Effect of cerebral microhemorrhages on neurocognitive functions in patients with end-stage renal disease.

BACKGROUND: Death is the most serious complication of intracerebral hemorrhage. Microbleeding can be a precursor of intracerebral hemorrhage. Susceptibility weighted imaging (SWI) should be included in imaging protocols for some specific groups such diabetic hemodialysis patients in terms of prediction of macrohemorrhages. PURPOSE: To investigate intracerebral microbleeding in hemodialysis patients and the correlation between microbleeding and neurocognitive impairment. MATERIAL AND METHODS: Forty-nine hemodialysis cases were involved in the study. Locations of microbleeding, correlation between microbleeding and hypertension, diabetes mellitus (DM), age, and duration of dialysis were analyzed. Standardized mini-mental test was performed. The tested cases were divided into two groups: intracerebral microbleeding (group 1, n = 26) and without intracerebral microbleeding (group 2, n = 17). RESULTS: Incidence of microbleeding and macrohemorrhage was noted as 59% and 14%, respectively, in all cases. All macrohemorrhagic cases also have microbleeding. In group 1, neurocognitive impairment was detected in 10 (38.4%) cases: six and four cases with moderate and mild impairment, respectively. In group 2, neurocognitive impairment was detected in 2 (11.7%) cases, both with mild impairment. A significant positive correlation was detected between microbleeding and neurocognitive impairment (P = 0.031). Although there was no correlation between attention disorder and microbleeding, a positive correlation was detected between close memory impairment and microbleeding (P = 0.027). A positive correlation was detected between DM and microbleeding (P = 0.027). CONCLUSION: In hemodialysis patients, microbleeding can be a cause of neurocognitive impairment which will be important for guide to treatment protocols. SWI should be included in the imaging protocol of diabetic hemodialysis patients with neurocognitive deterioration.

Effects of fasting during the month of Ramadan on renal function in patients with autosomal dominant polycystic kidney disease
.

BACKGROUND: In this study, we aimed to examine the impact of fasting during the month of Ramadan on autosomal dominant polycystic kidney disease (-ADPKD) patients with normal to near-normal glomerular filtration rate (GFR). MATERIALS AND METHODS: This was a prospective observational study of patients with ADPKD, the majority of whom had normal or near-normal GFR. Patients were divided into two groups: the fasting group (FG) and the nonfasting group (NFG). Assessments in the NFG were performed 1 week before and 1 month after Ramadan, while FG patients were assessed on the last day of fasting in addition to the abovementioned visits. The following parameters were checked at each visit: blood pressure (BP), weight, sodium, potassium, blood urea nitrogen (BUN), creatinine, calcium, phosphorus, glucose, lipid profile, bicarbonate, urine density, 24-hour urine volume, 24-hour urine protein, GFR, neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1). Kidney function tests were carried out on the 7th day of fasting in the FG for the identification of early kidney damage. RESULTS: Of the overall group of 54 patients, 23 were in FG (19 female) and 31 were in NFG (18 female). There were no significant differences between the two groups in terms of age, gender, ADPKD duration, and presence of hypertension. The mean estimated glomerular filtration rate (eGFR) values of FG and NFG were 86.4 ± 18.5 and 66.1 ± 36.5 mL/min/1.73m2, respectively. During the follow-up period, no significant changes occurred in BP, weight, creatinine, 24-hour urine volume, NGAL, KIM-1, or GFR in either group (p > 0.05), while 24-hour urinary protein was significantly decreased in FG (p < 0.001). CONCLUSION: A fasting duration of ~ 17 hours a day did not affect renal function negatively in patients with early-stage chronic kidney disease due to ADPKD. Also, no significant changes occurred in acute renal failure markers.
.

Protective effect of dexpanthenol against nephrotoxic effect of amikacin: An experimental study.

