The urinary fistula is a common serious complication after renal transplantation.It can occur in any parts of the urinary tract,such as renal calices,renal pelvis,ureter and bladder.The majority of urine fistula occurred in 3 weeks after renal transplantation,may occurred in a few month later,or even half a year.According to the principles of classification of urethral damages,the urinary fistulae after kidney transplantation was classified in terms of the cause,location and extent of them.Moreover,why it was difficult to cure urinary fistulae was discussed,and the key points in the diagnosis were illuminated.The conclusion is that the only way to ensure the best treatment is determining the leaking location and selecting the optimal therapeutic schedule.Furthermore,the diagnosis of urinary fistula must include the leaking location and the classification of the simple one or complex one according to the location and extent of the fistula,which may make the diagnosis of urinary fistula after renal transplantation more accurate and standardized.

Renal transplantation is the best method for end-stage renal diseases in clinic. With the development of immunosuppressive agents, renal transplantation has been quite successful. Various complications after renal transplantation still threaten the function of graft and the life of patients. Some medical complications are difficult to prevent, but surgical complications are effective to prevent. The article comprehensively analyzes the etiology, diagnosis, treatment and prevention of some common urological complications such as urinary fistula, ureteral obstruction and ureteric reflux. The urological complications as the common complication are correlated to surgical skill. It has been an important link in improvement of transplantation quality to reduce incidence of urological complications and to diagnose and manage.

Objective To analyse the clinical risk factors of multiple organ dysfunction syndrome(MODS) after renal transplantation. Methods 650 cases were retrospectively studied,and the related risk factors of patients with MODS or SIRS were analyzed by undertaking ? 2 tests Results In all of 650 cases,there were 38 cases with SIRS,and 7 cases with MODS.The study showed a significant relation between MODS with lower blood pressure(71.4%),lower blood oxygen(85.7%),severe infection(85.7%) and chronic organ failure(28.6%).The incidence for patients of MODS with more than two kinds of risk factors are obviously higher than those with two or less than two kinds of risk factors.The incidence for patients of renal failure(85.7%) and respiratory failure(71.4%) are highest in patients of organ failure. Conclusions Lower blood pressure,lower blood oxygen,severe infection and chronic organ failure are clinical risk factors to MODS.

Objective To evaluate the clinical effects,CT features and side-effects of percutaneous microwave coagulation therapy(PMCT) in the treatment of peripheral lung cancer.Methods CT-guided PMCT was applied to 16 cases of peripheral lung cancer from August 2003 to October 2004 in this hospital.Pathological or cytological findings showed 9 cases of squamous carcinoma and 7 cases of adenocarcinoma.A needle microwave antenna was applied into the tumor percutaneously under CT guidance.In each emission of microwave,the tumor was ablated with a 2 450 Hz microwave coagulation output of 65~75 W for 3~5 min.According to the size and shape of the tumor,single or multiple ablation emission was selected.Results The operation time was(15~60) min(mean,35 min).Complete remission(CR) was achieved in 1 case,partial remission(PR) in 4 cases,and no changes(NC) in 11.Follow-up observations in the 16 cases for 3~15 months(mean,9.5 months) found 2 cases of tumor metastasis and 1 case of death.Conclusions Percutaneous microwave coagulation therapy is a safe,micro-invasive,and effective treatment for the management of peripheral lung cancer.

Background Left ventricular hypertrophy(LVH) is a cardiovascular risk factor independent of the blood pressure. JAK/STAT pathway has been confirmed to participate in cardiac hypertrophy and hyperplasia. Our previous reports have shown that sodium tanshinone ⅡA sulfonate(STS) reversed LVH,inhibited the myocardial cells Ca2+ influx,lowered left ventricular myocardial tumor necrosis factor-?(TNF-?)and the proto-oncogene c-fos,Bcl-2,and p53 protein expression. Objective To study the effect of sodium tanshinone ⅡA sulfonate(STS) on JAK/STAT pathway in left ventricular hypertrophy(LVH) induced by abdominal aorta stenosis in rats. Methods Twenty-four 9-weeks-old rats submitted to abdominal aorta constriction,were randomized to receive STS 10 mg/(kg?d)(n=8)or sterilized distilled water (1 mL/d)(n=8),or valsartan 10 mg/(kg?d) by gavage(n=8),with age and sex matched sham operated rats(n=8) as control. HE,VG and immunohistonchemical staining were used to evaluate the myocardial fiber dimension(MFD). Expressions of JAK1 and STAT3 were assessed by using Western blot. Results Compared with the control group,pressure loaded rats had higher SBP[(117.3?8.3) vs LVH: (186.5?13.5)mmHg,P

