Objective To evaluate factors such as renal injury grade （Sargent Method）, blunt or penetrative renal injury, injury severity score（ISS）, and shock influencing the need for operation or nephrectomy, and predictive of mortality in renal injury. Methods A well~tesigned questionnaire was used to collect medical records retrospectively. Two hundred and twenty-one cases of renal injury in West China Hospital from 1998 to 2002 were included, logistic regression analysis was used for multi-factors analysis. Results The average age of the 221 cases was 31.6, with 191 males （86.4%） and 30 females （13.6% ）, 175 blunt injuries （79.2%） and 46 penetrative injuries （20.8%）, and 101 concomitant injuries （45.7%）. Six cases died of renal injury （2.7%）. The results of logistic regression showed that the need of operation was related to injury grade, Type of renal injury, and shock significantly. ORs （odd ratios） were 5. 965 with 95% CI 2. 767 to 12. 859, 4. 667 with 95% CI 1. 725 to 12. 628, and 2. 547 with 95% CI 1. 684 to 3. 936 respectively. The need of nephrectomy was significantly related to injury grade with OR 11. 550 and 95% CI 4. 253 to 31. 366. The death was significantly related to ISS with OR 1. 263 and 95% CI 1. 082 to 1. 411. Conclusions The results of our data suggest the need of operation depends on injury grade, blunt or penetrative renal injury, and shock. The need of nephrectomy depends on injury grade. The death is related to ISS.
Objective To explore the effect of renal microcirculation following severity acute pancreatitis （SAP） on renal injury and to explore the protection effect of urokinase on them. Methods A total of 192 Wistar rats were randomized divided into normal control group， SAP group， and urokinase group， then rats of 3 groups were sub-divided into 2， 6， 12， and 24 hours group， each group enrolled 16 rats. Of the 16 rats in each subgroup， 8 rats underwent blood flow of renal test， other 8 rats were sacrificed to get blood samples and to perform histopathological examination. The rat models of SAP were established by retrograde injecting with 5% sodium taurocholate into the cholangiopancreatic duct. Radioactive biomicrosphere technique was used to measure the blood flow of renal， levels of plasma thromboxane B2（TXB2） and 6-keto-prostaglandin F1α （6-Keto-PGF1α） were tested by the TXB2 kit and 6-Keto-PGF1α kit， and histopa-thological changes of renal tissues were observed by using HE staining. Results Compared with normal control group at the same time point， the blood flow of renal were lower （P＜0.05）， activity ratio of TXB2 to 6-Keto-PGF1α were higher（P＜0.01）， and the histopathological injury were worse （P＜0.01） in rats of SAP group and urokinase group. Compared with SAP group， the blood flow of renal at 2， 6， and 12 hours in urokinase group were higher （P＜0.01）， the activity ratios of TXB2 to 6-Keto-PGF1α were lower （P＜0.01）， and the histopathological injury were lighter （P＜0.05） in all the 4 time points of urokinase group. Conclusions The renal microcirculation dysfunction and increase of activity ratio of TXB2 to 6-Keto-PGF1α may play an important role in renal injury following SAP in early stage. Urokinase can protect the renal from such injuries.
ObjectiveTo investigate the effect of emodin on the expression of hypoxia inducible factor (HIF)-1α protein in rats with severe acute pancreatitis-associated renal injury and explore the possible mechanisms. MethodsA total of 72 rats were randomly divided into sham-operated group (n=24), severe acute pancreatitis with renal injury group (injury group, n=24), and treatment group (n=24). The sham-operated and injury groups were given 1.5 mL saline through intragastric administration before operation while the treatment group was fed with the same amount of 50 mg/kg emodin diluent. The pancreas and pancreatic tail-segment was dissociated and the head of pancreas was occluded in rats to form the model, and blood vessel forceps were loosed after three hours. All the rats were sacrificed 12, 24 and 36 hours after modeling. The level of ascites, serum amylase, creatinine, blood urea nitrogen were detected. Hematoxylin-eosin staining was used to observe the pancreatic and renal pathological changes, and immunohistochemical method was used to detect the expression of HIF-1α protein level in the kidney. ResultsCompared with the sham-operated group, the level of ascites, serum amylase, creatinine, blood urea nitrogen and the expression of HIF-1α protein level increased significantly. The tissue damage of pancreas and the kidney became more serious. Compared with the injury group, the kidney and pancreas function of the treatment group had a better performance. HIF-1α protein level significantly increased in the treatment group, and the difference had a statistical significance (P<0.05). ConclusionEmodin has a good protective effect on severe acute pancreatitis-associated renal injury. It may function through up-regulation expression of HIF-1α protein level to improve the ability of the kidney to tolerate hypoxia, and then reduce the cell apoptosis and necrosis of the kidney.
