The prevention and control of chronic kidney disease(CKD)and end-stage renal disease(ESRD)has become an important public health problem.This article has outlined the status,hazards,and problems in prevention of CKD and ESRD,briefly described the work having been done by the Chinese Society of Nephrology of the Chinese Medical Association,and proposed countermeasures for future prevention and treatment of ESRD,aiming at improving knowledge of the urgency of combating ESRD by the society,government,public,and medical staff in order to improve the prevention and treatment of ESRD in China.

Objective To introduce the current development of nephrology during the period of "Eleventh-Five-Year Plan" in PLA medical circles,to serve as a reference for the further development of nephrology in PLA.Methods Literature concerning nephrology published domestically and abroad in past 5years were retrieved,and the progresses,achieved domestically and abroad,especially in PLA,on new concept,diagnoses and therapy of common nephropathy,and clinical applications of new drugs and techniques were emphatically analyzed.Results Great progresses have been made during the period of "Eleventh-Five-Year Plan" on basic researches,clinical applications and substitution therapy in nephrology,and outstanding achievements have been acquired on basic and clinical researches of chronic nephropathy and acute renal injury,drug treatment of renal diseases and continuous renal replacement therapy.The PLA medical personnel participated in the formulation of "Diagnostic and Therapeutic Standard of Renal Diseases" ,furthered the academic exchanges between the military and civilian circles,both domestically and abroad.The academic level of PLA in nephrology was raised markedly with obvious features and preponderance.Conclusion During the period of "Twelfth-Five-Year Plan" ,the focus of nephropathy researches should be put on the enhancement of the ability of military health service,integrated control and comprehensive remedy of acute renal injury induced by combat wound,trauma and stress injuries.It is important to stably retain the superiority on basic and clinical researches of chronic nephropathy,acquire more achievements,make greater contributions to raising the professional level of diagnosis and treatment of kidney diseases.

Alterations in the balance between synthesis and degradation of extracellular matrix (ECM) and its remodeling may result in an accumulation of ECM molecules and lead to glomerulosclerosis. Recent studies have focused on the role of degradative systems, especially the roles of plasminogen activators/plasminogen activator inhibitors (PA/PAI), matrix metalloproteinases, and their inhibitors[GK2*4/5!2*4/5] (MMP/TIMP) in the initiation and pathogenesis of renal diseases. Previously, attention has been paid to the study of inhibitors of ECM degrading enzymes, such as PAI and TIMP. Recent researchs showed that there existed complex dynamic expressions of enzymes and their inhibitors. Although many studies have tried to elucidate the pathogenesis of renal diseases, the exact underlying mechanisms are still not completely understood. For better understanding of the mechanism of chronic progressive renal diseases, the underlying genetic and molecular regulation of each component of PA/PAI and MMP/TIMP systems should be elucidated in different renal physiological and pathophysiological processes. Future studies are needed to manipulate activity or expression of these proteinases in order to treat and/or prevent glomerular diseases.

Chronic kidney disease(CKD)is increasingly recognized as a global public health problem.Uncontrolled complications of CKD,especially cardiovascular diseases,contribute greatly to the premature death and unfavorable prognosis.Recent evidence shows that CKD complications may occur earlier than previously thought.CKD complications deserve early detection and active treatment.Periodical follow-up and regular check should be done to adjust the therapeutic condition.Clinical practice guideline or recommendation based on evidence-based medicine is essential for management of CKD complications.Personalized treatment should be considered to improve survival and quality of life,and to make patient return to society.

Animal model of aged rat nephrotoxicity was induced by i. p. administrationof gentamycin in a dose of 140mg/kg/day. Part of those rats were treated with CordycepsSinensis(CS), Epimedium(Ep) and Astragalus Membranaccus (AM) in form of decoc-tion per Os and others seryed as control. The results were summarized as. 1. The nephro-toxicity of gentamycin was aggrevated with age. CS, Ep and AM are effective drugs inpreventing the tdeular damage caused by gentamycin in rats. The pathological changes ofrenal tuoules of the rat groups which treated with CS, Ep and AM were less severe thanthat of the control. 2. CS, Ep and AM could prevent the decline of renal cortical Na~+-K~+-ATPase activity of aged rat induced by gentamycin.

BACKGROUND: Nucleus raphe magnus(NRM) is an important nucleus located in the median raphe of ventral medulla. Many studies have been focused on the crucial role which plays in acupuncture analgesia, cardiovascular regulation, respiratory regulation and other aspects of health. However,little attention has been paid to its role in the regulation of digestive system heretofore.OBJECTIVE: To investigate the effect of NRM on gastric movement and gastric electric activity in rabbits.DESIGN: Comparative study based on the experimental animals.SETTING: A laboratory of functional medicine in a traditional Chinese medical university. PARTICIPANTS: From September 2002 to April 2004, the study was conducted in the functional medicine laboratory of Heilongjiang University of Chinese Medicine(Provincial Key Laboratory). Seventy healthy New Zealand white rabbits were used including male and female, which weighed 2 - 2. 5 kg on average, supplied by the Laboratory Animal Center of Heilongjiang University of Chinese Medicine(Class I) . The rabbits were randomly divided into 7 groups: saline group, 5-hydroxytryptamine(5-HT)group, cyproheptadine group, substance P group, substance pantagonist group, morphine group and noradrenaline group.METHODS: Through cannula, microinjection of 5-HT, cyproheptadine, substance P, substance P antagonist, morphine and noradrenaline were given into NRM. Synchronously, gastric movement and changes in the amplitude and frequency of gastric electric slow wave in rabbits were recorded.MAIN OUTCOME MEASUREMENTS: Gastric movement and gastric electric activity were observed after microinjection of 5-HT, cyproheptadine,substance P, substance P antagonist, morphine and noradrenaline into NRM.RESULTS: After microinjection of 5-HT and substance P into NRM,gastric movement and gastric electric slow waves in rabbits were inhibited ( P ＜ 0. 05, P ＜ 0. 01 ). After microinjection of cyproheptadine, substance P antagonist, gastric movement and gastric electric slow waves in rabbits were increased( P ＜ 0.05, P ＜ 0.01) . Meanwhile, it turned out that microinjection of morphine and noradrenaline into NRM had no effect on gastric movement and gastric electric slow waves in rabbits ( P ＞ 0.05).CONCLUSION: 5-HT and substance P in NRM contribute to the regulation of gastric movement and gastric electric slow wave in rabbits by NRM, while morphine and noradrenaline presumably have no relation with the regulation.

