The effect of hemodialysis on cardiac enzyme levels and echocardiographic parameters.

BACKGROUND: Cardiac troponins are specific and sensitive markers of myocardial damage. Troponin levels may increase without an obvious active cardiac disease in hemodialysis patients. In this study, we aimed to investigate the effect of a single hemodialysis session on echocardiographic parameters and cardiac enzyme levels, including cTn-I, creatine phosphokinase (CPK), and creatine kinase-MB (CK-MB). PATIENTS AND METHODS: Forty patients under chronic hemodialysis treatment enrolled in this prospective study. All the patients had a physical examination and underwent echocardiography before and after hemodialysis. cTn-I, CPK and CK-MB levels were also determined before and after hemodialysis in all patients. RESULTS: Post-dialysis cTn-I levels were significantly higher compared to pre-dialysis levels (p = 0.03). cTn-I levels increased in 26 patients, did not change in 1 patient and decreased in 13 patients after hemodialysis when compared to the values determined before hemodialysis. There was no significant increase in CPK and CK-MB levels after dialysis. Statistically significant changes were detected in the end-systolic diameter of the left ventricle, end-diastolic diameter of left ventricle, ejection fraction, diameter of the left atrium, diameter of the right atrium, pulmonary artery pressure and end-diastolic diameter of the right ventricle. However, there was no significant relation between these echocardiographic changes and ultrafiltration volume, blood flow rate, age, and gender. CONCLUSIONS: Hemodialysis leads to an increase in cTnI levels. However, the effect of increased cTnI levels on survival rates in hemodialysis patients with underlying coronary artery disease has not yet been determined. Prospective multi-center studies with large sample size are required to clarify this issue.

Lack of nephrotoxicity of gadopentetate dimeglumine-enhanced non-vascular MRI and MRI without contrast agent in patients at high-risk for acute kidney injury.

BACKGROUND: Gadolinium chelates (GCs) have been traditionally considered as non-nephrotoxic magnetic resonance imaging (MRI) contrast materials. However, it has been suggested in some recent articles that GCs may have a nephrotoxic potential, but most of these reports are retrospective. However, the evaluated contrast agents, their doses, and the tests used to determine the kidney function were not consistent across studies. We aimed to investigate the effect of magnetic field and an MRI contrast agent, gadopentetate dimeglumine (GD), on renal functions in patients at high risk for acute kidney injury (AKI). MATERIAL AND METHODS: We designed a prospective case-control study with 2 age- and sex-matched groups of patients at high-risk for AKI (n=72 for each group). Patients in Group 1 received a fixed dose of (0.2 mmol/kg) GD-enhanced non-vascular MRI and patients in Group 2 received MRI without GD. Before the MRI and at 6, 24, 72, and 168 hours after the MRI, biochemical tests, estimated glomerular filtration rate (eGFR), albumin/creatinine ratio in spot urine, and early AKI biomarkers (cystatin C, N-Acetyl-Glucosaminidase [NAG], Neutrophil gelatinase-associated lipocalin [NGAL]) were measured. RESULTS: Serum creatinine, albumin/creatinine ratio, and eGFR were not different between Group 1 and 2 (p>0.05). There were no significant changes in renal function tests and AKI biomarkers (∆serum creatinine, ∆albumin/creatinine ratio, ∆GFR, ∆cystatin C, ∆NAG, and ∆NGAL) for either groups 6, 24, 72, and 168 hours after the procedures (p>0.05). CONCLUSIONS: MRI without contrast agent and non-vascular contrast-enhanced (GD, 0.2 mmol/kg) MRI are not nephrotoxic procedures for patients at high risk for AKI.

Community-acquired hypernatremia in elderly and very elderly patients admitted to the hospital: clinical characteristics and outcomes.