BACKGROUND: Amikacin has the largest spectrum among aminoglycosides, its nephrotoxic effect limits its utilization. Our purpose in this study is to review the protective effect of dexpanthenol against the nephrotoxic effect of amikacin, accompanied with histopathological and biochemical parameters. METHODS: 32 rats were randomly separated into four groups with eight in each (amikacin (1.2mg/kg/day), amikacin (1.2mg/kg/day)+dexpanthenol (500mg/kg/day), dexpanthenol (500mg/kg/day) and control). In order to assess the oxidative balance and renal damage between groups, biochemical parameters (total antioxidant capacity (TAS), total oxidant stress (TOS), catalase (CAT), paraoxonase (PON), arylesterase (ARES), urea, and creatinin) were studied from the blood samples. At the end of the 14th day, renal tissues were reviewed blindly by a pathologist. RESULTS: TOS and oxidative stress index (OSI) values were significantly lower in the group which was administered with dexpanthenol+amikacin compared to the group which only received amikacin (respectively, p=0.001, p=0.002). Antioxidant biochemical parameters (TAS, CAT, PON, and ARES) were significantly higher in the group which was administered with dexpanthenol+amikacin compared to the group administered only with amikacin (respectively, p=0.007, p=0.001, p=0.003, p=0.003). Urea and creatitin values were found to be significantly lower in the group which was administered with dexpanthenol+amikacin compared to the group administered only with amikacin (respectively, p=0.002, p=0.001). Histopathologic changes such as glomerular and tubular epithelium changes and interstitial edema were clearly observed in the group administered only with amikacin, such findings were insignificant in the group administered with dexpanthenol+amikacin. CONCLUSION: It was revealed with biochemical and histopathologic data that nephrotoxic effects created by amikacin administration can be limited with dexpanthenol by using them together, and further advanced clinical studies are required.

Endocan and albuminuria in type 2 diabetes mellitus.

BACKGROUND: Endocan is a newly identified proteoglycan released from endothelium, stimulating angiogenesis and when increased, indicates endothelial activation (inflammation). Our aim was to examine the association between serum endocan levels and urine albumin-creatinine ratio (UACR). METHOD: One hundred and thirty-seven patients with type 2 diabetes mellitus and normal serum creatinine who had no co-morbidities other than hypertension, diabetic nephropathy, retinopathy, or neuropathy were divided into normoalbuminuria (G1), microalbuminuria (G2), and macroalbuminuria (G3) groups and compared cross-sectionally regarding serum endocan levels. RESULT: There were 55, 47, and 35 patients in G1, G2, and G3, respectively. The groups were comparable in terms of gender, age, duration of diabetes, diabetic neuropathy/retinopathy, fasting glucose, HbA1c, serum creatinine level, and eGFR. Patients in G3 had significantly higher blood pressure but lower serum albumin and endocan levels. UACR showed a negative bivariate correlation with serum endocan levels (r = -.282, p = .001). There was bivariate positive correlation between endocan and systolic blood pressure (r=.185, p = .030). In linear regression analysis, UACR was negatively correlated with endocan while positively correlated with systolic blood pressure, duration of diabetes, and platelet distribution width. CONCLUSION: Patients with macroalbuminuria had lower endocan levels, and increasing UACR was associated with decreasing serum endocan levels. Despite the occurrence of angiogenesis and glomerular hypertrophy in the early phase of diabetic nephropathy, ensuing significant renal injury over time may reduce the expression of endocan. Serum endocan levels may represent a novel marker for nephropathy progression.

GAS6 intron 8 c.834 + 7G > A gene polymorphism in diabetic nephropathy.

