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OBJECTIVES Incidence of new-onset diabetes after transplant negatively affects graft and patient survival. Obesity, impaired fasting glucose before transplant, and a history of diabetes in first-degree relatives are well-defined risk factors. TCF7L2 and CDKAL1 gene polymorphisms have been implicated in the pathogenesis. We investigated the effect of single gene polymorp-hisms of TCF7L2 (rs7903146) and CDKAL1 (rs7754840) on new-onset diabetes in renal transplant recipients. MATERIALS AND METHODS We evaluated 239 renal transplant recipients. TCF7L2 and CDKAL1 gene polymorphisms were assessed by polymerase chain reaction. RESULTS Mean patient age was 43 ± 13 years. There were 148 male patients (61.9%), and 91 were female (38.1%). New-onset diabetes was detected in 55 patients (23%). In 20 cases (36%), the glycemic disorder was transient; 61% of patients required insulin therapy. In terms of CDKAL1, 108 patients had the wild-type allele, 112 had a single-allele mutation, and 19 had a 2-allele mutation (45.2%, 46.9%, and 7.9%, respectively). In terms of TCF7L2, 163 of the patients had the wild-type allele, 49 had a single-allele mutation, and 27 had a 2-allele mutation (68%, 20%, and 11%, respectively). New-onset diabetes-related factors were age at transplant, body mass index after transplant (calculated as weight in kilograms divided by height in meters squared), tacrolimus, mycophenolate, and TCF7L2 polymorphism but not CDKAL1 polymorphism. After multiple regression analysis, the effect of TCF7L2 polymorphism persisted. A single allelic change resulted in a risk factor 1.4 times higher for new-onset diabetes after transplant (P = .043; 95% CI, 1.142-1.874) and a double allelic change was 2.7 times higher (P < .01; 95% CI, 1.310-4.073) Conclusions: TCF7L2 (rs7903146) gene polymorphism is an independent risk factor for new-onset diabetes in Turkish renal transplant patients. This study is the first in Turkey to show the distribution and effect of these genes in kidney transplant patients.

Objectives Posttransplant erythrocytosis affects 8% to 26% of kidney transplant recipients. In this study, our aim was to define associations among hypercalcemia, persistent hyperparathyroidism, and posttransplant erythrocytosis. We also investigated the effects of biologic sex, age, and dialysis modality before transplant on posttransplant erythrocytosis development. Materials and methods We enrolled 247 patients [159 (64%) male and 88 (36%) female] who underwent kidney transplant between 2009 and 2018. All demographic and laboratory parameters were retrospectively analyzed as possible factors associated with posttransplant erythrocytosis. Results Fifty-nine (24%) of total patients had posttransplant erythrocytosis. The median time to posttransplant erythrocytosis development was 16 months (range, 8-34 mo). Male sex, the use of peritoneal dialysis as maintenance renal replacement therapy before kidney transplant, and persistent hyperparathyroidism were defined as independent risk factors for posttransplant erythrocytosis development in our multivariate logistic regression analyses (odds ratio = 5.228, 3.963, and 4.109, respectively). In addition, high serum creatinine levels were associated with a lower incidence of posttransplant erythrocytosis (odds ratio = 0.253). Although significance did not remain after multivariate analysis, hypercalcemia was found to be significantly associated with posttransplant erythrocytosis in univariate analyses (odds ratio = 1.768). In subgroup analyses, where only male patients were evaluated, persistent hyperparathyroidism and peritoneal dialysis were found to be independent risk factors for posttransplant erythrocytosis development (odds ratio = 4.176 and 5.003). Conclusions Persistent hyperparathyroidism and hypercalcemia could precipitate development of posttransplant erythrocytosis. The preserved residue renal function may be associated with increased endogenous erythropoietin, which could lead to posttransplant erythrocytosis development.

The purpose of this study was to determine the prevalence of oral Candida spp. in HD patients and to investigate its relation with systemic inflammation and atherosclerosis. Microbiological samples were taken from buccal mucosa, palate, and dental prosthesis with a cotton swab. High-sensitivity CRP (hsCRP) and IL-6 were measured as inflammation markers. A total of 69 patients (58% male and median age 62 years) were enrolled in this study; 53.6% of total patients had oral Candida colonization. HsCRP and IL-6 levels were found to be significantly higher in the oral Candida colonization positive group than in the Candida colonization negative group (P = 0.002 and P = 0.01, respectively). HDL levels were significantly lower in the Candida colonization positive group (P = 0.03). Peripheral artery disease (P = 0.05) and oral Candida colonization (P = 0.002) were significantly associated with inflammation. In addition to conventional risk factors such as age (P = 0.03), diabetes (P = 0.001), and peripheral artery disease (P = 0.002), oral Candida colonization is associated with coronary artery disease (P = 0.04). Oral Candida colonization might be associated with chronic inflammation and development of atherosclerosis in HD patients.

Hypertension, non-dipper blood pressure (BP) pattern and decrease in daily urine output have been associated with left ventricular hypertrophy (LVH) in peritoneal dialysis (PD) patients. However, there is lack of data regarding the impact of different PD regimens on these factors. We aimed to investigate the impact of circadian rhythm of BP on LVH in end-stage renal disease patients using automated peritoneal dialysis (APD) or continuous ambulatory peritoneal dialysis (CAPD) modalities. Twenty APD (7 men, 13 women) and 28 CAPD (16 men, 12 women) patients were included into the study. 24-h ambulatory blood pressure monitoring (ABPM) and transthoracic echocardiography besides routine blood examinations were performed. Two groups were compared with each other for ABPM measurements, BP loads, dipping patterns, left ventricular mass index (LVMI) and daily urine output. Mean systolic and diastolic BP measurements, BP loads, LVMI, residual renal function (RRF) and percentage of non-dippers were found to be similar for the two groups. There were positive correlations of LVMI with BP measurements and BP loads. LVMI was found to be significantly higher in diastolic non-dippers compared to dippers (140.4 ± 35.3 vs 114.5 ± 29.7, respectively, P = 0.02). RRF and BP were found to be independent predictors of LVMI. Non-dipping BP pattern was a frequent finding among all PD patients without an inter-group difference. Additionally, higher BP measurements, decrease in daily urine output and non-dipper diastolic BP pattern were associated with LVMI. In order to avoid LVH, besides correction of anemia and volume control, circadian BP variability and diastolic dipping should also be taken into consideration in PD patients.