BACKGROUND: The clinical features, outcome and cost burden of community-acquired hypernatremia (CAH) in elderly and very elderly patients are not well known. Our aim was to investigate the etiologies, reasons for admission, clinical courses, outcomes, complications, and cost assessments of the elderly patients with CAH. MATERIAL/METHODS: We conducted a retrospective study in our tertiary hospital. Elderly and very elderly patients evaluated in the emergency department (ED) from January 1, 2010 to December 31, 2010 (n=4960) were included. Totally, 102 patients older than 65 years and diagnosed with CAH were evaluated. The patients were divided into 2 main groups according to their age: elderly (65-74 years old) (group 1) (n=38), and very elderly (>74 years) (group 2) (n=64). RESULTS: Our overall observed prevalence of CAH was 2.0% (n=102, 102/4960). In particular, the prevalences of CAH in group 1 and group 2 were 1.0% (38/3651) and 4.8% (64/1309), respectively (p<0.001). Totally, 62 patients had been treated by renin-angiotensin system (RAS) blockers (ie, ACE-inhibitors). Alzheimer's disease had been diagnosed in 46.1% of the subjects. The mean Katz scores at the time of admission were 2.4 ± 1.9 and 1.1 ± 1.0 in group 1 and 2, respectively (p<0.001). The mean cost was higher in group 2 than in group 1 (2407.13 ± 734.54 USD, and 2141.12 ± 1387.14 USD, respectively) (p<0.01). The need for intensive care was significantly greater in group 2 as compared to group 1. CONCLUSIONS: The important determinants of "CAH" in elderly subjects are accompanying Alzheimer's disease, oral intake impairment, and concomitant treatment with RAS blockers.

Peripheral DNA damage in active pulmonary tuberculosis.

In pulmonary tuberculosis patients, little is known about peripheral DNA damage, although increased oxidative stress is a well documented entity. Therefore, we aimed to investigate DNA damage along with oxidative status parameters in pulmonary tuberculosis patients. Twenty-seven pulmonary tuberculosis patients and 26 controls were included. DNA damage was assessed by comet assay. Total oxidant and antioxidant status, and oxidative stress index were determined. DNA damage, total oxidant status and oxidative stress index were higher in pulmonary tuberculosis patients than controls (all P < 0.05), while total antioxidant status was lower (P < 0.05). DNA damage was correlated with total oxidant and antioxidant status, and oxidative stress index (r = 0.69, P < 0.05; r = 0.48, P < 0.05, r = -0.47, P < 0.05; respectively) in pulmonary tuberculosis patients. Oxidative stress and DNA damage are increased in pulmonary tuberculosis patients. Increased oxidative stress associated DNA damage may be one of the pathogenetic mechanisms involved in the disorders suggested to be associated with pulmonary tuberculosis.

Nonsteroidal anti-inflammatory drug-induced severe hyponatremia.

Hyponatremia (serum sodium level, <135 mmol/L) occasionally may develop in the course of treatment with nonsteroidal anti-inflammatory drugs, which are usually used in daily clinical practice. Nonsteroidal anti-inflammatory drugs diminish the normal inhibitory effect of prostaglandins on the activity of antidiuretic hormone and can therefore reduce free water excretion, leading to water retention and induction or exacerbation of hyponatremia. In this report, we present a case of hyponatremia in a 78-year-old man who had received meloxicam, a nonsteroidal anti-inflammatory drug.

Peripheral lymphocyte DNA damage and oxidative status after eradication therapy in patients infected with Helicobacter pylori.

INTRODUCTION: Helicobacter pylori infection has been shown to cause inflammation, increased production of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. However, the effect of eradication treatment on DNA damage in patients infected with H. pylori is unclear. OBJECTIVES: The objective of this study was to investigate the effect of eradication treatment on peripheral DNA damage and oxidative status in patients wth H. pylori infection. PATIENTS AND METHODS: The study involved 42 patients positive for H. pylori (Hp+) and 25 patients negative for H. pylori (Hp-). Peripheral lymphocyte DNA damage was assessed using the alkaline comet assay and plasma oxidative status was determined. Measurements were conducted at baseline and 2 weeks after eradication treatment. RESULTS: The total antioxidant status (TAS) was lower in Hp+ patients than in Hp- patients (P <0.05), while the total oxidant status (TOS), oxidative stress index (OSI), and peripheral lymphocyte DNA damage were higher (P <0.001 for all parameters). TOS, OSI, and peripheral lymphocyte DNA damage were significantly lower after eradication treatment (P <0.001 for all parameters), while TAS was significantly higher (P <0.05). There was no correlation between TOS, OSI, peripheral lymphocyte DNA damage, and TAS and the histopathological degree of antral gastric inflammation in the Hp+ group (P >0.05). CONCLUSIONS: Our results suggest that H. pylori eradication significantly decreases peripheral lymphocyte DNA damage and oxidative stress. Eradication treatment might help prevent the development of gastric cancer in patients with H. pylori infection.