Objective To determine the changes in expressions of thrombin receptor and fibrin deposit in glomeruli during the process of senility. Method Rats were divided into 3 groups (8 rats in each group): 3-month-old group (3m), 12-month-old group (12m) and 24-month-old group (24m). Fibrin deposition was detected by Martius-Scarlet-Blue staining and direct immunofluorecence method. Immunohistochemical studies were performed to detect the expression of thrombin receptor (PAR-1) and transforming growth factor-? (TGF-?). Semi-quantitative PCR was performed to detect the changes in PAR-1 mRNA expression. A quantitative analysis of the expressions was performed by image analysis system. Result Significant pathological changes were found in glomeruli during the process of senility. Fibrin deposition was not observed in glomeruli in different groups. Significant expression of PAR-1 was found in glomerular endothelial cells, mesangial cells and epithelial cells in 3m rats. On the contrary, in 24m rats, PAR-1 expression in glomeruli was significantly decreased. Expression of TGF-? was increased with senility in glomeruli. PAR-1 gene expression, barely detectable in control tissue, was strikingly increased in 24m rats. Conclusion Thrombin receptor activation could be found in glomeruli of senile rat, and it is independent of fibrin deposition. Activation of PAR-1 may play an important role in the process of renal senility.

Objective To explore the changes of E-cadherin expression in renal ischemia-reperfusion injury.Methods For the in vitro analysis of epithelial ischemia,confluent monolayers of MDCK cells growing in DMEM were depleted of ATP for 4 h by incubation in PBS (supplemented with 1.5 mM CaCl2 and 2 mM MgCl2) containing 10 ?M antimycinA.For the in vivo studies of epithelial ischemic injury,adult Sprague-Dawley rats were subjected to bilateral renal artery ligation.Renal pathological changes were measured by PAS stain.Location and expression of E-cadherin were detected by immunohistochemistry and western blot respectively.Results E-cadherin were primarily found in a linear pattern at the lateral portions of the plasma membrane in normal MDCK.After ATP depletion for 4 hours,the linear pattern altered and manifested by the appearance of intracellular staining.In invivo ischemia-reperfusion model rats,E-cadherin expression was changed from normal tubular epithelial cell basal membrane to cytoplasma.Western blot suggested that in sham-operated rats,E-cadherin was 120 ku lane vs 80 ku lane in ischemia for 60 min rats,while in ischemia for 45 min rats,both the 120 ku and 80 ku lanes were detected.Conclusion In renal ischemia-reperfusion,the location and expression of E-cadherin are obviously altered in vivo and in vitro study and E-cadherin are degradated as ischemia time prolongs.These changes may be the reason why tubular epithelial cell exfoliated from TBM in ischemia-reperfusion injury.

Objective To investigate the protective effects of low-molecular heparin and urokinase on glomerular inflammation. Methods Forty 3-month-old female Wistar rats were randomly divided into five groups with 8 rats in each group: normal control (NC) group; lipopolysaccharide (LPS) group; LPS and tranexamic acid (LT) group; LPS, tranexamic acid and low-molecular heparin (LTH) group; and LPS, tranexamic acid and urokinase (LTU) group. Fibrin deposition and CD11b positive cells were identified by immunohistochemical staining. Western blotting was used to determine the ICAM-1 expression. Results No fibrin depositions and CD11b positive cells were found in glomeruli of rats in NC group. Compared with NC group, fibrin deposit (9.1%?1.6%), CD11b positive cell (11.2?2.1) and ICAM-1 expressions (0.23?0.09) were significantly increased in L group (P0.05). Conclusion Both low-molecular heparin and urokinase can effectively decrease fibrin deposits and alleviate inflammation.

Objective To investigate the effects of Na +-dependent high-affinity dicarboxylate cotransporter 3(NaDC3) and glucose on the transport of succinate in human proximal tubular epithelial cells (HKC) . Methods Western blot was used to detect the expression of hNaDC3 protein in the pcDNA3-hNaDC3, pcDNA3-AhNaDC3 and pcDNA3, transfected HKC, and normal HKC cell. Analysis of succinate contents in the intaking-buffer at the various time points and in the variouse concentrations of glucose were determined by capillary zone electrophoresis. Results The cell transfected with pcDNA3- hNaDC3 was found to have over-expression of hNaDC3 protein for about 1.5 times that of the normal HKC, while succinate content in intaking-buffer was decreased. Although the cells transfected with pcDNA3-AhNaDC3 showed lower expression of hNaDC3 protein, being about 0.6 times that of normal HKC cells, the decrease of succinate in intaking buffer was not obviously effected. There were no differences in hNaDC3 protein content and succinate intaking between the cells transfected with pcDNA3 and normal HKC cells. With the increase in glucose concentration, the decrease of succinate in intaking-buffer was accelerated. Conlusion The results suggested that the overexpression of hNaDC3 protein can cause the succinate-intake more quickly in HKC.