ObjectiveTo investigate the effect of Curcumin combined with Rhodiola on rats with severe acute pancreatitis (SAP) associated renal injury and explore the possible mechanisms. MethodsA total of 24 rats were randomly divided into SAP with renal injury group (SAP group, n=8), Curcumin group (n=8), Curcumin combined with Rhodiola group (n=8).The SAP group was given 1.5 mL saline through intragastric administration before operation while the Curcumin group was fed with same amount of Curcumin diluent.The Curcumin combined with Rhodiola group was given 1.5 mL Curcumin diluent through intragastric administration and 6 g/kg Rhodiola diluent through intraperitoneal injection before operation.The pancreas and pancreatic tail-segment was dissociated and the head of pancreas were occluded in rats to make the model, blood vessel forceps was loosed after three hours.All the rats were sacrificed at 18 h after modeling.The levels of serum amylase, creatinine, blood urea nitrogen were detected and pathological changes of pancreas and the left kidney were observed under the light microscope.The cell apoptosis was analyzed using TUNEL staining.The serum levels of interleukin (IL)-1β, IL-6, and IL-10 among the three groups were detected by enzyme-linked immunosorbent assay.The expression of inducible nitric oxide synthase (iNOS) mRNA in the right kidney was detected by real-time polymerase chain reaction.The superoxide dismutase (SOD) activity of the renal tissue was determined by hydroxylamine method. ResultsCompared with the SAP group, the levels of serum amylase, creatinine, blood urea nitrogen, IL-1β, IL-6, the cell apoptosis index, and the expression of iNOS mRNA were significantly decreased, the serum level of IL-10 and the activity of SOD were significantly increased (P < 0.05), the pancreas and the kidney damaged more slightly in the Curcumin group and Curcumin combined with Rhodiola group.Compared with the Curcumin group, the above situations were more better in the Curcumin combined with Rhodiola group. ConclusionsCurcumin combined with Rhodiola has a better protective effect on SAP associated renal injury.It might be through inhibiting the expressions of IL-1β, IL-6, stimulating the expression of IL-10, down-regulating the expression of iNOS mRNA, and improving the activity of SOD.It could reduce the cell apoptosis and necrosis of the kidney and improve the ability of the kidney to tolerate hypoxia.
ObjectiveTo investigate the effects of curcumin on expression of iNOS mRNA, study the protective and therapeutic effects on rats with severe acute panceratitis associated renal injury, and explore the possible mechanisms. MethodsA total of 24 rats were randomly divided into control group (n=8), severe acute panceratitis with renal injury group (injury group, n=8), and curcumin-treated group (treated group, n=8).The rats of control group and injury group were given 1.5 mL saline through intragastric administration at 3 h before operation, while the rats of treated group were fed with same amount of curcumin diluent at 3 h before operation.The rats of injury group and treated group with pancreatic head clamping method to establish the model of severe acute pancreatitis.At 12 h after modeling, rats in control group and injury group were perfused with 1.5 mL saline, and rats in treated group were intragastrically administrated to the same volume of curcumin diluent.All the rats were sacrificed at 18 h after modeling.The levels of serum amylase, creatinine, and blood urea nitrogen were detected and pathological chang of pancreas and the left kidney were observed under light microscope.The renal cell apoptosis were analyzed using TUNEL staining in three groups.The serum levels of interleukin-1β(IL-1β), interleukin-6 (IL-6), and interleukin-10 (IL-10) in three groups were detected by enzyme-linked immunosorbert assay (ELISA).The expressions of inducible nitric oxide synthase (iNOS) mRNA in the right kidney were detected with realtime polymerase chain reaction (RT-PCR) in three groups. ResultsCompared with the control group, the levels of serum amylase, creatinine, blood urea nitrogen, IL-1β, IL-6, and IL-10, the cell apoptosis and the expressions of iNOS mRNA in injury group and treated group were significantly increased (P < 0.05).In the treated group, the level of IL-10 was higher than the injury group (P < 0.05), and the difference of other indexes were lower than the injury group (P < 0.05). ConclusionsCurcumin has a better protective effect on severe acute pancreatitis associated renal injury.It may be through inhibited the expressions of IL-1βand IL-6, stimulated the expression of IL-10, and down-regulation of iNOS mRNA expression to reduce the generation of oxygen free radicals and NO damage to cell and reducing the cell apoptosis and necrosis of kidney.