Background: Diabetic nephropathy (DN) is a leading cause of diabetes-related morbidity and mortality. The aim of this study was to evaluate the relationship of AGT M235T and apoprotein E (APO E) gene polymorphism with DN in Turkish patients of Type 2 diabetes, and to compare genotype and allele distributions among DN patients, non-DN patients, and healthy controls. Methods: AGT M235T and APO E genotype and allele analysis were performed in 111 DN patients, 108 non-DN patients, 106 healthy control subjects for APO E genotype, and 100 for AGT M235T genotype polymorphism. APO E and AGT M235T genotype were determined by RFLP-PCR. Results: The frequencies of APO E epsilon 2/3, epsilon 3/3, epsilon 3/4 genotypes were 22.7%, 60%, 60%, respectively, among DN patients and 6.6%, 80%, 10.4%, respectively (p < 0.001), in the non-DN patients. The frequencies of AGT M235T MM, MT, TT genotypes among the same groups were 17%, 46%, 37% and 21%, 63%, 16%, respectively (p < 0.02). Having the epsilon 2/3 genotype and TT genotype increased the risk for DN nephropathy [4.8-fold (95% Cl: 1.94-11.67), 2.9-fold (95% Cl: 1.27-6.69), respectively]. Conclusion: Our study has shown that AGT M235T TT genotype and APO E epsilon 2/3 genotype may be linked to a risk for DN among Turkish population.

Capusa, Cristina/0000-0002-3748-8164; Akar, Harun/0000-0002-0936-8691; Mircescu, Gabriel/0000-0002-8606-3699; Rui, Hong-Liang/0000-0002-7584-9610 WOS: 000252812500022 PubMed: 18089456 Objective: It is known that skeletal changes due to secondary hyperparathyroidism (SH) can be severe in chronic kidney disease (CKD). Recently decribed Sagliker syndrome (SS) is a very striking and prominent feature of SH in CKD, including an uglifying appearance to the face, short stature, extremely severe maxillary and mandibulary changes, soft tissue in the mouth, teeth/dental abnormalities, fingertip changes, knee and scapula deformities, hearing abnormalities, and neurological and, more important, severe psychological problems. Design, Setting, Patients: In the past 8 years, we have encountered 40 cases of SS in SH and CKD by performing an international study in Turkey, India, Romania, Egypt, Maleysia, Tunis, and China. Results: The medical history of these patients showed that they did not receive proper therapy. Changes, particularly in children and teenagers, become irreversible, which was disastrous for the patients both aesthetically and psychologically. Conclusion: Treatment must begin early and be the appropriate treatment given in centers with sophisticated skills. Otherwise, the inability to correct all the changes in the skull and face, to remodel a new face, to extending the height, and, most important, to convince the patients to face the dramatic psychological problems can be catastrophic for those patients. (c) 2008 by the National Kidney Foundation, Inc.

Transforming growth factor-beta-1 (TGF-1) stimulates the expression of collagen mRNA in cultured human peritoneal mesangial cells, which may predispose them to developing peritoneal fibrosis. Polymorphisms in the signal sequence genetically may be responsible for increased TGF-beta 1 production (i.e., a substitution at amino acid position 10 and 25, +869 Leu(10)-Pro and +915 Arg(25)-Pro, respectively). The aim of this study was to find out whether there is any relation between peritoneal equilibration test (PET) results and TGF-1 gene polymorphism. Thirty-two CAPD patients and 72 healthy subjects were included into the study. Each CAPD patient had undergone two PET with a two-year interval. The patients were classified according to the results of a baseline PET as high (high-high average) and low (low-low average) transporters. In high transporters group (n = 20), the genotype frequencies were found as 45% Leu/Leu, 55% Leu/Pro for codon 10; and 85% Arg/Arg, 15% Arg/Pro for codon 25. In low transporters group (n = 12), the genotype frequencies were detected as 66.7% Leu/Leu and 33.3% Leu/Pro for codon 10; and 83.3% Arg/Arg, 16.7% Arg/Pro for codon 25. The distribution of the TGF-beta 1 genotypes in our control population was compatible with a Hardy-Weinberg equilibrium. We found no relation between TGF-beta 1 genotypes and peritoneal transport group (chi(2) test, p > 0.5). There was no relation between TGF-beta 1 genotype and longitudinal change in peritoneal transport. This study is the first study analyzing the possible link between TGF-beta 1 gene polymorphisms and the characteristics of peritoneal transport and longitudinal change of peritoneal transport characteristics in CAPD patients. Further work is needed to clarify the functional importance of these two polymorphisms in TGF-beta 1 production and in the development of peritoneal fibrosis.

In patients with chronic renal failure, the main cause of mortality is cardiovascular disease. Cardiac troponin T (cTnT) and brain natriuretic peptide (BNP) are found to be related with decreased survival in both the normal population and in patients with chronic renal failure in different studies. Our aim is to investigate the relationship between cTnT and BNP in patients with chronic renal failure.58 chronic haemodialysis patients were enrolled prospectively for the study. Blood samples for measurement of cTnT and BNP were collected after the haemodialysis. The patients are divided into 3 groups according to cTnT measurements. Group I included the patients with cTnT0.05 ng/ml, Group II included the patients with cTnT between 0.05 and 0.1 ng/ml and group III included the patients with cTnT0. 1 ng/ml. We performed echocardiography in all patients to measure the left ventricular ejection fraction and thickness of septum and posterior wall. When BNP levels were compared among the 3 groups, we found that the BNP level was lowest in group I and highest in group III (165.13 +/- 125.44 pg/dl; 236.0 +/- 107.83 pg/dl; 280.71 +/- 153.25 pg/dl, respectively) (P = 0.01).The difference in BNP levels among groups was statistically significant and independent from left ventricular hypertrophy, left ventricular ejection fraction and volume overload in multiple regression analysis. We also searched the relationship between plasma cTnT and BNP levels and found a positive correlation (r = 0.3; P = 0.023).cTnT and BNP levels were related to each other in patients with chronic renal failure.These parameters can help to identify the patients with a high risk for cardiovascular diseases.

