary amenorrhea, nausea, vomiting, and anorexia and was suspected to be pregnant. The diagnosis of pregnancy was confirmed by ultrasonography (USG), which revealed that she was 11 weeks pregnant. Her physical examination was normal. Her residual Kt/Vurea was 4.38 and weekly residual creatinine clearance was 161.97 mL/min. She came to her routine follow-ups every month until intrauterine growth retardation was detected by USG and her blood pressure was found to be 170/110 mmHg while she was 35 weeks pregnant. A Caesarean section was performed and a 1900 g healthy baby was born. She continued CAPD after termination of pregnancy.

OBJECTIVE: Our main purpose was to evaluate the epidemiological properties and mortality rate of this study and to evaluate the etiology and factors associated with mortality in patients with ARF. MATERIAL and METHODS: In this prospective observational study a total of 541 patients with ARF were assessed between January 2008 - January 2012. The etiological spectrum and predictors of mortality were evaluated in this population. RESULTS: The mean age was 64.9 ± 15.6 years and the majority of patients were male. The most common etiology of ARF was medical causes. Diarrheal disease and drug-induced ARF were the major medical causes. One hundred and fi fty four patients needed dialysis. The most common cause of death was cardiopulmonary failure. In multivariate analysis, dialysis necessity, age, C-reactive protein, serum sodium, serum phosphorus, serum albumin, and hemoglobin were independently associated with death after adjusting for other variables. CONCLUSION: ARF resulting from medical diseases was higher compared to surgical causes. Use of medication with antibiotics and non-steroid anti-infl ammatory drugs was predominantly increased; however the main cause was diarrheal disease. Hypoalbuminemia, anemia, dialysis requirement and hyperphosphatemia were found to be the main predictors of mortality in patients with ARF.

Renal amyloid A (AA) amyloidosis is one of the systemic etiologies of nephrotic syndrome (NS) in adults. Chronic inflammatory conditions including rheumatoid arthritis, familial periodic fever syndromes, spondyloarthropathies, and chronic bacterial infections such as tuberculosis and chronic osteomyelitis are the common causes of secondary AA amyloidosis. In this case report, we reported a patient presented with nephrotic syndrome and secondary AA amyloidosis due to chronic hepatitis B infection in the absence of any glomerulonephritis.

A 54-year-old female who had been receiving continuous ambulatory peritoneal dialysis therapy for 5 years because of end-stage renal disease, was admitted to hospital because of peritonitis due to Candida albicans. Ultrasonography showed locular fluid in abdominal subcutaneous tissue. E. coli was isolated from the peritoneal fluid culture and cephoperazone-sulbactam therapy was started. Nose bleeding manifested on the 9th day after initial treatment. Prothrombin time, activated partial thromboplastin time, and INR were found to be 61.1 sec, 159.2 sec, and 5.55, respectively. She had no liver disease, obstructive jaundice, or other disease disrupting the intestinal absorption of vitamin K. Hepatitis markers were negative and liver function tests were normal. Warfarin and conventional heparin were also not used. The coagulation disorder was attributed to treatment with cephoperazonesulbactam and the treatment was discontinued. The bleeding stopped with intravenous vitamin K and fresh frozen plasma and the coagulation tests returned to normal range. Empirical meropenem and vancomycin were started due to ongoing fever. She was connected to a mechanical ventilator because of respiratory failure due to aspiration pneumonia. She later died due to aspiration pneumonia. Cephoperazone-sulbactam may lead to coagulopathy by affecting the metabolism of vitamin K. Clinicians should therefore be careful if they use this drug.

The main causes of renal dysfunction in renal transplant recipients are acute or chronic allograft rejection, recurrent and de-novo glomerular diseases, BK virus nephropathy, renal artery stenosis, and rarely ureter obstruction.Renal infarction is a rare condition which is caused by renal artery occlusion and it might be resulted in renal parenchymal damage.The most common etiology of renal infarction is atheroembolic diseases.Other causes are trauma, autoimmune diseases and hypercoagulability.Renal infarction of the kidney is very rare and its incidence is not clear in patients with kidney transplantation.Herein we presented a renal transplant recipient with renal dysfunction due to renal infarction as a result of embolism due to atrial fibrillation, resulting in permanent renal dysfunction.