Objective To explore the mechanism of chronic intermittent hypoxia (CIH) on renal damage with normal diet and high-fat diet. Methods Twenty-four healthy male Wistar rats of SPF grade were randomly divided into 4 groups (n=6 in each group), namely group A (normoxia and common diet), group B (normoxia and high fat diet), Group C (CIH and common diet), and group D (CIH and high fat diet). The serum cystatin C (Cys-C) was measured and the renal CHOP protein was detected by immunohistochemistry. The ultrastructural changes of glomeruli and renal tubules were observed under electron microscope. Results The levels of Cys-C in group B, group C and group D were significantly higher than those in group A (P<0.05). The mean density of endoplasmic reticulum stress (ERS) marker protein CHOP in group B, group C and group D was significantly higher than that in group A (P<0.05). Electron microscope revealed focal nuclear pyknosis in the partly renal tubular epithelial cells, sparse and scattered brush border in group B and group C, also revealed nuclear pyknosis in a large number of tubular epithelial cells, sparse and scattered brush border in group D. Conclusion CIH can activate the ERS mediated renal tubular epithelial apoptosis, thus induce ultrastructure changes and damage of kidney.
ObjectiveTo explore the optimal conditions of rat model of hyperuricemia (HUA) induced by different doses of potassium oxanate (PO) combined with adenine, and to provide reference for the treatment of HUA.MethodsMale Sprague-Dawley rats (220-240 g body weight) were divided into normal control group, potassium oxanate (1000, 1500 mg/kg) and adenine (0, 50, 100 mg/kg) combined model groups, with 8 rats in each group. After 5 weeks of intragastric administration, blood were collected from tail vein of rats every week, and serum uric acid, creatinine and blood urea nitrogen level were measured. At the 6th week, the changes of the pathological characteristics, expression of inflammatory and fibrosis-related factors in the kidneys were observed.ResultsIn the 1500 mg/kg potassium oxanate combined with 100 mg/kg adenine group, rats died after 2 weeks of molding, and the survival rate at the 6th week was 62.5%; but there was no significant difference between the other groups and the normal control group in survival rate (P>0.05). Compared with the normal group, the level of serum uric acid in each model group increased significantly after 1 week of molding (P<0.05), but recovered to the pre-model level after stopping intragastric administration in week 6. After 5 weeks, in model groups the levels of serum creatinine and blood urea nitrogen were higher than those in the normal control group; and the inflammation and fibrosis-related factors mRNA and protein expression of kidney tissue in model groups increased with the increase of ademine dose, and there was a significant difference in the PO 1 000 mg/kg with adenine 100 mg/kg group, PO 1 500 mg/kg with Adenine 50 mg/kg group compared to the normal control group (P<0.05). The results of renal anatomy and histology testing in rats showed that with the increased of the dosage of PO and adenine in the model groups, the increase of white deposition of renal medulla, tubulointerstitial fibrosis, and tubular epithelial cell necrosis was found, and the glomerular atrophy aggravated. Compared with the indexes in the normal control group, the expression levels of inflammation and fibrosis related genes and proteins in the 50 mg/kg adenine combined with 1 500 mg/kg PO group were higher, and inflammatory cell infiltration and fibrosis were observed, which was consistent with the clinical manifestation of hyperuricemia induced renal injury.ConclusionPO (1500 mg/kg) combined with adenine (50 mg/kg) can establish a stable hyperuricemic nephropathy model in rats.