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Objective To investigate the effects of ulinastatin on renal expression of endothelin￣1 and nitric oxide (NO) in rats with toxic acute kidney injury(AKI). Methods Twenty￣four male SD rats were randomly divided into the normal control group,model control group and treatment groups, with 8 rats in each group. Except normal control group, rats were subcutaneously injected with gentamicin (300 mg.kg-1 .d-1 ) for 3 days to establish a model of toxic AKI.Rats in the treatment group were intraperitoneally injected with a 7￣day course of ulinastatin (30 000 U.kg-1 .d-1 ) from the fourth day.While the other two groups were injected with 0.9% sodium chloride injection (3 mL.kg-1 .d-1 ). The serum level of creatinine and cystatin￣C,urinary concentration of kidney injury molecule￣1(Kim￣1) and neutrophil gelatinase￣associated lipocalin (NGAL), level of endothelin￣1 and NO,expression of endothelin￣1 mRNA,endothelial nitric oxide synthase (eNOS),induced nitric oxide synthase (iNOS),eNOS mRNA and iNOS mRNA in homogenate of renal tissues in each group were detected on the eleventh day. Results Compared with the normal control group,serum level of creatinine and Cystatin￣C,urinary concentration of Kim￣1 and NGAL,level of endothelin￣1 and NO,expression of endothelin￣1 mRNA,iNOS and iNOS mRNA in homogenate of renal tissues were higher in model control group (P<0.01, respectively), while which were lower in treatment group than those in model control group ( P < 0. 01, respectively). And no statistical significant difference of eNOS and eNOS mRNA expression in homogenate of renal tissues existed among the three groups. Conclusion Ulinastatin possesses curative role against rat with toxic AKI via down￣regulating renal expression of endothelin￣1,NO and iNOS.
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Objective To explore the curative effect of ulinastatin against toxic acute kidney injury(AKI) in rats and its mecha-nism .Methods Twenty-four male SD(Sprague Dawley) rats were randomly divided into 3 groups ,control group ,model group and treatment group with 8 rats in each group .Rats were subcutaneously injected gentamicin(300 mg/kg of body weight per day) for 3 days to establish models of toxic AKI .Rats in treatment group were intraperitoneally injected with a 7-day course of ulinastatin(30 000 U/kg of body weight per day) from 4th day .Dectetion of serum level of creatinine and Cystatin-C(Cys C) ,urinary concentra-tion of kidney injury molecule-1 (Kim-1 ) and neutrophil gelatinase-associated lipocalin (NGAL ) ,activity of superoxide dismutase (SOD) and glutathione peroxidase(GSH-Px) ,content of malondialdehyde ,levels of tumour necrosis factor-alpha(TNF-α) and inter-leukin-1β(IL-1β) in homogenate of renal tissues as well as observation of renal pathological changes and semiquantitative score in each group were conducted on 11th day .Results In model group ,degeneration and necrosis of renal tubular epithelial cell ,dilatation of renal tubular cavity and inflammatory cell infiltration in renal interstitial were observed .Renal pathological changes were milder in treatment group ,when compared with the model group .Renal pathological semiquantitative score ,serum level of creatinine and Cys C ,urinary concentration of Kim-1 and NGAL ,content of malondialdehyde ,levels of TNF-α and IL-1β in homogenate of renal tissues were higher in model group than in control group ,while those in treatment group were lower than in model group(P<0 .01 , respectively) .And activity of SOD and GSH-Px in homogenate of renal tissues were lower in model group than in control group ,and those in treatment group were higher than in model group and control group(P<0 .01 ,respectively) .Conclusion Ulinastatin pos-sesses a curative role in toxic AKI in rat via inhibiting oxidative stress and down-regulating levels of proinflammatory factor in renal tissues .