UNLABELLED: BACKGROUND - AIM: In animal experiments, growth arrest-specific 6 (Gas6) protein plays a key role in the development of mesangial cell and glomerular hypertrophy in the early phase of diabetic nephropathy, and diabetic nephropathy is prevented by warfarin-induced inhibition of GAS6 protein. It was shown that GAS6 intron 8 c.834 + 7G > A polymorphism is protective against type 2 diabetes mellitus, and AA genotype is associated with higher blood levels of GAS6 protein. Our aim is to investigate whether this polymorphism is a risk factor for diabetic nephropathy in type 2 diabetes mellitus. METHOD: Eighty-seven patients with diabetic nephropathy were compared with 66 non-diabetic controls in terms of GAS6 intron 8 c.834 + 7G > A polymorphism. Patients with history of stroke, ischemic heart disease were excluded. Each patient was examined by the ophthalmologist to determine diabetic retinopathy. RESULTS: Frequency of GG, GA and AA genotypes are similar in diabetic nephropathy and control groups according to GAS6 intron 8 c.834 + 7G > A polymorphism (p = .837). Rate of diabetic retinopathy was 54.02%. In the subgroup analysis, GA genotype was significantly more frequent than GG genotype in patients with diabetic retinopathy when compared to without diabetic retinopathy (p = .010). CONCLUSION: In our study, GAS6 intron 8 c.834 + 7G > A polymorphism was not associated with diabetic nephropathy in type 2 diabetes mellitus. However, heterozygous state of this polymorphism may be a risk factor for diabetic retinopathy in patients with diabetic nephropathy.

Geriatric patients with known acute kidney injury and normal renal function at the time of admittance to the intensive care unit/assessment of RRT requirement and mortality: retrospective case-control study.

BACKGROUND: The objective of our study was to investigate the renal functions on admittance, chronic disease status, the diagnosis on admittance to the intensive care unit (ICU), need for mechanical ventilation and medication groups and their impact over mortality and renal replacement treatment (RRT) requirement in geriatric patients with and without known acute kidney injury (AKI) at the time of admittance. METHODS: A total of 168 patients over 65 years of age having been monitored for more than 24 h in our Respiratory ICU and were assessed retrospectively. Factors influencing the RRT requirement and the mortality rates of patients with known AKI and normal renal function at the time of admittance were reviewed. RESULTS: Of 80 patients, 8 (10 %) without AKI at the time of admittance to the ICU required RRT during the follow-up, however, 72 of those (90 %) completed the follow-up without developing AKI. Of 88 patients, 29 (33 %) with AKI at the time of admittance to the ICU required RRT, however, 59 of those (67 %) completed the follow-up without any need for RRT. CONCLUSIONS: Presence of known AKI in the geriatric population at the time of their admittance to the respiratory ICU remarkably increased both the need for RRT and the mortality with respect to the geriatric population with normal renal functions. After having assessed the reasons justifying RRT and increasing the mortality during the intensive care, gastrointestinal bleeding and hypotension which necessitate the combined use of dopamine and noradrenaline were concluded to be prominent.

Demographic and clinical characteristics of primary glomerular diseases in Turkey.

BACKGROUND: The aim of our study was to delineate the demographic and clinical properties of primary glomerular diseases of adult population in our country in the light of global knowledge. METHODS: All over the country, a total of 25 centers entered data between May 2009 and July 2012 to the database created by 'Glomerulonephritis Study Group' of Turkish Society of Nephrology. Demographic and clinical characteristics, specific diagnoses of glomerular diseases and biopsy findings recorded to the database were analyzed. RESULTS: Among the 1,274 patients, who had renal biopsy within the defined time period, 55 % were male and 45 % were female. The mean age was 40.8 ± 14.6 years. The most frequent indication for biopsy was nephrotic syndrome (57.8 %), followed by nephritic syndrome including rapidly progressive glomerulonephritis (16.6 %) and asymptomatic urinary abnormalities (10.8 %). The most frequent primary glomerular disease was membranous nephropathy (28.8 %), followed by focal segmental glomerulosclerosis (19.3 %) and IgA nephropathy (17.2 %). CONCLUSION: The presented study displayed important data about the epidemiology of primary glomerular diseases among adults in our country. The predominance of membranous nephropathy in contrast to other countries, in which the most frequent etiology is IgA nephropathy, seems to be due to differences in the indications for renal biopsy.