Monocyte chemotactic peptide 1(MCP 1) is a specific chemotactic and activating factor for monocytes in acute renal transplant rejection. The present study was to diagnose aimed at diagnosing acute renal transplant rejection by determination of MCP 1 concentration in urine of kidney recipients by avidin biotin complex enzyme linked immunosorbent assay(ABC ELISA).Among the 65 recipients, the urinary MCP 1 concentration was (1278?64)pg/ml in 17 with acute rejection, which was higher than that in 40 clinically stable ones(511?16 pg/ml, P

BACKGROUND: Present existed procedure protocol for urinary fistula has some limitations, which can not reflect diseased region, pathological change, or severe condition of patients, OBJECTIVE: To establish the procedure protocol for urinary fistula diagnosis and treatment following renal transplantation, in addition, to investigate its significance in clinical practice. METHODS: A total of 102 cases with urinary fistula, including 67 male and 35 female, range in age from 21 to 57 years. According to the business management mode, we have designed the "five-step procedure protocol" for the diagnosis and treatment of urinary fistula after renal transplantation. Four diagnosis steps consisting of qualitative, located, quantitative and classified, as well as one treatment step. Among 102 cases of urinary fistula, 34 were adopted conservative treatment, including 24 cases with drainage tube and retention type catheter, 10 cases with indwelling ureteric stents at tubal bladder. Other 68 cases received surgical treatment. In 47 cases with simple fistula, 36 cases received ureter/bladder replantation, 11 cases with ureteral anastomosis. Twenty-one cases with complex fistula were treated with surgical prosthesis using omentum majus after repairing. RESULTS AND CONCLUSION: Among the 34 cases receiving conservative treatment, 2 got urinary tract infection repeatedly, and 5 got the stenosis of ureterovesical anastomotic stoma. Among the 68 cases receiving surgical treatment, 2 had ureteral stoma stricture, 1 ureterovesical anastomotic stoma stricture, and 1 ureteral countercurrent. In the surgical treatment series, 3 cases died from severe pulmonary infection elicited by urinary fistula. 77 cases were available for long-term follow-up, 22 were dropped out. In the 57 cases with simple fistula were followed up for 1-10 years, the transplanted renal function was normal in 40 cases, and 17 cases suffered from chronic rejection. 20 cases with complex fistula treated with surgical prosthesis using omentum majus were followed up for 1-7 years, 19 cases were normal, 1 patient had increased creatinine, which was returned to normal after intravenous glucocorticoid therapy. The design of "qualitative, located, quantitative and classified" standard for urinary fistula diagnosis following renal transplantation, and the establishment of "five-step procedure protocol", make urinary fistula diagnosis and treatment more ordered and standard, which is more feasible for selecting optimal therapeutic scheme.

BACKGROUND:Among the factors causing vascular endothelial cell injury,angiotensin Ⅱ(Ang Ⅱ) caused by renin-angiotensin system (RAS), especially by local RAS, plays an important patho-physiological role.OBJECTIVE: To observe the effect of tanshinone ⅡA on the vascular endothelial cells secreting nitric oxide (NO) and endothelial nitric oxide synthase (eNOS) gene expression as well as intracellular Ca2+ level induced by Ang Ⅱ, and investigate the protective effect of tanshinone ⅡA on vascular endothelial cells.DESIGN: Controlled observation experiment.SETTING: Department of Emergency, Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology.MATERIALS: This experiment was carried out in the Experimental Center for Basic Medicine, Tongji Medical College,Huazhong University of Science and Technology from March 2006 to October 2006. Porcine aorta used in this experiment was provided by the Department of Pathophysiology of Tongji Medical College.METHODS: Nitric acid deoxidization method and reverse transcription-polymerase chain reaction (RT-PCR) were used to detect the effects of Ang Ⅱ of different concentrations (10-8 to 10-6 mol/L) on endothelial cells secreting NO and eNOS mRNA expression in cultured porcine aortic endothelial cells at different time points (1,6 and 24 hours) separately, then 50 mg/L tanshinone Ⅱ A was respectively added at different time point (0, 6 hours) when Ang Ⅱ was at 10-6 mol/L, and changes in NO production and eNOS gene expression were detected respectively at 1, 6 and 24 hours. Intracellular Ca2+ level was also detected with laser scanning confocal microscopy.MAIN OUTCOME MEASURES: ① NO content. ②eNOS mRNA expression. ③Intracellular Ca2+ level.RESULTS: ① NO production and eNOS mRNA expression were decreased with increase of Ang Ⅱ concentration and prolongation of time (P ＜ 0.01). ② NO production and eNOS mRNA expression in each tanshinone ⅡA-treated group were significantly higher than those in the Ang Ⅱ group. At 1 and 6 hours of tanshinone ⅡA treatment, production of NO and eNOS mRNA expression in the Ang Ⅱ + tanshinone ⅡA group were significantly higher than those in the Ang Ⅱ 6 hours + tanshinone ⅡA group (P ＜ 0.05); There were no significant differences in NO production and eNOS mRNA expression between two groups at 24 hours (P ＞ 0.05). ③Intracellular Ca2+ level in the Ang Ⅱ group was significantly higher than that of control group (P ＜ 0.01), and intracellular Ca2+ level in the tanshinone ⅡA + Ang Ⅱ was significantly lower than that in the Ang Ⅱ group (P ＜ 0.05).CONCLUSION: Tanshinone Ⅱ A has a protective effect on vascular endothelial cells and their functions by suppressing the inhibition of Ang Ⅱ on NO level and eNOS gene expression in cultured porcine aortic endothelial cells.

