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Plasma Creatinine Levels (plasma + creatinine_level)
Selected AbstractsProtective Effect of Ebselen, a Selenoorganic Drug, against Gentamicin-Induced Renal Damage in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2006R. Dhanarajan However, its clinical use is limited by its nephrotoxicity. Oxidative stress and nitrosative stress are reported to play important role in gentamicin nephrotoxicity. In the present study we investigated whether ebselen, an inhibitor of oxidative stress and nitrosative stress prevents or reduces gentamicin-induced renal damage in the rat. For this purpose male Wistar rats were divided into five groups and treated as follows. Group 1 (control group): dimethyl sulphoxide, intraperitoneally, Group 2: Gentamicin 100 mg/kg b.wt. subcutaneously, Group 3: 5 mg/g b.wt. ebselen intraperitoneally, Group 4: 2.5 mg/kg b.wt. ebselen followed by 100 mg/kg b.wt. gentamicin subcutaneously one hour later, and Group 5: 5 mg/kg b.wt. of ebselen followed by 100 mg/kg b.wt. gentamicin one hour later for four consecutive days. Nephrotoxicity was evaluated histopathologically by light microscopy, and biochemically by the measurement of the plasma creatinine and urea levels. Parameters of oxidative stress such as reduced glutathione, malondialdehyde, and activities of superoxide dismutase and glutathione peroxidase were measured in the kidney. Serum nitrite and nitrate were measured as indicators of nitrosative stress. Treatment of rats with gentamicin resulted in statistically significant reduction in reduced glutathione levels (51%) and the activities of antioxidant enzymes superoxide dismutase (56%) and glutathione peroxidase (39%) as compared with the controls in the kidneys. Renal malondialdehyde level was increased significantly (43%) as compared with the controls. Plasma creatinine levels, urea levels and nitrite levels were significantly increased (4, 4.5 and 160% times respectively) as compared with the controls. Histologically, damage to the renal cortex and medulla was observed moderate to severe tubular necrosis and glomerular congestion. Pretreatment with 2.5 mg/kg b.wt. ebselen prevented gentamicin induced damage to medulla; however, renal cortex showed mild damage and biochemically indicators of oxidative stress and nitrosative stress were significantly reduced. Pretreatment with 5 mg/kg b.wt. ebselen prevented gentamicin-induced oxidative damage and nitrosative damage and renal damage almost completely in 78% of the rats, in the other 22% of the rats, ebselen pretreatment reduced gentamicin-induced renal damage. The results of the present study suggest that ebselen may be useful as a nephroprotective agent. [source] Long-term evolution of the acute tubular necrosis (ATN) induced by glycerol: role of myofibroblasts and macrophagesINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 4 2002Telma J. Soares Summary. Late structural changes such as interstitial fibrosis in the renal cortex and tubular atrophy have been detected after severe acute tubular necrosis (ATN). The aim of this study was to investigate the expression of fibronectin, ,-smooth muscle actin and macrophages during the evolution of the ATN induced by glycerol and their relationship with the late structural changes observed in the kidneys of these animals. Forty-nine male Wistar rats were injected with a 50% glycerol solution, 8 mL/kg (4 mL/kg applied i.m. to each hind leg) and 14 with 0.15 m NaCl solution. Before glycerol injection on day 1, water was removed for 17 h. Blood and urine samples were collected 1 day after the injection to quantify sodium and creatinine. The animals were killed 5, 30 and 60 days after the injections and the kidneys removed for histological and immunohistochemical studies. The results of the histological and immunohistochemical studies were scored according to the extent of lesion or staining in the cortical tubulointerstitium, respectively. The percentage of tubulointerstitial lesions was determined by morphometry. Glycerol-injected rats presented a transitory increase in plasma creatinine levels and in fractional sodium excretion. The immunohistochemical studies showed increased fibronectin, ,-smooth muscle actin (,-SM-actin), TGF-, and ED-1 (macrophages) staining in the renal cortex from rats killed 5, 30 and 60 days after glycerol injection (P < 0.05) compared to control. The animals killed on day 30 and 60 also presented chronic lesions (fibrosis, tubular dilatation and atrophy) in the renal cortex, despite the recovery of renal function. Macrophages, TGF-, and myofibroblasts may have contributed to the development of renal fibrosis in these rats. [source] Sodium Bicarbonate versus Sodium Chloride and Oral N-Acetylcysteine for the Prevention of Contrast-Induced Nephropathy in Advanced Chronic Kidney DiseaseJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 6 2009LINDA SHAVIT M.D. Introduction: Contrast-induced acute kidney injury (CI-AKI) is one of the leading causes of hospital-acquired acute kidney injury. Multiple clinical studies have proposed several preventive strategies. Aims: To examine the efficacy of sodium bicarbonate compared with sodium chloride and oral N-acetylcysteine (NAC) for preventive hydration after cardiac catheterization. Methods: We conducted a prospective, single-center trial. Patients with chronic kidney disease (CKD) stage III,IV undergoing cardiac catheterization were allocated to