The present study was designed to evaluate angiotensinogen (AGT) M235T and plasminogen activator inhibitor-1 (PAI-1) (4G/5G) polymorphisims in relation to the occurrence of atherosclerotic renal artery stenosis (ARAS) and recurrent stenosis. In this study, 30 patients were enrolled after angiographic demonstration of ARAS; 100 healthy subjects for AGT polymorphism and 80 healthy subjects for PAI-1 polymorphism were considered the control group. The patients were followed for a mean 46.1 ± 9.2 months. The patients had significantly higher frequencies of the MT genotype and the T allele than control group (χ2 = 18.2, p < 0.001 and χ2 = 11.5 p < 0.001). There were no significant differences in the PAI-1 genotype and allele findings when the data for all patients were compared with that for the controls (χ2= 2.45, p = 0.29 and χ2 = 0.019, p = 0.89). There were no significant differences in the genotype and allele findings for the patients with and without restenosis (p > 0.05). The C-reactive protein (CRP) level was higher in the patients with restenosis than in the patients without restenosis (7.694 ± 0.39 mg/L and 1.56 ± 1.08 mg/L) (p = 0.001). Our results suggest that the M235T MT genotype and T allele might be associated with increased risk of atherosclerotic renal artery stenosis. The CRP level might be an independent predictor for recurrent stenosis. © Springer Science+Business Media, Inc. 2005.

Glycerol-induced acute renal failure is an experimental model for myoglobinuric nephropathy. Amifostine is a cytoprotective agent which scavenges the free radicals. Since there is enhanced production of reactive oxygen metabolites in glycerol-induced acute renal failure, we wanted to examine whether amifostine has a protective role against vascular reactivity and histological changes in kidneys isolated from glycerol-pretreated rabbits. Perfusion pressure was recorded from kidneys obtained from rabbits injected with glycerol 3 hr before the experiments and from glycerol-pretreated and non-pretreated rabbits injected with amifostine 30 min. before the experiments. Acetylcholine-induced (10(-8)-10(-5) M) vasodilatation was tested following the construction of submaximal vasoconstriction by phenylephrine. Histological investigation was performed using light microscope. Acetylcholine-induced vasodilatation was found to be significantly decreased in glycerol, glycerol+ amifostine and amifostine groups compared to controls at all concentrations. Reduction in acetylcholine-induced vasodilation was more prominent in arnifostine group compared to arnifostine +glycerol group. There was histological renal damage in all experimental groups and this damage was more pronounced in glycerol +amifostine group. In conclusion, contrary to expectation, arnifostine per se led to histological damage and potentiated the histological damage caused by glycerol and produced a decrease in acetylcholine-induced vasodilatation. The mechanisms by which arnifostine exerts its effects are not known.

Atherosclerosis is a disease of the arterial wall, with increasing wall thickness representing an early event in the progression of the disease. It has been suggested that iron overload, as assessed by increased serum ferritin concentration, may be a risk factor for atherosclerosis. The aim of this study was to investigate the relationship between the influence of intravenous (IV) iron therapy and ferritin levels and carotid intima media thickness (C-IMT) in dialysis patients. Sixty patients (51 +/- 14) years were divided into two groups according to their IMT obtained by ultrasound; group I (high risk) and group II (low risk). The parameters assessed were serum creatinine, urea, calcium, phosphorus, hemoglobin, albumin, uric acid, iron, ferritin, and lipid levels. Thirty-eight patients (88%) in group I and 5 patients (12%) in group II received IV iron therapy while 5 patients (29%) in group I and 12 patients (71%) in group II (P < 0.001) did not receive IV iron therapy. Ferritin levels were higher in group I than in group II (581 +/- 303 and 306 +/- 224) (P < 0.001). C-IMT measurements correlated with serum ferritin and with the intravenous iron dose received during the 24 months preceding the study (r = 0.315, P = 0.015; r = 0.471, P = 0.001). The findings indicate that IV iron therapy and elevated serum ferritin levels may cause an increase in the incidence of atherosclerosis.

Elevated cardiac troponin T (cTnT) has been associated with shorter survival in hemodialysis patients. Moreover, intravenous (IV) iron treatment has been held responsible for oxidative stress and accelerated atherosclerosis in these patients. In the present study, we investigated the relationship between cTnT concentration, IV iron treatment, and parameters of iron status. In addition, parameters of oxidative stress, inflammation, and atherosclerosis were evaluated. Predialysis blood samples of 78 chronic hemodialysis patients were analyzed for cTnT, malondialdehyde, creatine kinase (CK), and CK-isoenzyme MB (CK-MB). In addition, the mean value of predialysis serum samples collected during the last year, were considered for homocysteine, ferritin, iron, iron binding capacity, blood cell counts, blood urea nitrogen, creatinine, albumin, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), calcium, phosphate, iPTH, cholesterol, and triglyceride. The quantity of IV iron sucrose administered during the last two years was counted from the patients' files. Echocardiography, all events related to ischemic heart disease, and urine volume were also recorded. Elevated cTnT levels (greater than or equal to 0.10 ng/mL) were found in 18 patients (23.1%). The amount of iron administered was 2264 +/- 1871 mg with a range 0-7000 mg. Patients with elevated cTnT levels received more IV iron than those with normal cTnT (3692 +/- 1771 vs. 1761 +/- 1595 mg, p