An unusual cause of peritonitis in peritoneal dialysis patients: Pantoea agglomerans.

Peritonitis is a serious infection and early diagnosis and treatment is mandatory. A variety of microorganisms are identified in these cases and during recent years a new one was included, Pantoea agglomerans. In this case report, a female patient on continuous ambulatory peritoneal dialysis therapy with a peritonitis episode caused by this organism is described. The source of infection was thought to be due to contact of catheter with non-sterile surfaces. In microbiologic culture, this organism was identified and the patient successfully treated with a three week course of gentamicin therapy. The number of reported cases with this organism has increased in last years and various infection localizations and clinical progress patterns have been identified. In peritoneal dialysis patients presenting with peritonitis, this organism must be kept in mind.

Effect of vildagliptin add-on treatment to metformin on plasma asymmetric dimethylarginine in type 2 diabetes mellitus patients.

AIMS: A close association has been demonstrated between increased cardiovascular risk and high asymmetric dimethylarginine (ADMA) levels in type 2 diabetes mellitus (DM) patients. We planned to measure serum ADMA levels in type 2 DM patients using vildagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor. MATERIALS AND METHODS: A total of 68 type 2 DM patients who were on metformin were enrolled in the study. Based on the glycemic levels of patients, vildagliptin was added on to treatment in 33 patients. Patients were followed for 6 months. Serum ADMA, C-reactive protein, and fibrinogen levels were compared in groups of patients using metformin or metformin + vildagliptin, after 6 months. RESULTS: Serum ADMA levels were found to be significantly lower in the group using vildagliptin compared to the group using metformin + vildagliptin (P<0.001). However, serum C-reactive protein and fibrinogen levels were statistically similar in the two study groups (P=0.34 and P=0.23, respectively). CONCLUSION: Metformin + vildagliptin treatment was observed to lower serum ADMA levels in type 2 DM patients. Our findings notwithstanding, large-scale prospective randomized controlled studies are warranted to conclude that vildagliptin provides cardiovascular protection along with diabetes regulation.

Assessment of serum apelin and lipocalin-2 levels in patients with subclinical hypothyroidism.

OBJECTIVES: Subclinical hypothyroidism is the precursor to hypothyroidism because it has a tendency to transform into hypothyroidism. Subclinical hypothyroidism is considered one of the risk factors causing metabolic syndrome. Metabolic syndrome can be characterized by plasma levels of apelin and lipocalin-2, both released from adipocytes. In the present study, we aimed to measure serum apelin and lipocalin-2 levels of patients with subclinical hypothyroidism and compare them with serum apelin and lipocalin-2 levels from healthy individuals. METHODS: This was a cross-sectional study. A total of 80 subjects were enrolled in the study and divided into two groups: Group A included 39 patients (females, n=34) diagnosed with subclinical hypothyroidism, and Group B (the control group) comprised 41 healthy volunteers (females, n=38). Serum samples were obtained from each participant for the measurement of apelin and lipocalin-2. These were then stored at minus 80°C until the time of analysis, when serum apelin and lipocalin-2 levels of the two groups were compared. RESULTS: Patients with subclinical hypothyroidism (Group A and Group B subjects [healthy controls]) were comparable with respect to gender, age, and body mass index (BMI) (P=0.412, P=0.863, and P=0.269, respectively), nor was there a statistically significant difference between groups in terms of apelin and lipocalin-2 levels (P=0.87, and P=0.67, respectively). Apelin levels showed a positive and significant correlation with BMI (P=0.034). Serum lipocalin-2 levels showed significant positive correlations with BMI and creatinine levels (P=0.002, and P=0.025, respectively). CONCLUSION: In the present study, no significant difference of serum apelin and lipocalin-2 levels was observed between patients with subclinical hypothyroidism and healthy control subjects. Positive correlations were found, however, between serum apelin level and BMI as well as between serum lipocalin-2 and BMI and creatinine levels.