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ObjectiveTo investigate the predictor and prophylaxis of cardiovascular events in diabetic nephropathy (DN) patients. MethodsFifty-eight cases of DN patients were assigned randomizedly to two groups. Conventional treatment group(33 cases) received conventional treatment, and ginkgo biloba extract group(30 cases) received extra ginkgo biloba extract capsules treatment. Plasma examination for blood fat, blood pressure(Bp), brain natriuretic peptide(BNP) and echocardiogram was performed every 3 months. All the patients were followed-up for the occurrence of cardiovascular events. ResultsThere were no significant differences in age, sex, Bp, blood fat, serum creatinine, hemoglobin,BNP, left ventricular E/A and left ventricular ejection fraction (LVEF) in two groups at the time of recruitment. After treatment of 12 months, the level of plasma BNP decreased significantly in ginkgo biloba extract group and maintained in the lower levels throughout the follow-up compared with that in conventional treatment group(P＜ 0.01 ). After treatment of 18 and 24 months, left ventricular E/A and LVEF were better in ginkgo biloba extract group than those in conventional treatment group(P ＜ 0.01 or ＜ 0.05 ). In ginkgo biloba extract group, the level of plasma BNP after treatment of 12 months had correlation with left ventricular E/A and LVEF after treatment of 24 months (r =0.61, -0.68, P ＜ 0.05 ). Survival analysis indicated that the level of plasma BNP was a predictor of cardiovascular event in DN patients. ConclusionThe level of plasma BNP can be used as a predictor of cardiovascular event in DN patients,and ginkgo biloba extract capsules can decrease the level of plasma BNP and reduce the incidence of cardiovascular events in DN patients.
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Objective To explore the value of combined measurement of urine N-acetyl-beta-D-glucosaminidase (NAG) activity and serum Cystatin C in diagnosing diabetic nephropathy (DN) in early phase. Methods Sixty-two cases with type 2 diabetes (diabetic group) were divided into three groups according to their 24 hours urinary albumin excretion (24hUAE) : group A (normal albuminuria, 20 cases), group B (microalbuminuria, 22 cases) and group C (macroalbuminuria, 20 cases). Furthermore, 30 healthy people were involved in control group. 24hUAE,NAG,serum creatinine (SCr) and serum Cystatin C were measured, and endogenous creatinine clearance rate (Ccr) was calculated by Cockcroft-Gault formula. All these indexes among three groups were compared. Results The levels of urinary NAG activity and serum Cystafin C in diabetic group was significantly higher and Ccr was significantly lower than those in control group(P < 0.01). The levels of urinary NAG activity and serum cystatin C gradually increased in group A, B and C(P< 0.05 or < 0.01). While no significant difference was observed between group A and group B in the level of SCr (P > 0.05). There were significant positive correlations among the levels of urinary NAG activity, serum Cystatin C,24hUAE and SCr (P< 0.01),and all above showed negative correlations with Ccr (P<0.01). Co-detection of urinary NAG activity and serum Cystatin C had significantly higher positive rate [80.6%(50/62)] than single one [58.1%(36/62),61.3%(38/62)](P<0.05). Conclusion Co-detection of urinary NAG activity and serum Cystatin C may indicate early renal damage in DN, and it is valuable in diagnosing DN in early phase.
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Objective To investigate the feasibility of serum cardiac troponin T(cTnT) as a marker of cardiovascular events and hemodialysis (HD) adequacy in maintainence hemodialysis (MHD) patients.Methods Forty-seven cases of MHD patients were randomly divided into two groups (group A and group B).Group A received intermittent HD 4 h thrice one week,and group B received intermittent HD 4 h twice one week plus high-flux hemodiafiltration(HDF) 4 h once one week.Serum examination for blood biochemical indicator,cTnT and echocardiogram was performed every three months and at the time of recruitment.All the patients were followed up until the occurrence of death or cardiovascular events.Results After 3 months treatment,serum cTnT deceased significantly in group B compared with group A,and maintained the lower levels throughout the follow-up.E/A and LVEF had been reduced since 3 months treatment in group A,but stable in group B,E/A was lower in group A after 18 months treatment than that in group B,LVEF was lower in group A after 12 months treatment than that in group B.There were positive correlations between cTnT and E/A or LVEF in 42 cases who accomplished the follow-up of 12 months (r =0.54,0.66,P ＜0.05).Kaplan-Meier survival curve showed that the occurrence of cardiovascular events in patients with cTnT≥0.1μ g/L was higher than that with cTnT ＜0.1 μg/L in (28.5 ± 9.7) months' follow- up (Log-rank test: P =0.02).Both survival analysis and Cox analysis indicated that serum cTnT was a predictor of cardiovascular events in MHD patients.Conclusions Serum level of cTnT can be used as a marker of HD adequacy,and it is a predictor of cardiac events in MHD patients.Regular high-flux HDF increases the adequacy of HD treatment and improves the quality of life in MHD patients.