Background: This study has been undertaken to investigate the possible alterations of oxidant/antioxidant status in uremic patients undergoing hemodialysis (HD) and the effects of vitamin E supplementation. Methods: Erythrocyte antioxidant enzyme activities [glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT)] and thiobarbituric acid reactive substance (TBARS) concentrations as a measure of lipid peroxidation in HD patients have been determined and compared with healthy controls. The patient group consisted of 36 uremic patients 21-75 years of age undergoing maintenance HD three times weekly for an average of 41 months. The efficiency of Vitamin E therapy in dialysis patients was also assessed by re-evaluating antioxidant status of the same patients after supplementation of the vitamin E in a dosage of 600 mg/daily for 14 weeks. Results: A significant decrease in the activities of erythrocyte SOD, CAT and GSHPx and a significant increase in TBARS concentrations were found in patient group compared to control group (p < 0.001). A significant correlation between GSHPx activities and duration of HD therapy was also observed (r= - 0.46,p < 0.01). Vitamin E supplementation caused an increase in GSHPx and SOD activities and a decrease in TBARS concentrations. A slight but not significant increase in CAT activity was also observed by Vitamin E. Conclusions: The results suggest the presence of an oxidative activity and the possible preventive role of Vitamin E therapy in uremic patients undergoing HD. (C) 2003 Elsevier B.V. All rights reserved.

Background: Fixed-dose combination antihypertensive therapy has been recommended for patients with essential hypertension who are unresponsive to monotherapy or as a first-line treatment. Objective: We investigated the effects of a fixed-dose combination of the phenylalkylamine-type calcium channel blocker verapamil slow release (SR)plus the angiotensin-converting enzyme inhibitor trandolapril on blood pressure (BP), serum lipid profile, urinary albumin excretion (UAE), left ventricular mass (LVM), and LVM index (LVMI), as well as the adverse events associated with this treatment. Methods: Patients aged 30 to 65 years with mild to moderate essential hypertension were included in the study. All of the patients received capsules containing combination treatment with verapamil SR 180 mg plus trandolapril 2 mg orally, daily for 12 weeks. Mean arterial pressure (MAP), systolic BP (SBP), diastolic BP (DBP), and heart rate (HR) were measured at baseline and at 4, 8, and 12 weeks of treatment. Serum lipid profile, UAE, LVM, LVMI, and body mass index (BMI) were determined at baseline and at the end of the study period. All patients underwent electrocardiography and echocardiography at baseline and week 12. The primary end point of the study was to achieve an SBP/DBP ≤140/≤90 mm Hg (ie, normotensive) during week 12. All adverse events were assessed as mild, moderate, or severe at each visit. According to the response rate at week 12, patients were divided into 2 groups: those who became normotensive (responders) or those who remained hypertensive (SBP/DBP >140/>90 mm Hg; nonresponders). Results: Forty-one patients (29 women, 12 men; mean [SD] age, 47.7 [7.8] years; mean [SD] BMI, 29.4 [3.5] kg/m2) were enrolled. The median durationof hypertension prior to enrollment was 5 months. Mean MAP, SBP, DBP, UAE, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), LDL-C/highdensity lipoprotein cholesterol (HDL-C) ratio, LVM, LVMI, and BMI decreased significantly after 12 weeks of combination treatment; HR and triglyceride level did not change significantly. Treatment-related adverse events occurred in 31.7% of patients, and none were severe or caused any patient to withdraw from the study. The most common adverse events were cough, constipation, headache, and dryness in the throat. Microalbuminuria, which may be a marker of endothelial dysfunction, was found in 7 (17.1%) patients at baseline and regressed significantly after 12 weeks. Conclusions: In this study population, the fixed-dose combination of verapamil–trandolapril was an effective and well-tolerated antihypertensive therapy. This combination significantly reduced MAP, BP, TC, LDL-C, LDL-C/HDL-C ratio, UAE, LVM, and LVMI. Also, microalbuminuria decreased after this treatment. Verapamil–trandolapril may be useful in preventing microalbuminuria and left ventricular hypertrophy in patients with essential hypertension.

The aim of the present study was to investigate the effects of treatment with antioxidant stobadine (ST) on the activities of enzymes related with pentose phosphate pathway and glutathione-dependent metabolism and the other markers of oxidative stress in brain and peripheral organs of diabetic rats, and to compare the effects of ST treatment alone with the effects of treatments with another antioxidant vitamin E and ST plus vitamin E. Rats were made diabetic by the injection of streptozotocin (STZ; 55 mg/kg IP), and, 2 days later, some control and diabetic rats were left untreated or treated with ST (24.7 mg/kg/day, orally), vitamin E (400–500 U/kg/day, orally), or both substances together. In the brain, although 6-phosphogluconate dehydrogenase activity (6-PGD) did not change, glucose-6-phosphate dehydrogenase activity (G-6PD) was markedly increased in diabetic rats compared with controls; only combined treatment with ST and vitamin E produced a partial prevention on this alteration. The aorta G-6PD and 6-PGD of diabetic rats were 52% and 36% of control values, respectively. Neither single treatments with each antioxidant nor their combination altered the G-6PD and 6-PGD in aorta of diabetic rats. Glutathione peroxidase (GSHPx) activity was increased by STZ-diabetes in brain, heart, and kidney. In diabetic brain, vitamin E alone or combination with ST kept GSHPx at normal levels. Diabetes-induced stimulation in GSHPx did not decrease in response to the treatment with vitamin E in heart and kidney, but was greatly prevented by ST alone. The activity of glutathione reductase (GR) was decreased in brain and heart of diabetic rats. The treatment with each antioxidant or with a combination of both agents completely prevented this deficiency and resulted in further activation of GR in diabetic tissues. Glutathione S-transferase (GST) activity did not significantly change in diabetic brain and aorta. GST was stimulated by all treatment protocols in the brain of diabetic rats and was depressed in aorta of control rats. Catalase (CAT) was activated in diabetic heart but depressed in diabetic kidney. Diabetes-induced abnormalities in CAT activity did not respond to vitamin E alone in heart, was moderately ameliorated by the treatment with this vitamin in kidney, and was completely prevented by ST alone in both tissues. Superoxide dismutase (SOD) activity of brain and heart was unchanged by the diabetes but inhibited in diabetic kidney after the treatment ST alone or ST plus vitamin E. The lipid peroxidation (MDA) was increased in diabetic brain and heart. ST or vitamin E alone partly prevented diabetes-induced increase in MDA in brain and heart; however, antioxidant combination achieved a completely amelioration in MDA of these tissues of diabetic rats. Kidney MDA levels were similar in control and untreated diabetic animals. ST and vitamin E treatments, when applied separately or together, significantly reduced kidney MDA in both control and diabetic rats; and the combined effect of antioxidants was greater than that of each alone. These results are consistent with the degenerative role of hyperglycemia on cellular reducing equivalent homeostasis and antioxidant defense, and provide further evidence that pharmacological intervention of different antioxidants may have significant implications in the prevention of the prooxidant feature of diabetes and protects redox status of the cells.