A case of rhabdomyolysis complicated with acute renal failure after resumption of fenofibrate therapy: a first report.

Adverse effects due to use of fibrates often relate to the skeletal muscle, kidneys, or liver. Rhabdomyolysis is a most serious potential adverse effect. We present a case of resumed fenofibrate induced rhabdomyolysis complicated with acute renal failure.

Serum malondialdehyde levels, myeloperoxidase and catalase activities in patients with nephrotic syndrome.

OBJECTIVES: Some studies have indicated the pathophysiological importance of reactive oxygen species (ROS) in patients with nephrotic syndrome. Myeloperoxidase (MPO) is a leukocyte-derived enzyme-generating ROS that has been proposed to exert a wide array of pro-atherogenic effects throughout all stages of the atherosclerotic process. The aim of this study was to investigate the serum malondialdehyde (MDA) levels, MPO and catalase activities in patients with adult nephrotic syndrome. PATIENTS AND METHOD: s Twenty-four patients with nephrotic syndrome and 24 healthy controls were enrolled. Serum MPO activity, catalase activity, and MDA levels were assessed. RESULTS: Serum MPO activity and MDA levels were significantly higher in patients with nephrotic syndrome than controls (both, P<0.001), while catalase activity was significantly lower (P<0.001). Serum catalase activity was found to be significantly correlated with MPO activity (r=-0.417, P=0.003) and MDA levels (r=-0.532, P=0.007). The serum MDA levels were also found to be significantly correlated with MPO activity (r=0.419, P=0.003). CONCLUSIONS: We concluded that serum MPO activity and oxidative stress were increased and that serum catalase activity was decreased in patients with adult nephrotic syndrome. In addition, these results indicate that increased MPO activity is associated with an oxidant-antioxidant imbalance that may contribute to atherosclerosis in patients with adult nephrotic syndrome.

The effect of sleep apnea syndrome on the development of diabetic nephropathy in patients with type 2 diabetes.

AIMS: Type 2 diabetes mellitus and obstructive sleep apnea syndrome (OSAS) are serious comorbidities. Effects of OSAS on diabetic microvascular complications are ongoing research subjects. We evaluated the incidence of OSAS in Type 2 diabetes mellitus patients with nephropathy and with no renal involvement. METHODS: A total of 52 people with diabetes were enrolled in this study. Patients body mass indices were calculated and fasting glucose, glycosylated hemoglobin, urea, creatinine, total lipid profile, and urinary albumin excretion were evaluated. Full polysomnography was used to detect sleep disorders. RESULTS: Baseline characteristics and laboratory results of the patients were similar. Meeting criteria for OSAS was detected in 35 of the 54 patients (67.3%). 25 patients (48%) had mild, six patients (11.5%) had moderate, and four patients (7.7%) had severe sleep disorders. There was no significant relationship between respiratory obstructive parameters and microalbuminuria (R=0.91, p=0.362). Substantial correlation was detected between lower values of serum triglyceride levels and lower respiratory indices (R=0.299, p=0.031). CONCLUSIONS: In type 2 diabetes accompanying OSAS affects glucose regulation but its effect on nephropathy development is currently a subject of research.

Assessment of internal jugular vein thrombosis due to central venous catheter in hemodialysis patients: a retrospective and prospective serial evaluation with ultrasonography.

AIM: We aimed to evaluate the frequency of catheter-related internal jugular vein (IJV) thrombosis, associated factors, and the anatomical variations of IJV in hemodialysis patients. MATERIAL AND METHODS: Hemodialysis patients were evaluated with B-mode ultrasonography (USG). Participants in the prospective group were evaluated using USG prior to catheter insertion, 10 days after catheter insertion, at the time of catheter removal, and 15 days after removal. RESULTS: The rate of thrombosis was increased correlated with the number of catheter insertions. These rates were 14%, 15%, and 47% in those undergoing catheter insertion once, twice, and three times, respectively (P < .05). The anatomical variations of IJV were 21% in the retrospective cases. No significant relationship was found between anatomical variations and thrombosis and between some biochemical parameters and thrombosis. CONCLUSION: Catheter-related IJV thrombosis is frequent in hemodialysis patients. Long catheter remaining time and repeated catheterization increase the thrombosis rate.