Development of high-output heart failure after correction of central venous occlusion: a case report.

Temporary or permanent central venous catheter (CVC) insertion has been performed frequently for hemodialysis treatment. One of the most important long-term complications of CVC is the central venous occlusion (CVO). Treatment of CVO consists of percutaneous angioplasty (PTA), PTA and stent implantation, or surgical procedure for resistant occlusions. Clinical outcome and long-term results of the revascularization procedures are well documented. However, there is no clear information about acute medical complications of the procedures. High-output heart failure (HOHF) is associated with several diseases including chronic anemia, psoriasis, systemic arteriovenous fistula, sepsis, hypercapnia, multiple myeloma, and hyperthyroidism. Herein, we report a case of chronic kidney disease with CVO that developed acute HOHF immediately after the revascularization procedure (PTA and stenting).

Serum paraoxonase enzyme activity and oxidative stress in obese subjects.

INTRODUCTION: Obesity is an important risk factor for atherosclerotic cardiovascular disease. Paraoxonase-1 (PON1) may play a significant role in the prevention of obesity-related accelerated atherosclerosis by hydrolyzing lipid peroxides in oxidized low-density lipoproteins. OBJECTIVES: The aim of this study was to evaluate PON1 and arylesterase enzyme activities and lipid hydroperoxide (LOOH) levels, and to investigate whether there is increased susceptibility to atherogenesis in obese subjects, which might be reflected by increased oxidative stress and decreased PON1 activity. We also aimed to investigate the association between PON1 activity and body mass index (BMI) in this patient group. PATIENTS AND METHODS: The study involved 25 obese subjects and 23 controls. Serum PON1 and arylesterase activity was measured spectrophotometrically. LOOH levels were measured by the FOX-2 assay. RESULTS: Serum basal/salt-stimulated PON1 and arylesterase activities were significantly lower in obese subjects than in controls (P <0.001 for both enzymes), while LOOH levels were significantly higher (P <0.001). BMI was significantly correlated with PON1, arylesterase and LOOH levels (P <0.001, r = -0.720; P <0.001, r = -0.634; P <0.001, r = 0.491; respectively). Serum high-density lipoprotein (HDL) levels were positively correlated with PON1 activity (r = 0.347, P <0.05). CONCLUSIONS: Our results indicate that obese subjects have increased oxidative stress and decreased PON1 activity, which might contribute to accelerated atherosclerosis. A decrease in PON1 activity seems positively correlated with BMI and inversely correlated with HDL levels.

Peripheral lymphocyte DNA damage and oxidative stress in patients with ulcerative colitis.

INTRODUCTION: Ulcerative colitis (UC) is a fairly common chronic inflammatory disorder. Chronic inflammation may contribute to the risk of colorectal cancer through the accumulation of specific products resulting from DNA damage. Previous studies reported that DNA damage and oxidative stress play a significant role in the pathophysiology of UC, but the results are inconsistent. OBJECTIVES: In the present study, we investigated peripheral DNA damage and oxidative stress in patients with UC. PATIENTS AND METHODS: The study included 20 patients with UC and 20 controls. Peripheral lymphocyte DNA damage was measured using the alkaline comet assay. Plasma total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) were determined. RESULTS: DNA damage levels, TOS, and OSI were significantly higher in patients with UC than in controls (P <0.001 for all parameters), while TAC was significantly lower (P <0.001). DNA damage was significantly correlated with TOS, TAC, and OSI (r = 0.604, P <0.001; r = -0.593, P <0.001; and r = 0.716, P <0.001, respectively). Moreover, TAC levels were significantly correlated with TOS and OSI (r = 0.604, P <0.001; r = -0.399, P <0.05; and r = -0.513, P <0.05, respectively). CONCLUSIONS: Our results show that increased peripheral DNA damage and oxidative stress seem to be associated with decreased antioxidant levels and thus may in part contribute to the development of colorectal cancer associated with UC.