It has been shown that beta-glucan (BG), which has antioxidant and immunomodulatory effects, attenuats renal ischemia-reperfusion injury. We aimed to investigate whether BG might have a preventive role against the development of contrast-induced nephropathy and to compare its effect with nebivolol (Nb) and N-acetylcysteine (NAC).Thirty-six Wistar albino female rats were randomly divided into six groups (n = 6 each): control, contrast media (CM), BG, BG + CM, Nb + CM, and NAC + CM. With the exception of control and CM groups, the others were given drugs orally once a day for 5 days. Kidney function parameters, inflammatory parameters, and serum and renal tissue oxidative stress markers were measured.Increases of serum creatinine and blood urea nitrogen levels were significantly higher (p 0.05) in the CM group only. Absolute changes of serum creatinine levels in BG, BG + CM and Nb + CM groups were significantly lower than those in the CM group (p 0.05). Serum levels of advanced oxidation protein products and malondialdehyde were significantly less (p 0.05) in the BG group compared to the CM group. Histopathological lesions in the CM group were more advanced (p 0.05). No significant differences between the BG + CM, Nb + CM and NAC + CM groups were found with regard to histopathological findings.This study suggests that BG protects or ameliorates against contrast-induced nephropathy. Its beneficial effects may be similar to or greater than those of Nb or NAC.

We present a 62-year-old man, with a prior history of diabetes mellitus, atherosclerotic heart disease, and chronic renal failure requiring peritoneal dialysis, who developed accelerated uremic sensorimotor polyneuropathy. Our patient significantly improved after effective hemodialysis. Although renal transplantation is a curable therapy for uremic neuropathy, effective dialysis is still an important treatment for the group of patients who cannot undergo renal transplantation.

A case of adenomatoid tumor of the uterus in a 34-year-old patient, who had received a renal transplant and was undergoing immunosuppresive therapy is presented. At surgery, there were a total of eight nodular intramural and subserous masses thought to be leiomyoma nodules, and tumor excision was unusually, hardly performed because the nodules were strictly adherent to the myometrium. All the specimens yielded the same pathological diagnosis - adenomatoid tumor. This case is unusual because of the multiple nodular pattern and its association with the immunocompromised status of the patient. Although adenomatoid tumors have not been shown to recur, we are in doubt in our case, because the uterus is still intact and the immunocompromised status of the patient might have a role in the extensive growth and also in the possibility of recurrence. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.

WOS: 000258002700006 PubMed: 18661412 Visfatin was recently defined as an adipocytokine; however, the pathophysiological role of visfatin is not completely understood. A few studies suggest that visfatin may be a new proinflammatory adipocytokine. The aim of the present study was to compare serum visfatin levels between hemodialysis and continuous ambulatory peritoneal dialysis (CAPD) patients and evaluate the relationship between visfatin levels to IL-6, TNF-alpha, and left ventricular hypertrophy. Serum visfatin, IL-6, and TNF-alpha levels were measured by using the ELISA method, and echocardiographic evaluations were performed in 31 hemodialysis patients, 30 CAPD patients, and 21 healthy volunteers. Serum visfatin levels were higher in the CAPD group (265.27 +/- 387.86 ng/mL) than hemodialysis (97.68 +/- 244.96 ng/mL,) and control (41.33 +/- 48.87 ng/mL) groups (p = 0.04, p = 0.01, respectively). No significant difference was observed between the hemodialysis and control groups. In univariate analysis, visfatin levels were positively correlated with IL-6 (r = 0.24, p = 0.03), TNF-alpha (r = 0.34, p = 0.002), and BMI (r = 0.26, p = 0.03) and negatively correlated with some left ventricular diastolic parameters [ Em and Em/Am (r =-0.305, p = 0.01), (r =-0.251, p = 0.03), respectively]. No relationship was found between visfatin and left ventricular mass index. In the linear regression analysis, visfatin levels independently related with TNF-((beta = 0.369, p = 0.001) and IL-6 (beta = 0.284, p = 0.015). This study has found significantly higher levels of serum visfatin in CAPD patients when compared to healthy individuals. Increased visfatin levels seem to associate with proinflammatory cytokines such as IL-6 or TNF-alpha. As for the effects of on left ventricular structure and functions, visfatin might have negative effects on left ventricular diastolic function parameters but have no effects on left ventricular mass index.

