Epicardial Adiposity is Associated with Microalbuminuria in Patients with Essential Hypertension.

BACKGROUND: Measurement of epicardial adipose tissue (EAT) is suggested as a novel cardiometabolic risk factor. Microalbuminuria is a marker of endothelial dysfunction and is associated with an increased risk for cardiovascular disease in patients with systemic hypertension. The aim of this study was to investigate the relationship of echocardiographic epicardial adipose tissue (EAT) thickness and microalbuminuria in hypertensive patients. METHODS: 75 essential hypertensive patients were included into the study. All subjects underwent transthoracic echocardiography to measure EAT thickness. Spot urine sample was collected for the assessment of microalbuminuria. Patients were divided into two groups according to their spot urine albumin to creatinine ratio (UACR); Group 1 included normoalbuminuria (0-30 µg/mg); and Group 2: included microalbuminuria (30-300 µg/mg). Thereafter, we evaluated patient characteristics including smoking status, blood pressure, body mass index (BMI), antihypertensive treatment, statin therapy and serum levels of total cholesterol, low-density lipoprotein cholesterol, triglicerides, albumin, C-reactive protein (CRP), creatinine and hemoglobin. RESULTS: There was no difference in baseline characteristics between Group 1 and Group 2. Patients with microalbuminuria had significantly higher mean EAT thickness values compared to the normoalbuminuria group (7.1 ± 0.9 vs. 6.6 ± 0.9, p = 0.01). There were positive significant correlations between EAT and age (r = 0.267, p = 0.020), serum creatinine (r = 0.292, p = 0.01), UACR (r = 0.251, p = 0.03), left ventricular mass (r = 0.257, p = 0.03) and left ventricular mass index (r = 0.242, p = 0.04). UACR was independently associated with EAT (p = 0.01) after adjustments were made for age and BMI. CONCLUSIONS: Epicardial Adipose Tissue (EAT) thickness could be associated with microalbuminuria in patients with essential hypertension. This association could support the recognition of EAT as a credible marker in cardiovascular risk stratification.

Protective effect of beta-glucan on contrast induced-nephropathy and a comparison of beta-glucan with nebivolol and N-acetylcysteine in rats.

BACKGROUND: 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). METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Could nephrotoxicity due to colistin be ameliorated with the use of N-acetylcysteine?

PURPOSE: The protective effect of N-acetylcysteine (NAC) on nephrotoxicity due to contrast nephropathy and reperfusion-induced ischemia has been reported in experimental models. However, its efficacy on colistin-induced nephrotoxicity has not been elucidated yet. The primary aim of this study was to evaluate the nephrotoxic effect of colistin and to investigate the possible protective effect of NAC on colistin-induced nephrotoxicity. The secondary aim was to research the systemic effects of nephrotoxicity-induced oxidative stress on the lung. METHODS: Eighteen female Sprague-Dawley rats were randomly assigned and were given (a) 1 ml/kg sterile saline, (b) 300,000 IU/kg/day colistin, and (c) 300,000 IU/kg/day colistin and 150 mg/kg NAC for six consecutive days. RESULTS: Plasma blood urea nitrogen (BUN), creatinine, urinary creatinine, urinary protein, plasma TNF-alpha levels, renal tissue superoxide dismutase (SOD) and malondialdehyde (MDA) activity and immunocytochemical findings were evaluated. Colistin exerted nephrotoxicity and achieved a significant increase in plasma BUN and creatinine levels and renal tissue SOD levels. NAC exhibited no significant effect on biochemical parameters but reduced renal tissue SOD level and reversed immunocytochemical staining of inducible nitric oxide synthase (i-NOS) and neurotrophin-3. Increased oxidative stress in the lung tissue of the rats treated with colistin has also been documented. Additionally, NAC significantly reduced the immunostaining of endothelial NOS (e-NOS) and i-NOS in the lung tissue. CONCLUSIONS: Colistin-induced renal toxicity may be attributable to oxidative damage. The combined treatment of colistin plus NAC seems to have a beneficial role in restoration of the oxidant injury which may be related to its antioxidant effect.

A spontaneous spinal epidural hematoma in a hemodialysis patient: a rare entity.

Hemodialysis patients are at an increased risk of bleeding due to the platelet dysfunction caused by uremia and the use of anticoagulants during dialysis. Spontaneous spinal hematoma is a rare disorder as a complication in hemodialysis patients. Also it includes the hematoma secondary to coagulopathy, vascular malformation and hemorrhagic tumors. Here, we report the case of 77-year-old woman who presented with spinal cord compression due to spontaneous spinal epidural hematoma associated with hemodialysis. When an end-stage renal disease patient suffers from back pain and neurological deficits, the clinician should be alerted for the spontaneous spinal epidural hematoma as well as cerebrovascular events.

Renal cell carcinoma associated immunosuppressive therapy: a case report with Wegener's granulomatosis.

Development of uroepithelial tumors after cyclophosphamide and azathioprine therapy in Wegener's granulomatosis (WG) have been reported in the literature but renal cell carcinoma (RCC), rarely. RCC associated with WG has been previously reported in a few cases. Most of them have simultaneous diseases. Here, we report a case, which developed RCC 8 years after initiation of WG. Long-term immunosuppressive treatment is a risk factor for the development of malignancies; it should be suggested that RCC in our patient might be due to immunosuppressive therapy.

The relationship of visfatin levels to inflammatory cytokines and left ventricular hypertrophy in hemodialysis and continuous ambulatory peritoneal dialysis patients.

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.