receive either an infusion of 0.9% sodium chloride and oral NAC or 154 mEq/L sodium bicarbonate. Main: Outcome measure CI-AKI, defined as an increase of 25% or 0.3 mg/dL or more in plasma creatinine within 2 days of contrast administration. Results: Ninety-three patients were allocated to one of the two groups: 42 patients in the saline plus NAC group and 51 patients in the bicarbonate group. There were no statistically significant differences between the groups in the most important clinical and procedural characteristics. Baseline plasma creatinine levels, estimated glomerular filtration rate, incidence of diabetes mellitus, hypertension, congestive heart failure, and contrast medium volume were similar. Mean plasma creatinine concentration was 1.76 ± 0.54 mg/dL in the saline and NAC group and 1.9 ± 1 mg/dL in the bicarbonate group (P = 0.23). The rate of CI-AKI was 9.8% in the bicarbonate group and 8.4% in the saline plus NAC group. No patient required renal replacement therapy. Conclusion: Hydration with sodium bicarbonate is not more effective than hydration with sodium chloride and oral NAC for prophylaxis of CI-AKI in patients with CKD stage III,IV undergoing cardiac catheterization. [source] Maximum limits of organic and inorganic mercury in fish feedAQUACULTURE NUTRITION, Issue 2 2004M.H.G. Berntssen Abstract The relatively high levels of mercury found in fish feeds might form a fish health and food safety risk. The present study aims to establish sublethal toxic threshold levels in fish and assess feed-fillet transfer of dietary mercury. Atlantic salmon (Salmo salar L.) parr were fed for 4 months on fish meal-based diets supplemented with mercuric chloride (0, 0.1, 1, 10 or 100 mg Hg kg,1 dry weight (DW)) or methylmercuric chloride (0, 0.1, 0.5, 5 or 10 mg MeHg kg,1 DW). At the end of the experiment, dietary inorganic mercury mainly accumulated in intestine (80% of body burden) and assimilation was low (6%). In contrast, methylmercury readily accumulated in internal organs and muscle (80% of body burden) and had a relatively high assimilation (23%). Highest accumulation of dietary inorganic mercury was observed in the gut and kidney. Fish fed 10 mg Hg kg,1 had an early (after 2 months) significant increase in renal metallothionein (MT) level and intestinal cell proliferation, followed by intestinal pathological conditions after 4 months of exposure. At 100 mg Hg kg,1, intestinal and renal function were reduced as seen from the significantly reduced protein and glycogen digestibility and increased plasma creatinine levels. For dietary methylmercury (MeHg), highest accumulation was found in blood and muscle. Intestinal cell proliferation and liver MT significantly increased at 5 mg MeHg kg,1 after 2 months of exposure. At the end of the experiment, blood haematology was significantly affected in fish fed 5 mg MeHg kg,1 and these fish exceeded the current food safety limit for mercury. Tissue MT induction and intestinal cell proliferation appeared to be useful and quantifiable early indicators of toxic mercury exposures. Based on the absence of induction of these early biological markers such as MT and cell proliferation, nonobserved effect levels (NOELs) could be set to 0.5 mg Hg kg,1 for dietary methylmercury and 1 mg Hg kg,1 for inorganic mercury. Lowest observed effect levels (LOELs) levels could be set to 5 mg kg,1 for methylmercury and 10 mg Hg kg,1 for inorganic mercury. [source] INTRAPERITONEAL GLYCEROL INDUCES OXIDATIVE STRESS IN RAT KIDNEYCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 8 2008Elenara Rieger SUMMARY 1Glycerol has been used for the treatment of intracranial hypertension, cerebral oedema and glaucoma. Experimentally, intramuscular administration of hypertonic glycerol solution is used to produce acute renal failure. In this model, glycerol causes rhabdomyolysis and myoglobinuria, resulting in the development of renal injury. The pathogenesis is thought to involve vascular congestion, the formation of casts and oxidative stress. However, the effect of glycerol itself independent of rhabdomyolysis has not been investigated. Therefore, the aim of the present study was to investigate the effects of i.p. glycerol on some biochemical and oxidative stress parameters in the kidney of young rats. 2Rats received 10 mL/kg, i.p., hypertonic glycerol solution (50% v/v) or saline (NaCl 0.85 g%) followed by 24 h water deprivation. Twenty-four hours after the administration of glycerol, rats were killed. Creatinine levels and the activity of creatine kinase (CK) and lactate dehydrogenase (LDH) were determined in the plasma. In addition, CK, pyruvate kinase and LDH activity and oxidative stress parameters (free radical formation, lipid peroxidation and protein carbonylation) were measured in renal tissue. 3Glycerol did not alter plasma CK activity and increased plasma creatinine levels, suggesting renal insufficiency and the absence of rhabdomyolysis. Renal CK and pyruvate kinase activity was decreased, suggesting diminution of energy homeostasis in the kidney. Plasma and renal LDH activity was decreased, whereas the formation of free radicals, lipid peroxidation and protein carbonylation were increased, suggesting oxidative stress. 4These results are similar to those described after the intramuscular administration of glycerol. Therefore, it is possible that glycerol may provoke renal lesions by mechanisms other than those induced by rhabdomyolysis. [source] | ||||||||||