Familial Mediterranean fever (FMF) is an autosomal recessive hereditary disease characterized by recurrent attacks of fever, usually accompanied by sterile polyserositis. Although colchicine is the main medical treatment option for FMF, potential adverse effects and drug interactions should be considered during the follow-up of these patients. Herein, we presented a case of a hemodialysis patient with FMF, who developed rhabdomyolysis due to concomitant use of colchicine and clarithromycin for pneumonia treatment.

OBJECTIVE: To investigate the effects of renal transplantation on left ventricular (LV) function and morphology in patients with end-stage renal disease (ESRD) in the late posttransplant period. MATERIAL and Methods: The prospective study included 40 patients (mean age 33.2 ± 7.7 years;25 female /15 male) with ESRD. In all of these patients, renal transplantation was performed successfully; and the serum creatinine levels were less than 2 mg/dL. The echocardiographic evaluations were performed before renal transplantation and 12. month after renal transplantation. Left ventricular diastolic diameter (LVDD), left ventricular systolic diameter (LVESD), left ventricular mass (LV Mass), left ventricular mass index (LVMI), LV ejection fraction (LVEF), Doppler and tissue Doppler parameters were obtained in all patients. RESULTS: At the twelfth month, LVDD (48 ± 5 vs 45 ± 6, p: 0.01), LVSD (33 ± 4 vs 29 ± 4, p< 0.001) LVMI (114 ± 31 vs 98 ± 13, p: 0.007) decreased significantly compared to the pretransplant period. There was a significant increase in the LVEF in at the twelfth month (59 ± 5 vs 67 ± 6, p< 0.001). There was a significant improvement between pretransplant period and late posttransplant period with regard to diastolic cardiac function. CONCLUSION: Renal transplantation had beneficial effects on diastolic and systolic functions and cardiac morphology in the late posttransplant period.

BackgroundAfter the first genome had been sequenced in 2003 with an international project, Human Genome Project, the 1000 Genomes Project also revealed the analysis of 1092 and 2504 genomes respectively. Whole exome sequencing of human samples was reported to detect approximately 20,000–30,000 SNV and indel calls on average. It is very important to choose the best tool that suits the related study.MethodsIn this study, it is aimed to demonstrate the results of an in-house method (SELIM) for variant prioritization of WES data without using in-silico methods.ResultsBy this method, the annotated data have been decreased by 7.4–13.8 times (mean=10.9).ConclusionBy the initiation of 1.000.000 genome project, powerful databases are needed. In this respect, SELIM is an in-house workflow that can easily be used for simplifying the annotated data without using any in-silico methods.

The risk of neoplasm increases after transplantation in patients with organ transplantation. Immunosuppressive treatments or oncogenic viruses are major risk factors. Epstein-Barr virus (EBV) and Human Herpesvirus-8 (HHV-8) are the most frequently shown types among oncogenic viruses. Herein, we present a case of spindle cell neoplasm in a 70-year-old renal transplant recipient who underwent immunosuppressive treatment for 4 years, and presented with jaundice and fatique.

Objective: Hemodialysis (HD) requires a well-functioning temporary or permanent vascular access. Arteriovenous fistula (AVF) is frequently used in chronic kidney disease (CKD) patients for vascular access. Cytokines direct inflammation and immune response. Inflammation is one of the prevalent risk factors in renal patients. Inflammatory cytokine gene polymorphisms have an effect on vascular access. Therefore, we aimed to investigate a cytokine gene, IL-1α -889 C>T, promoter polymorphism in HD patients with and without AVF thrombosis. Materials and Methods: Eighty-one HD patients and 62 healthy controls were enrolled in the study. Polymorphism was studied using a polymerase chain reaction and restriction fragment length polymorphism. The Mann–Whitney U test and Pearson chi-square analysis were used for statistical analysis. Results: There was no significant difference between the groups. However, the wild genotype was found to be much higher in the group without thrombosis compared to the thrombosis group (59.1% versus 48.6%). This difference was not statistically significant. In the patients’ group, the heterozygous genotype was found to be more prevalent (37.8% versus 27.3%). Conclusions: Polymorphisms in the promoter region of the genes affect the transcriptional activity and also the gene products. According to our results, the IL-1α -889 C>T gene promoter polymorphism is not associated with a risk of thrombosis in HD patients.