WOS: 000259221300003 PubMed: 18758126 Objective The existence of microalbuminuria (MAU) in patients with essential hypertension is a strong indicator of microvascular damage. Although endothelial dysfunction and increased vascular permeability both have a role in the development of MAU, its ethiopathogenesis in hypertensive patients is not yet clearly understood. Vascular endothelial growth factor (VEGF) is the most important regulator of pathological or physiological angiogenesis and it additionally leads to increased vascular permeability. This study aims to assess the relationship of serum VEGF levels to MAU in non-complicated, newly-diagnosed essential hypertensive patients (EHs). Methods This study included 30 newly-diagnosed EHs with MAU, 46 newly-diagnosed EHs without MAU and 46 healthy controls. None of the EHs had diabetes, renal impairment or atherosclerotic diseases. Serum VEGF levels were measured using the ELISA method. Results Serum levels of VEGF were significantly higher in EHs with MAU when compared with patients without MAU (225.15+/-109.34 pg/mL versus 166.78+/-114.35 pg/mL, p: 0.04) or controls (225.15+/-109.34 pg/mL versus 144.91+/-96.60 pg/mL, p: 0.007). On the other hand, no significant difference was observed between the non-MAU and control groups. In the univariate analysis, serum levels of VEGF, were positively correlated with systolic blood pressure (R: 0.253 p: 0.001), diastolic blood pressure (R: 0.162 p: 0.04), mean arterial pressure (R: 0.239 p: 0.002), creatinine clearance (R: 0.172 p: 0.04) and MAU (R: 0.338 p: 0.002). In the multiple linear regression analysis, VEGF levels were independently related to MAU (beta: 0.248, p: 0.02). Conclusion VEGF levels are higher in EHs in the presence of MAU. These high values may be important in the early diagnosis of vascular damage in EHs. Additionally, VEGF may increase glomerular permeability and lead to MAU in EHs.

Abnormalities in the metabolism of essential fatty acids and the results of increased oxidative stress have been implicated in cardiovascular disorders observed in diabetes mellitus. This study, therefore, aimed to investigate the effects of cod liver oil (CLO, Lysi Ltd, Iceland), which comprises mainly an antioxidant vitamin A, n:3 polyunsaturated fatty acids (n:3 PUFAs), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), on cardiovascular abnormalities in streptozotocin (STZ)-diabetic rats. Two days after single STZ (55 mg kg−1, i.p.) or vehicle injection, diabetes was verified by increased blood glucose, and non-diabetic and diabetic rats were left untreated or treated with CLO (0.5 mL kg−1 daily, by intragastric probing) for 12 weeks. Plasma glucose, triacylglycerol and cholesterol concentrations were significantly elevated in 12-week untreated-diabetic rats; CLO provided better weight gain, entirely prevented the plasma lipid abnormalities, but partially controlled the glycaemia in diabetic rats. In isolated aorta rings, diabetes resulted in increased phenylephrine-induced vasoconstriction and isoprenaline-induced vasorelaxation, impaired endothelium-dependent vasodilatation and unchanged responsiveness to sodium nitroprusside. CLO treatment completely prevented endothelial deficiency, partly corrected the phenylephrine-induced vasoconstriction and did not affect the responses to isoprenaline and sodium nitroprusside in diabetic aorta. Diabetes also produced a marked decrease in the rate of spontaneously beating right atria and a significant increase in basal contractile force of left ventricular papillary muscle. The responsiveness of right atria to the positive chronotropic effect of isoprenaline was significantly decreased in diabetic rats, and was increased in CLO-treated diabetic rats. The positive chronotropic effect of noradrenaline was markedly increased in diabetic atria, but prevented by CLO treatment. Diabetes also resulted in an increased positive inotropic response of papillary muscle to both noradrenaline and isoprenaline, which were prevented by CLO treatment. CLO treatment also resulted in lower tissue sensitivity (pD2) to these agonists in diabetic papillary muscle. Ventricular hydroxy-proline content was found to be unchanged among the experimental groups. The ultrastructure of diabetic myocardium displayed various degenerations (i.e. intracellular oedema, myofibrillar fragmentation, condensed pleomorphic mitochondria, thick capillary irregular basement membrane, swollen endothelial cells), which were partially prevented by CLO treatment. We conclude that the supplementation with CLO is effective in preventing cardiovascular disorders observed in experimental diabetes.

Objectives To determine the significance of a newly described marker of inflammation procalcitonin (PCT), and to investigate its relationship to conventional markers of inflammation, such as C-reactive protein (CRP), fibrinogen, and erythrocyte sedimentation rate (ESR), in patients on peritoneal dialysis (PD) and with peritonitis. Design A prospective, observational clinical study. Setting The Nephrology Division of a University-affiliated teaching hospital. Patients and Methods 51 consecutive patients on PD were included in the study. Of this number, 16 developed peritonitis during the observational period. Baseline PCT, CRP, and fibrinogen concentrations and ESR of 51 PD patients were determined at a time point (TB) prior to any evidence of infection. These results were compared with laboratory values from 74 hemodialysis patients and 34 nonuremic control subjects. All PD patients then were followed prospectively for evidence of peritonitis. In addition to routine blood tests, including hemoglobin and leukocyte count, and routine biochemical tests, blood samples were taken to measure PCT, CRP, and fibrinogen concentrations and ESR at the time (T0) when patients first were diagnosed with PD peritonitis and also on the 4th (T4) and the 14th (T14) days after treatment for peritonitis was initiated. PCT was assayed by immunoluminometry. Results No significant difference was observed between baseline median serum PCT concentrations in PD and hemodialysis patients; however, in both groups, baseline median PCT concentrations were significantly higher than those of nonuremic controls ( p < 0.05). The 16 patients on PD who developed peritonitis had 21 PD peritonitis episodes during the study period. The increased PCT concentration observed at T0 in PD peritonitis episodes decreased with therapy, and this change was statistically significant ( p < 0.05). In a receiver operating characteristic curve analysis for peritonitis, the area under the curve (AUC) for PCT was 0.80, which was significantly lower than the AUC for CRP and greater than the AUCs for fibrinogen and ESR. The sensitivity of PCT for peritonitis was lower than the sensitivity of conventional markers of inflammation; however, the specificity of PCT was higher. Conclusions Median serum PCT concentration in PD patients was significantly higher than in nonuremic controls but not hemodialysis patients. Serum PCT concentrations may serve as a useful adjunct to traditional markers of inflammation in detecting and monitoring inflammation and peritonitis in PD patients.