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sing guidewire through temporary catheter is an alternative strategy, because of avoiding this avoids vein re-puncturation and doesn't increase catheter related complication.
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Objective To characterize the expression of surfactant protein A (SP-A) in normal and acute pyelonephritic rat kidneys and to study the correlation of infection and inflammation with SP-A expression. Methods Twenty-one rats were randomly assigned into three groups: control, sham operation and pyelonephritic group. HE staining was used to determine tubulointerstitial inflammation. Reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting were used to determine the mRNA expression and protein level of SP-A. Immunohistochemical staining was used to label the localization and intensity of SP-A expression in kidney tissue. The correlation between intensity of SP-A expression and interstitial inflammation was also evaluated. Results In pyelonephritic group, tubulointerstitial inflammation was more prominent than that in control and sham groups (54.3?11.5,6.4?1.4, 8.6?1.9,respectively). RT-PCR and Western blotting revealed that SP-A expression was up-regulated in pyelonephritic group (in mRNA level: 2.2+0.58, 0.9?0.25, 1.1? 0.30; in protein level: 0.45?0.09, 0.24?0.05, 0.26?0.05, respectively). Immunohistochemical staining demonstrated that SP-A expression was mainly localized on epithelial cells in outer medullary and collecting tubules in normal group and sham group, but strong staining extended to collecting tubules in pyelonephritic group. The tubulointerstitial inflammation score was positively correlated with the intensity of SP-A expression (r=0.67,P
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Objective To investigate the effect of artorvastatin on macrophage accumulation in tubulointerstitium of unilateral ureteral obstructive (UUO) nephropathy and its possible mechanism.Methods Twenty-one rats were randomly divided into three groups: sham-operatipn, UUO, UUO+ artorvastatin. Immunohistochemistry staining of CD68 and M-CSF was used to define the macrophage accumulation and expression of interstitial M-CSF. Lipid profile in these groups was also determined. Results CD68 + cells and M-CSF expression were significantly increased at day 10 after UUO operation, this kind of CD68 + cell accumulation and M-CSF expression up-regulation were ameliorated by artorvastatin treatment. In UUO and atorvastatin treated groups, the number of macrophage was positively correlated with tubulointerstitial M-CSF expression. There was no significant difference about serum lipid among the three groups. Conclusion Atorvastatin can reduce interstitial macrophage accumulation in UUO nephropathy. This therapeutic effect might relate to down-regulation of tubulointerstitial M-CSF expression.
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Objective To investigate the effect of surfactant protein A (SP-A) on the production of MIP-2 and binding activity of NF-?B in rat tubular epithelial cells, and evaluate its possible role in renal inflammation. Methods Confluent cultures of NRK-52E cells (a renal tubular epithelial cell line of rat origin) were pretreated with various concentrations of SP-A(0 to 80 ?g/ml) and stimulated by lipopolysaccharide (LPS) (10 ?g/ml) with 2% serum. MIP-2 expression was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR). The effect of SP-A on NF-?B binding activity was assessed by electrophoretic mobility shift assay (EMSA). Results MIP-2 mRNA and protein was expressed and up-regulated in NRK-52E cells stimulated by LPS. The expression of MIP-2 was down-regulated by SP-A. NF-?B binding activity was inhibited by SP-A in a concentration-dependent manner. Conclusion SP-A binding activity and down-regulates the expression of MIP-2 in renal tubular epithelial cells, which may play an important role in the modulation of renal tissue inflammation.