The influence of hemodialysis membrane permeability on serum paraoxonase-1 activity and oxidative status parameters.

We aimed to measure oxidative stress parameters and paraoxonase-1 (PON-1) enzyme activities in chronic hemodialysis (HD) patients and to investigate whether HD membrane permeability has any influence on those measures. Forty-seven HD patients and 24 controls were enrolled. At the first step of the study, all HD patients had undergone HD treatment via "low-flux" membranes for 4 weeks. At the second step of the study, the membranes were switched to "high-flux" membranes and HD treatments were also performed via "high-flux" membranes for 4 weeks. Blood samples were withdrawn after completion of 4 weeks treatment for each membrane. Total oxidant status (TOS), total antioxidant status (TAS), and paraoxonase and arylesterase activities were measured in blood samples of the patients and the controls. TOS and oxidative stress index (OSI) of both membranes were higher than controls (all, P < 0.05), while TAS and paraoxonase and arylesterase activities were lower (all P < 0.05). Paraoxonase (P < 0.05, r = -0.437 and P < 0.05, r = -0.453, respectively) and arylesterase (P < 0.05, r = -0.333 and P < 0.05, r = -0.371, respectively) activities of "low-flux" and "high-flux" membranes were inversely correlated with OSI. There were no significant differences between "low-flux" and "high-flux" membranes in regard to oxidative stress parameters or PON-1 enzyme activities (all, P > 0.05). HD patients have increased oxidative stress and decreased serum PON-1 activities inversely correlated with oxidative stress. Membrane permeability seems to have no influence on oxidative stress parameters and PON-1 enzyme activities.

The effect on serum myeloperoxidase activity and oxidative status of eradication treatment in patients Helicobacter pylori infected.

OBJECTIVES: Myeloperoxidase activity has been investigated after eradication of Helicobacter pylori (H. pylori) in infected patients in previous studies but the results are controversial. The aim of this study was to investigate effect on serum myeloperoxidase activity and oxidative status of eradication treatment in H. pylori-infected patients. DESIGN AND METHODS: Gastric biopsy specimens were obtained from 30 H. pylori infected patients. Serum myeloperoxidase activity was measured by enzyme-linked immunoassay. Oxidative status was determined using total antioxidant capacity (TAC) and total oxidant status (TOS) measurement and calculation of oxidative stress index (OSI). RESULTS: After 2 weeks of the eradication treatment, serum myeloperoxidase activity, TOS and OSI values were significantly lower (all; p<0.001), while TAC was significantly higher (p<0.001). CONCLUSIONS: Our results indicate that eradication treatment in H. pylori-infected patients may affect both oxidative stress and myeloperoxidase activity which is an important biomarker in pathogenesis of atherosclerosis.

Risk factors for infections caused by multidrug-resistant bacteria in patients with solid tumours.