This study was performed to investigate the potential relationship between left ventricular hypertrophy (LVH) and proinflammatory cytokines in hemodialysis (HD) patients and the effect of HD on cytokine production. Serum interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) measurements and echocardiographic studies were performed in 35 stable HD patients. A variety of probable risk factors for LVH including age, HD duration, blood pressure (BP), body mass index, lipid profile, hemoglobin, albumin, parathormone and homocysteine levels were also investigated. Additionally, the effect of HD procedure on cytokine levels was evaluated. Predialysis serum levels of IL-1 beta, IL-6, TNF-alpha, and homocysteine in HD patients were compared with 12 healthy subjects. Left ventricular hypertrophy was demonstrated in 20 (57%) of HD patients by echocardiography. Left ventricular mass index (LVMI) was correlated positively with systolic BP (r=0.556, p=0.001), diastolic BP (r=0.474, p=0.004), and serum levels of TNF-alpha (r = 0.446, p = 0.009). Multiple regression analysis showed that systolic BP and TNF-alpha levels were significant independent predictors of LVH. No relationship was observed between LVH and other parameters. The mean predialysis serum level of IL-6 was significantly higher in HD patients compared to healthy controls (15.7 +/- 8.7 vs. 7.3 +/- 0.7 pg/ mL, p=0.001). Predialysis serum levels of TNF-alpha in HD patients were higher when compared to healthy subjects, but the difference was not statistically significant (8.3 +/- 3 vs. 7 +/- 1.45 pg/mL, respectively, p>0.05). However, serum levels of IL-6 and TNF-alpha significantly elevated after HD, when compared to predialysis levels (from 15.7 +/- 8.7 to 17.8 +/- 9.5 pg/mL, p = 0.001 and from 8.3 +/- 3.0 to 9.9 +/- 3.5 pg/mL p=0.004, respectively). As a conclusion, in addition to BP, proinflammatory cytokines, TNF-alpha in particular, seem to be associated with LVH in ESRD patients.

SUMMARY: Background: Sleep complaints are common in end-stage renal disease. We aimed to investigate the relationship between sleep-related complaints and inflammatory cytokines in haemodialysis (HD) patients, and also the effects of HD on sleep patterns and cytokine levels. Methods: Predialysis serum interleukin-1beta (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) levels in nine patients with sleep complaints were compared with those of nine patients without sleep complaints and nine healthy controls. Patients with sleep complaints underwent polysomnography the night after HD and the following night. Results: Patients with sleep complaints had significantly higher predialysis IL-1β levels compared with those without and healthy controls (P = 0.004 and P = 0.000, respectively). They also had higher predialysis IL-6 and TNF-α levels than those without sleep complaints; however, the difference was not significant. Patients without sleep complaints had higher mean IL-6 and TNF-α and similar mean IL-1β levels compared with healthy controls (P = 0.001, P = 0.024, P = 0.26, respectively). Obstructive sleep apnoea syndrome (OSAS) was found in six out of nine (66%) patients with sleep complaints. Sleep architecture and cytokine levels did not differ between the two nights. The mean serum IL-1β, IL-6 and TNF-α levels did not differ in the pre- and post-polysomnographic samples. There was no correlation between IL-1β, IL-6 or TNF-α levels and the apnoea-hypopnoea index. Conclusions: Proinflammatory cytokines, IL-1β in particular, might be associated with sleep complaints in HD patients. OSAS is not uncommon in HD patients with sleep-related complaints and sleep architecture does not appear to be effected by the HD procedure itself.

Background: Atherosclerotic lesions are heavily infiltrated by macrophages. Neopterin can be used as a marker of the activity of macrophages. Serum neopterin levels were elevated in non-renal patients with atherosclerosis. The intima-media thickness (IMT) of the carotid arteries in hemodialysis patients was significantly higher than in control subjects. In this study, we measured serum neopterin levels in hemodialysis patients and evaluated a possible correlation between neopterin levels and carotid IMT. Patients and Methods: Thirty-seven hemodialysis patients (26 male/11 female, mean age 47 ± 15 years) and 12 healthy subjects (8 male/4 female, mean age 43 ± 10 years) were included in this study. Serum neopterin levels were measured by using a commercial ELISA kit. Carotid IMT of the subjects were measured by high-resolution B-mode ultrasonography. Results: Carotid IMT values were 1.04 ± 0.29 and 0.77 ± 0.25 mm in hemodialysis patients and healthy controls, respectively (p < 0.01). Serum neopterin levels were 110.9 ± 19.1 and 3.8 ± 2.3 ng/ml in hemodialysis patients and healthy controls, respectively (p < 0.01). Serum neopterin levels were 103.2 ± 21.3 ng/ml in hemodialysis patients with IMT Conclusion: Our findings suggest that neopterin could be associated with the severity of carotid atherosclerosis in hemodialysis patients.

In addition to gastrointestinal tract symptoms such as nausea, vomiting, and loss of appetite, impaired gastric emptying time (GET) may be related to nutritional parameters and nutritional status of patients on renal replacement therapy (RRT). Patients on RRT are affected by several factors such as uremic toxins, the presence of dialysate in the peritoneal cavity, and the drugs used against renal allograft rejection. In this study, we investigated the gastric emptying time and its relationship with biochemical and nutritional parameters in patients on RRT: those on hemodialysis and peritoneal dialysis, and renal transplantation patients. Seventy-five patients, 44 on hemodialysis, 16 on peritoneal dialysis, and 15 renal transplant patients, were included in the study. They were examined for gastric emptying time using a radioisotopic method. The results were compared with the GET of healthy subjects. Each group of patients was evaluated in terms of hemoglobin, hematocrit, blood urea nitrogen (BUN), creatinine, blood glucose, total protein, albumin, serum lipids, parathyroid hormone (PTH) and body mass index and biceps and triceps skinfold. The mean GET of patients on RRT was significantly longer than the mean GET of healthy subjects (87.8 +/- 23.4 vs. 55 +/- 18 min, p0.05). In addition, time on replacement therapy inversely and blood glucose positively correlated with GET in renal transplant patients. In conclusion, GET was longer in patients on all three RRT modalities than in healthy subjects. GET was not significantly different in dialysis patients and renal transplant patients.