Skin bleeding time for the evaluation of uremic platelet dysfunction and effect of dialysis.

INTRODUCTION: In patients with chronic kidney disease (CKD) predisposition to bleeding is frequently seen due to disturbances in platelet adhesion and aggregation. Various tests have been utilized to evaluate the disturbance of hemostasis in end-stage renal disease patients. In this trial; we evaluated skin bleeding time in patients admitted to our hospital with uremic symptoms and having hemodialysis (HD) for the first time. We also examined the effects of HD and uremia on this test and investigated its effectiveness in predicting the hemorrhagic complications before implementation of invasive procedures in uremic patients. MATERIAL-METHOD: Twenty nine patients (13 men,16 women; mean age 59.7 ± 18.1) with CKD who presented with symptoms of uremia and treated with HD for the first time were enrolled in this trial. The skin bleeding time were measured before initiation of first hemodialysis and after the second hemodialysis session. RESULTS: The skin bleeding time after the second dialysis was significantly shorter when compared to pre-dialysis values (p < 0.05). Correlation analysis between the skin bleeding time and urea, creatinine, hemoglobin, platelet, and bicarbonate showed no correlation. CONCLUSIONS: Skin bleeding time could reveal the uremic platelet dysfunction and beneficial effect of dialysis in the patients who presented with uremic symptoms and treated with HD for the first time. We suggest that skin bleeding time may be an appropriate test for the evaluation of hemostasis disturbance in uremic patients and prediction of the bleeding risk before invasive procedures.

The course of hypercalciuria and related markers of bone metabolism parameters associated with corticosteroid treatment.

BACKGROUND AND OBJECTIVE: Prolonged corticosteroid (CS) use induces osteoporosis; the pathogenesis of this condition is multifactorial and includes CS-induced hypercalciuria. We investigated the course of hypercalciuria and related markers of bone metabolism parameters during and after the CS treatment. MATERIALS AND METHODS: We recruited 42 patients who were taking at least 10 mg/day of methylprednisolone or an equivalent dose of CSs for at least 30 days. The 24-h urinary calcium and sodium, a spot urinary calcium/creatinine ratio, and urinary deoxypyridinoline were measured prior to the treatment, at day 7, at days 30-60, and after the cessation of the treatment. Additionally, the serum levels of phosphorus, calcium, alkaline phosphatase (ALP), albumin, creatinine, osteocalcin, and parathyroid hormone (PTH) were analyzed. RESULTS: The 24-h urinary calcium excretion was significantly increased at day 7 (182.2 ± 158.6 mg/day; p < 0.001) and at days 30-60 (196.9 ± 167.8 mg/day; p < 0.001) compared with baseline (98.7 ± 88.1 mg/day) and returned to basal level after the cessation of the CSs (118.9 ± 90.2 mg/day; p = 0.725). The urinary deoxypyridinoline level was significantly higher at days 30-60 compared with basal level. The serum osteocalcin level was decreased at days 30-60 when compared with day 7. No significant changes were detected in the PTH, phosphorus, creatinine, and ALP levels. CONCLUSIONS: CS treatment induces hypercalciuria just after starting the treatment until the end of it. CS-induced hypercalciuria promptly improved after cessation of the treatment. By days 30-60, the excretion of urinary deoxypyridinoline was accompanied by hypercalciuria. The serum osteocalcin level was decreased at days 30-60 when compared with day 7.

Fenofibrate-induced rhabdomyolysis in a patient with chronic renal failure due to nephrotic syndrome: a rare case report.

