Background:Renal venous thrombosis (RVT) is the most common form of venous thrombosis in neonates,causing both acute and long term kidney dysfunction. Historical predisposing factors include dehydration,maternal diabe...Background:Renal venous thrombosis (RVT) is the most common form of venous thrombosis in neonates,causing both acute and long term kidney dysfunction. Historical predisposing factors include dehydration,maternal diabetes,and umbilical catheters,but recent reports highlight associations with prothrombotic abnormalities. Study:Twenty three patients with neonatal RVT were analysed over 15 years. Predisposing factors,presentation,and procoagulant status were compared with renal outcome using multilevel modelling. Results:Median presentation was on day 1:19/23 (83%) had pre/perinatal problems,including fetal distress (14),intrauterine growth retardation(five),and pre-identified renal abnormalities (two);8/18 (44%) had procoagulant abnormalities,particularly factor V Leiden mutations (4/18). Long term abnormalities were detected in 28/34 (82%) affected kidneys; mean glomerular filtration rate was 93.6 versus 70.2 ml/min/1.73 m2 in unilateral versus bilateral cases (differen- ce 23.4; 95%confidence interval 6.4 to 40.4; p=0.01 ). No correlation was observed between procoagulant tendencies and outcome,but presenting renal length had a significant negative correlation:mean fall in estimated single kidney glomerular filtration rate was 3 ml/min/1.73 m2 (95%confidence interval 3.7 to -2.2; p =0.001) per 1 mm increase,and kidneys larger than 6 cm at presentation never had a normal outcome. Conclusions:This subgroup of neonatal RVT would be better termed perinatal RVT to reflect antenatal and birth related antecedents. Prothrombotic defects should be considered in all patients with perinatal RVT. Kidney length at presentation correlated negatively with renal outcome. The latter,novel observation raises the question of whether larger organs should be treated more aggressively in future.展开更多
Objective To investigate the increased podocyte permeability by evidence of adriamycin (AD) and its molecular mechanism.Methods In this study, we explored the direct effects of AD on cultured mouse podocytes and the p...Objective To investigate the increased podocyte permeability by evidence of adriamycin (AD) and its molecular mechanism.Methods In this study, we explored the direct effects of AD on cultured mouse podocytes and the potential protection effects of Dexamethasome (Dex).Results After 24-hour AD (5×10 -7 mol/L) treatment, albumin passage through podocyte monolayers was increased by 2.27-fold (P<0.01). AD caused a 62% decrease in Zonula Occluden -1 (ZO-1) protein (P<0.05), suggesting that AD might increase podocyte permeability by disrupting tight junctions. Dex (1×10 -6 mol/L), co-administered with AD, protected podocytes from AD-induced increased albumin passage. This may be linked with an increased P-cadherin protein level to 1.93 fold of control (P<0.01).Conclusions AD has a direct, detrimental effect on podocyte permeability, probably through disrupting tight junctions; Dex could protect against AD-induced high podocyte permeability by upregulating adherent protein P-cadherin.展开更多
文摘Background:Renal venous thrombosis (RVT) is the most common form of venous thrombosis in neonates,causing both acute and long term kidney dysfunction. Historical predisposing factors include dehydration,maternal diabetes,and umbilical catheters,but recent reports highlight associations with prothrombotic abnormalities. Study:Twenty three patients with neonatal RVT were analysed over 15 years. Predisposing factors,presentation,and procoagulant status were compared with renal outcome using multilevel modelling. Results:Median presentation was on day 1:19/23 (83%) had pre/perinatal problems,including fetal distress (14),intrauterine growth retardation(five),and pre-identified renal abnormalities (two);8/18 (44%) had procoagulant abnormalities,particularly factor V Leiden mutations (4/18). Long term abnormalities were detected in 28/34 (82%) affected kidneys; mean glomerular filtration rate was 93.6 versus 70.2 ml/min/1.73 m2 in unilateral versus bilateral cases (differen- ce 23.4; 95%confidence interval 6.4 to 40.4; p=0.01 ). No correlation was observed between procoagulant tendencies and outcome,but presenting renal length had a significant negative correlation:mean fall in estimated single kidney glomerular filtration rate was 3 ml/min/1.73 m2 (95%confidence interval 3.7 to -2.2; p =0.001) per 1 mm increase,and kidneys larger than 6 cm at presentation never had a normal outcome. Conclusions:This subgroup of neonatal RVT would be better termed perinatal RVT to reflect antenatal and birth related antecedents. Prothrombotic defects should be considered in all patients with perinatal RVT. Kidney length at presentation correlated negatively with renal outcome. The latter,novel observation raises the question of whether larger organs should be treated more aggressively in future.
基金ThisstudywassupportedbytheNationalKeyBasicResearch"973"Project (No 2 0 0 1CB13 5 10 0 0 3 )andtheOverseasExchangeProgramme (No 990 3 5 )oftheJiangsuProvincialGovernment
文摘Objective To investigate the increased podocyte permeability by evidence of adriamycin (AD) and its molecular mechanism.Methods In this study, we explored the direct effects of AD on cultured mouse podocytes and the potential protection effects of Dexamethasome (Dex).Results After 24-hour AD (5×10 -7 mol/L) treatment, albumin passage through podocyte monolayers was increased by 2.27-fold (P<0.01). AD caused a 62% decrease in Zonula Occluden -1 (ZO-1) protein (P<0.05), suggesting that AD might increase podocyte permeability by disrupting tight junctions. Dex (1×10 -6 mol/L), co-administered with AD, protected podocytes from AD-induced increased albumin passage. This may be linked with an increased P-cadherin protein level to 1.93 fold of control (P<0.01).Conclusions AD has a direct, detrimental effect on podocyte permeability, probably through disrupting tight junctions; Dex could protect against AD-induced high podocyte permeability by upregulating adherent protein P-cadherin.