Vitamin E treatment has been found to be beneficial in preventing or reducing diabetic nephropathy. Increased tissue calcium and abnormal microsomal Ca2+-ATPase activity have been suggested as contributing factors in the development of diabetic nephropathy. This study was undertaken to test the hypothesis that vitamin E reduces lipid peroxidation and can prevent the abnormalities in microsomal Ca2+-ATPase activity and calcium levels in kidney of streptozotocin (STZ)-induced diabetic rats. Male rats were rendered diabetic by a single STZ injection (55 mg kg(-1) i.p.). After diabetes was verified, diabetic and age-matched control rats were untreated or treated with vitamin E (400-500 IU kg(-1) day(-1), orally) for 10 weeks. Ca2+-ATPase activity and lipid peroxidation (NIDA) were determined spectrophotometrically. Blood glucose levels increased approximately five-fold (> 500 mg dl(-1)) in untreated-diabetic rats but decreased to 340 +/- 27 mg dl(-1) in the vitamin E treated-diabetic croup. Kidney MDA levels did not significantly change in the diabetic state. However, vitamin E treatment 2 markedly inhibited NIDA levels in both control and diabetic animals. Ca2+-ATPase activity was 0.483 +/- 0.008 U l(-1) in the control group and significantly increased to 0.754 +/- 0.010 Ul(-1) in the STZ-diabetic group (p < 0.001). Vitamin E treatment completely prevented the diabetes-induced increase in Ca2+-ATPase activity (0.307 +/- 0.025 U l(-1), p < 0.001) and also reduced the enzyme activity in normal control rats. STZ-diabetes resulted in approximately two-fold increase in total calcium content of kidney. Vitamin E treatment led to a significant reduction in kidney calcium levels of both control and diabetic animals (p < 0.001). Thus, vitamin E treatment can lower blood glucose and lipid peroxidation, which in turn prevents the abnormalities in kidney calcium metabolism of diabetic rats. This study describes a potential biochemical mechanism by which vitamin E supplementation may delay or inhibit the development of cellular damage and nephropathy in diabetes. Copyright (C) 2003 John Wiley Sons, Ltd.

Primary malignant lymphoma of bladder is one of the rarest extranodal site for lymphomas. Less than 100 cases have been reported so far [1] . A history of chronic cystitis has been shown to be a preceding feature in many cases (40%) of primary bladder lymphoma [2] . Most of the cases reported in the literature have a low-grade lymphoma including the subtypes of mucosa-associated lymphoid tissue 3 , 4 . The diffuse large cell lymphoma is the most frequent type among the subtypes of high-grade bladder lymphomas [5] . In this report, a case with high-grade primary malignant lymphoma of bladder is reported and the clinical, pathological aspects of diseases are reviewed.

SUMMARY: Different papers have emphasized the presence of visual-evoked potential (VEP) abnormalities in metabolic disorders. The aim of this study was to perform pattern VEP (PVEP) recordings in patients with chronic renal failure just before and 24 h after dialysis to test the effect of this procedure on visual pathway generated parameters. Twenty-four haemodialysis patients (M/F:14/10; mean age: 48.8 ± 14.1 years) were examined. None of them were complaining from visual difficulties or from visual loss. The recording sessions were performed just before and 24 h after dialysis. The control group consisted from 27 healthy subjects matched for age and sex. Eight (33%) patients demonstrated abnormal P100 latency prolongation in at least one tested eye (six patients in one tested eye, two in both eyes) in the recording session just prior to dialytic treatment. In the post-treatment session, it was found that the abnormal P100 latencies that were present in six patients (75%) before dialysis had returned to normal, while in the remaining two (25%), the latency abnormality persisted. No correlation was found between VEP parameters and dialysis duration, serum blood urea nitrogen (BUN), creatinine, parathyroid hormone and haematocrit levels. However, a positive correlation in the intradialytic percentage variation of bodyweight with P100 latencies was found. Visual evoked potential is a reliable, simple and non-invasive technique that can be used for the investigation and follow up of subclinical involvement of visual pathways in patients with chronic renal failure. Detected abnormalities in some uraemic patients are reversible by using dialysis.

Although the role of reactive oxygen species (ROS) in chronic renal failure (CRF) is not definitely demonstrated, a consistent number of observations has provided evidence for the presence of oxidative stress in uremic patients undergoing maintenance dialysis. In order to investigate this hypothesis further and to understand the role of antioxidant supplementation, peripheral blood lymphocytes were taken from 36 dialysis patients before and after Vitamin E supplementation in a dosage of 600 mg per day (2 x 300 mg) for 14 weeks and examined in the alkaline Comet assay for DNA strand breakage. The results were also compared with those of 36 controls with comparable age, sex, and smoking habits, and with no history of renal disease. The DNA breakage observed in the lymphocytes of patients before Vitamin E supplementation was significantly higher than in the controls (P < 0.001) but a clear protective effect of Vitamin E supplementation were observed after 14 weeks of therapy. (C) 2002 Elsevier Science B.V. All rights reserved.

Background: Crush syndrome has been described as extensive muscle damage, leading to acute renal failure. The aim of this study was to evaluate the possible role of nitric oxide, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in crush syndrome. Patients and methods: A total of 17 patients suffering from crush syndrome, 7 patients without crush syndrome and 10 healthy controls were enrolled in the study. Plasma nitrate, TNF-alpha, IL-1beta levels and biochemical parameters were measured. Results: All patients with crush syndrome demonstrated acute renal failure. Plasma nitrate levels were elevated significantly in the crush syndrome patients compared with patients without crush syndrome (33.5 +/- 20.1 vs. 15.3 +/- 5 mumol/l, p = 0.014). There was no significant difference in TNF-alpha and IL-1beta levels between control and patient groups. Conclusion: Increased plasma nitrate levels in the crush syndrome may be related either to the elevated production of NO or the diminished excretion of nitrate or both. (C) 2002 Elsevier Science B.V. All rights reserved.