OBJECTIVES: Fenofibrate is a fibric acid derivative that is used alone or combination with statins in the treatment of hyperlipidemia. These drugs have potential risks, including rhabdomyolysis and acute renal failure. Despite reports of rhabdomyolysis with the use of fenofibrate alone or with statin-fibrate combinations, there have been no cases of rhabdomyolysis described when fenofibrate was used alone to treat patients with chronic renal failure owing to nephrotic syndrome. DESIGN AND METHODS: We report on a 26-year-old male who presented with fenofibrate-induced rhabdomyolysis with chronic renal failure due to nephrotic syndrome. RESULTS: After the discontinuation of fenofibrate, the patient was treated with intravenous fluid replacement and urine alkalization. Subsequently, his clinical and biochemical findings improved. CONCLUSIONS: Before starting fenofibrate therapy, the causes of secondary hyperlipidemia, especially nephrotic syndrome, should be investigated. In the presence of chronic renal failure and hypoalbuminemia, the fenofibrate dose should be adjusted. Physicians should be aware of the potential toxicities of fenofibrate, and patients should be informed about its potential side effects.

Fenofibrate-induced rhabdomyolysis in a patient with stage 4 chronic renal failure due to diabetes mellitus.

Rhabdomyolysis is defined as a pathological condition of skeletal muscle cell damage leading to the release of toxic intracellular components into the circulation. Several factors may lead to rhabdomyolysis. Fenofibrate is a fibric acid derivative agent that is used in the treatment of hyperlipidaemia. Although several case reports of rhabdomyolysis have been reported due to the combination of statin and fenofibrate, fenofibrate alone rarely causes rhabdomyolysis. When administering fenofibrate in chronic renal failure, dose should be adjusted. Here, we report a case with fenofibrate-induced rhabdomyolysis in a patient with chronic renal failure.

Relationship between visfatin and some clinical and biochemical parametres in peritoneal dialysis patients.

OBJECTIVE: To characterise the relationship between visfatin levels and various clinical and biochemical parameters in peritoneal dialysis patients. METHODS: The case-control study was conducted at the Medical Faculty Hospital, Yuzuncu Yil University, Van, Turkey, between May 2007 and December 2008, and involving 41 patients on peritoneal dialysis, 20 haemodialysis patients and 20 healthy controls. Fasting visfatin level was measured with enzyme-linked immunosorpent assay (ELISA) method, and patients on peritoneal dialysis were separated into two groups according to the visfatin levels - high and low. The groups were compared in terms of some clinical (height, weight, body mass index, waist circumference, hip circumference, waist/hip ratio, heart rate, systolic and diastolic blood pressure and the kt/V and CrCI (creatanine clearance) parameters which are indicative of the dialysis adequacy) and biochemical parameters (glucose, triglycerides, cholesterol, low density lipoprotein, high density lipoprotein, aspartate aminotransferase, alanine transminase, blood urea nitrogen, creatinine, total protein, albumin, globulin, sodium, potassium, magnesium, calcium, phosphorus, ferritin, venous blood gas, parathyroid hormone and insulin). SPSS 15 was used for statistcal analysis. RESULTS: No statistically significant difference in the visfatin levels was found between the patients and controls (7.71 +/- 4.04, 7.36 +/- 3.71, 7.70 +/- 1.61, respectively, p = 0.63). The triglyceride level of the high-visfatin group was significantly higher than that of the low-visfatin group (243.8 +/- 133.2, 150.8 +/- 65.8, respectively, p<0.05). However, there was no correlation between visfatin and triglyceride levels. No difference in the other clinical and biochemical parametres was observed between the two groups of peritoneal dialysis patients. CONCLUSIONS: No significant difference in the serum visfatin levels of peritoneal dialysis patients compared to haemodialysis patients or healthy individuals was noticed. Further studies are needed to confirm the effect of visfatin on triglyceride levels, and, if confirmed, the mechanism of this relation.