OBJECTIVES: We aimed to determine the risk factors for healthcare-associated infections (HCAI) caused by multidrug-resistant (MDR) bacteria in patients with solid tumours. METHODS: This retrospective study was performed in the Department of Clinical Microbiology and Infectious Diseases, Mersin Teaching and Research Medical Centre, between January 2004 and December 2008. SPSS version 11.5 program package was used for the statistical analyses. RESULTS: A total of 145 patients who had an HCAI were analyzed; 62% of the patients were male and their median age was 57.7 ± 16 y and median Charlson co-morbidity score was 4.94 ± 1.2. During the study period, 83 MDR bacteria were isolated from HCAIs that developed in 70 (48.3%) patients. In multiple binary logistic regression analysis, duration of hospital stay (odds ratio (OR) 1.041, 95% confidence interval (CI) 1.007-1.077; p = 0.019), surgery (OR 3.115, 95% CI 1.288-7.535; p = 0.012), use of glycopeptides (OR 5.394, 95% CI 1.960-14.850; p = 0.001), and use of third-generation cephalosporins (OR 5.521, 95% CI 2.017-15.110; p = 0.001) were found to be independent risk factors for the development of an MDR infection. CONCLUSIONS: Among hospitalized patients with a solid tumour, HCAIs caused by MDR bacteria occurred more frequently in patients undergoing surgery, receiving third-generation cephalosporins and glycopeptide antibiotics, and having a prolonged hospital stay.

Evaluation of oxidative status in iron deficiency anemia through total antioxidant capacity measured using an automated method.

OBJECTIVE: Oxidative stress, an increase in oxidants and/or a decrease in antioxidant capacity, is one of the potential biochemical mechanisms involved in the pathogenesis of iron deficiency anemia. The objective of this study was to evaluate the oxidative status and to determine whether there is any relationship between oxidative status and the severity of anemia in patients with iron deficiency anemia using an automated method. METHODS: Twenty-six subjects with iron deficiency anemia and 20 healthy controls were enrolled in the present study. Serum total antioxidant capacity, serum total peroxide level and oxidative stress index were determined in all study subjects. RESULTS: Serum total antioxidant capacity was significantly lower in patients with iron deficiency anemia than controls (p<0.05), while serum total peroxide level and oxidative stress index were significantly higher (both p<0.05). There was a significant correlation between hemoglobin level and serum total peroxide level, oxidative stress index and total antioxidant capacity (r=-0.504, p<0.05; r=-0.503, p<0.05; r=0.417, p<0.05, respectively). CONCLUSION: Increased oxidative stress may play a role in the pathogenesis of iron deficiency anemia. Supplementation of antioxidant vitamins in conjunction with iron replacement therapy may offer better responses and provide early resolution of symptoms related to iron deficiency anemia. The automated assay is a reliable and easily applied method for measurement of serum total antioxidant capacity in iron deficiency anemia.

Pulmonary hypertension in hemodialysis patients without arteriovenous fistula: the effect of dialyzer composition.

Pulmonary hypertension (PHT) increases mortality rate in hemodialysis (HD) patients. Numerous clinical, hemodynamic, and metabolic abnormalities have been suggested to be associated with the development of PHT in HD patients. We aimed to investigate the acute effects of two different dialyzer membranes on pulmonary arterial pressure (PAP) throughout a HD session in maintenance HD patients. Seventy-four HD patients dialyzed through permanent tunneled jugular central venous catheter were enrolled. A first-use cellulose acetate and high-flux polysulfone dialysis membrane were tested using a crossover design. For each membrane, pre- and post-dialysis pulmonary artery pressures were measured echocardiographically. Elevated pulmonary artery pressure was observed in 68.8% of patients (n = 51), whereas mild PHT was observed in 28.3% of patients (n = 21) and moderate PHT in 40.5% (n = 30). Decrease in pulmonary artery pressure following HD procedure performed using high-flux polysulfone membrane was significantly higher than the decrease observed following HD procedure performed using cellulose acetate membrane (p < 0.05). Significant decrease in pulmonary artery pressures was observed only after HD procedures performed using high-flux polysulfone membrane (p < 0.05). Ultrafiltered volume was only significantly correlated with the decrease in pulmonary artery pressure observed after HD procedure performed through high-flux polysulfone membrane (ß = 0.411, p < 0.05). PHT seems to be prevalent among HD patients even in the absence of AV fistula and abnormal cardiac functions. Membrane composition seems to be important, which may overwhelm the improving effects of ultrafiltration.