BACKGROUND: The urinary fistula rates following kidney transplantation are varying in each center, which lack of unified classification criteria and treatment standard. OBJECTIVE: To explore optimal treatments for urinary fistula following kidney transplantation by retrospective analyzing the characteristics, etiological factors and therapeutic efficacy of urinary fistula. METHODS: Totally 68 patients with urinary fistula were collected, including 42 males and 26 females, aged 21-57 years. The urinary fistula occurred at days 1-17 after operation. According to the location of urinary fistula, patients were divided into stomas fistula and ureter fistula groups. The location of fistula was determined by cystography, magnetic resonance hydrography (MRH) or operation research. In both groups, conservative treatment was first adopted, namely, placing a negative pressure drainage tube draining the wounds and placing a double-J catheter or a urinary canal in, however, if invalid, a surgical repair was performed. There were 45 patients underwent surgery. The location, onset period, therapeutic efficacies of urinary fistula was analyzed. RESULTS AND CONCLUSION: Among the 68 cases of fistula, 20(29.4%) were stomas fistula and 48 (70.6%) were ureter fistula. The onset period was (5.1±2.5) and (8.8±5.5) days after transplantation, respectively (P < 0.05). Fifteen of 20 stomas fistula (75.0%) were cured successfully by conservative treatment. Whereas, for the remaining 5 cases (25.0%), we attempted open surgery, among which 4 were cured, free of recurrence, and 1 case underwent nephrectomy because of acute rejection. For the 48 cases of ureter fisula, only 8 (16.7%) were cured by conservative treatment, but the other 40 (83.3%) must accept further open surgery, among which 35 were cured (including 6 cases of recurrent fistula). Three cases underwent nephrectomy failure of repair owing to acute rejection, besides 2 died of pulmonary infection. The achievement ratio of conservative treatment in lower fistulae was significantly higher than that of upper fistulae (P < 0.01). It is necessary to determine the location of urinary fistula following kidney transplantation. Compared to ureter fistula, stomas fistula occurred earlier with great leaked volume. Conservative treatment can first selected for stomas fistula, only if it is invalid can we resort to open surgery. However, for. ureter fistula, it is wise to adopt open surgery as soon as possible.

To investigate the molecular mechanism by which Tanshinone IIA (TSN IIA) prevents left ventricular hypertrophy (LVH), we examined the expression of AT1R, TGF-beta1 and Smads gene in the hypertrophic myocardium of hypertensive rats with abdominal aorta constriction. LVH model was established by creating abdominal aorta constriction. Four weeks later, animals were randomly divided into 4 groups with 8 animals in each. One group was used as model control, the other three groups were treated with TSN IIA (20 mg/kg), TSN IIA (10 mg/kg) and valsartan (10 mg/kg), respectively. Another 8 SD rats were subjected to sham surgery and served as blank control. After 8-week treatment, the caudal artery pressure of the animals was measured. The tissues of left ventricle were taken for the measurement of the left ventricular mass index (LVMI) and pathological sectioning and HE-staining were used for determining the myocardial fiber dimension (MFD). The mRNA expression of AT1R, protein expression of TGF-beta1 and activity of Smad-2, 4, 7 were detected by RT-PCR and Western blotting, respectively. Our results showed that (1) the blood pressure of rats treated with TSN IIA, either at high or low dose, was significantly higher than those in the control and valsartan-treated group (P<0.01, P<0.05); (2) LVMI and MFD in TSN IIA and valsartan-treated rats were higher than those in the control group (P<0.05) but significantly lower than those in the model control (P<0.01); (3) the high doses of TSN IIA and valsartan significantly down-regulated the mRNA expression of AT1R and protein expression of TGF-beta1 and Smad-3 in the hypertrophic myocardium (P<0.01), and TGF-beta1 in valsartan-treated animals was more significantly lower than that in rats treated with TSN IIA; (4) the two doses of TSN IIA and valsartan significantly up-regulated the protein expression of Smad-7 in the hypertrophic myocardium (P<0.01), and Smad-7 in the animals treated with high-dose TSN IIA was significantly higher than that in rats treated with valsartan. It is concluded that inhibition of myocardial hypertrophy induced by TSN IIA independent of blood pressure. The underlying mechanism might be the down-regulated expression of AT1R mRNA and Smad-3, increased production of Smad-7, and blocking effect of TSN IIA on TGF beta1/Smads signal pathway in local myocardium.