Serum prolidase enzyme activity and its relation to histopathological findings in patients with non-alcoholic steatohepatitis.

The aim of this study was to investigate serum prolidase enzyme activity and to find out its association with liver biopsy specimens' histopathological findings in patients with nonalcoholic steatohepatitis (NASH), which may progress to liver fibrosis and cirrhosis. Thirty-six patients with biopsy-proven NASH and 29 healthy controls were enrolled. Serum prolidase enzyme activity was measured spectrophotometrically. Serum prolidase enzyme activity was significantly higher in patients with NASH than controls (P=0.016). A significant correlation was observed between serum prolidase enzyme activity and fibrosis score in patients with NASH (r=0.661, P<0.001). Serum prolidase activity seems to be correlated with the level of fibrosis. Monitoring serum prolidase activity may be a useful adjunctive tool in predicting liver fibrosis, especially in the absence of advanced fibrosis and other conditions, which may affect the interpretation of prolidase activity.

Successful treatment of resistant antiglomerular basement membrane antibody positivity with mycophenolic acid.

Anti-glomerular basement membrane (GBM) antibody disease may progress to end-stage renal failure, requiring either dialysis or renal transplantation. In patients with end-stage renal disease (ESRD) due to anti-GBM-ab disease, the recurrence rate after transplantation is as high as 50% (2) and delaying renal transplantation until circulating anti-GBM antibody levels have been undetectable for at least 12 months reduces the recurrence rate to 5-15%. We report a case of ESRD due to renal limited anti-GBM disease with circulating anti-GBM-ab resistant to standard treatment approach who achieved undetectable anti-GBM-ab with mycophenolic acid.

Serum stem cell factor level in renal transplant recipients with posttransplant erythrocytosis.

The etiology of posttransplant erythrocytosis (PTE) remains unclear, and the most frequently suggested causative factors are still a matter of controversy. We aimed to investigate serum-soluble stem cell factor (sSCF) along with serum erythropoietin (EPO) levels in renal transplant recipients (RTRs) with PTE. Thirteen RTRs with PTE, 42 RTRs without PTE, and 42 healthy controls were included. Serum sSCF and EPO levels were determined using an enzyme-linked immunosorbent assay kit. Expected and observed/expected EPO levels were calculated. Serum sSCF levels and observed/expected EPO were significantly higher in RTRs with PTE than both RTRs without PTE and controls. In RTRs with PTE, sSCF level was significantly correlated with hematocrit and observed/expected EPO, respectively. Significant correlation was also observed between hematocrit level and observed/expected EPO in RTRs with PTE. Increased sSCF level and inadequate suppression of EPO production seem to have a role in the pathogenesis of PTE.

The influence of omentectomy on bacterial clearance: an experimental study.

BACKGROUND: The influence of an omentectomy on peritoneal defense mechanisms and its clinical consequences have not been fully elucidated. In the present study, we aimed to investigate the influence of omentectomy on bacterial growth in blood and tissue specimen cultures in rats with experimental peritonitis. METHODS: Fifty Wistar-Albino rats were included in the present study. Animals were assigned into five groups as follow: Group 1 (n = 10), omentectomy alone; Group 2 (n = 10), omentectomy + bacterial peritonitis; Group 3 (n = 10), bacterial peritonitis alone; Group 4 (n = 10), laparotomy alone; and Group 5 (n = 10), sham group. Culture positivity rate and bacterial growth (colony forming units [CFU]/gram tissue) were assessed in mesenteric lymphoid tissue and venous blood of all animals. RESULTS: Bacterial growth in lymphoid tissue was significantly higher in Groups 2 and 3 than others (both, p < 0.05). CFU of Escherichia coli in lymphoid tissue was significantly higher in Group 2 than in Groups 1 and 3 (both, p < 0.05/4). Blood culture positivity was significantly higher in Group 2 than the others (both, p < 0.05). CONCLUSION: The omentum has an important role in the host peritoneal defense system. Peritoneal infection may pursue a more severe course with increased bacterial entrance into the blood in the absence of the omentum.