Ischemia/reperfusion injury is an unavoidable relevant consequence after kidney transplantation and influences short term as well as long-term graft outcome. Clinically ischemia/reperfusion injury is associated with d...Ischemia/reperfusion injury is an unavoidable relevant consequence after kidney transplantation and influences short term as well as long-term graft outcome. Clinically ischemia/reperfusion injury is associated with delayed graft function, graft rejection, chronic rejection and chronic graft dysfunction. Ischemia/reperfusion affects many regulatory systems at the cellular level as well as in the renal tissue that result in a distinct inflammatory reaction of the kidney graft. Underlying factors of ischemia reperfusion include energy metabolism, cellular changes of the mitochondria and cellular membranes, initiation of different forms of cell death-like apoptosis and necrosis together with a recently discovered mixed form termed necroptosis. Chemokines and cytokines together with other factors promote the inflammatory response leading to activation of the innate immune system as well as the adaptive immune system. If the inflammatory reaction continues within the graft tissue, a progressive interstitial fibrosis develops that impacts long-term graft outcome. It is of particular importance in kidney transplantation to understand the underlying mechanisms and effects of ischemia/reperfusion on the graft as this knowledge also opens strategies to prevent or treat ischemia/reperfusion injury after transplantation in order to improve graft outcome.展开更多
BACKGROUND:Hospital mortality rates are higher among patients with sepsis-associated acute kidney injury(SA-AKI)than among patients with sepsis.However,the pathogenesis underlying SA-AKI remains unclear.We hypothesize...BACKGROUND:Hospital mortality rates are higher among patients with sepsis-associated acute kidney injury(SA-AKI)than among patients with sepsis.However,the pathogenesis underlying SA-AKI remains unclear.We hypothesized that the source of infection affects development of SA-AKI.We aim to explore the relationship between the anatomical source of infection and outcome in patients with SA-AKI.METHODS:Between January 2013 and January 2018,113 patients with SA-AKI admitted to our Emergency Center were identifi ed and divided into two groups:those with pulmonary infections and those with other sources of infection.For each patient,we collected data from admission until either discharge or death.We also recorded the clinical outcome after 90 days for the discharged patients.RESULTS:The most common source of infection was the lung(52/113 cases,46%),followed by gastrointestinal(GI)(25/113 cases,22.1%)and urinary(22/113,19.5%)sources.Our analysis showed that patients with SA-AKI had a significantly worse outcome(30/52 cases,P<0.001)and poorer kidney recovery(P=0.015)with pulmonary sources of infection than those infected by another source.Data also showed that patients not infected by a pulmonary source more likely experienced shock(28/61 cases,P=0.037).CONCLUSION:This study demonstrated that the source of infection infl uenced the outcome of SA-AKI patients in an independent manner.Lung injury may influence renal function in an asyet undetermined manner as the recovery of kidney function was poorer in SA-AKI patients with a pulmonary source of infection.展开更多
Background Animal models that demonstrate changes of renal function in response to acute lung injury （ALl） and mechanical ventilation （MV） are few. The present study was performed to examine the effect of ALl indu...Background Animal models that demonstrate changes of renal function in response to acute lung injury （ALl） and mechanical ventilation （MV） are few. The present study was performed to examine the effect of ALl induced by oleic acid （OA） in combination with conventional MV strategy on renal function in piglets. Methods Twelve Chinese mini-piglets were randomly divided into two groups： the OA group （n=6）, animals were ventilated with a conventional MV strategy of 12 ml/kg and suffered an ALl induced by administration of OA, and the control group （n=6）, animals were ventilated with a protective MV strategy of 6 ml/kg and received the same amount of stedle saline. Results Six hours after OA injection a severe lung injury and a mild-moderate degree of renal histopathological injury were seen, while no apparent histological abnormalities were observed in the control group. Although we observed an increase in the plasma concentrations of creatinine and urea after ALl, there was no significant difference compared with the control group. Plasma concentrations of neutrophil gelatinase-associated lipocalin （NGAL） and cystatin C increased （5.6＋1.3） and （7.4＋1.5） times in the OA group compared to baseline values, and were significantly higher than the values in the control group. OA injection in combination with conventional MV strategy resulted in a dramatic aggravation of hemodynamic and blood gas exchange parameters, while these parameters remained stable during the experiment in the control group. The plasma expression of TNF-a and IL-6 in the OA group were significantly higher than that in the control group. Compared with high expression in the lung and renal tissue in the OA group, TNF-a and IL-6 were too low to be detected in the lung and renal tissue in the control group. Conclusions OA injection in combination with conventional MV strategy not only resulted in a severe lung injury but also an apparent renal injury. The potential mechanisms involved a cytokine response of TNF-a and展开更多
文摘Ischemia/reperfusion injury is an unavoidable relevant consequence after kidney transplantation and influences short term as well as long-term graft outcome. Clinically ischemia/reperfusion injury is associated with delayed graft function, graft rejection, chronic rejection and chronic graft dysfunction. Ischemia/reperfusion affects many regulatory systems at the cellular level as well as in the renal tissue that result in a distinct inflammatory reaction of the kidney graft. Underlying factors of ischemia reperfusion include energy metabolism, cellular changes of the mitochondria and cellular membranes, initiation of different forms of cell death-like apoptosis and necrosis together with a recently discovered mixed form termed necroptosis. Chemokines and cytokines together with other factors promote the inflammatory response leading to activation of the innate immune system as well as the adaptive immune system. If the inflammatory reaction continues within the graft tissue, a progressive interstitial fibrosis develops that impacts long-term graft outcome. It is of particular importance in kidney transplantation to understand the underlying mechanisms and effects of ischemia/reperfusion on the graft as this knowledge also opens strategies to prevent or treat ischemia/reperfusion injury after transplantation in order to improve graft outcome.
基金supported by the National Natural Science Foundation of China(81873947)Hospital Development center(SHDC120161)
文摘BACKGROUND:Hospital mortality rates are higher among patients with sepsis-associated acute kidney injury(SA-AKI)than among patients with sepsis.However,the pathogenesis underlying SA-AKI remains unclear.We hypothesized that the source of infection affects development of SA-AKI.We aim to explore the relationship between the anatomical source of infection and outcome in patients with SA-AKI.METHODS:Between January 2013 and January 2018,113 patients with SA-AKI admitted to our Emergency Center were identifi ed and divided into two groups:those with pulmonary infections and those with other sources of infection.For each patient,we collected data from admission until either discharge or death.We also recorded the clinical outcome after 90 days for the discharged patients.RESULTS:The most common source of infection was the lung(52/113 cases,46%),followed by gastrointestinal(GI)(25/113 cases,22.1%)and urinary(22/113,19.5%)sources.Our analysis showed that patients with SA-AKI had a significantly worse outcome(30/52 cases,P<0.001)and poorer kidney recovery(P=0.015)with pulmonary sources of infection than those infected by another source.Data also showed that patients not infected by a pulmonary source more likely experienced shock(28/61 cases,P=0.037).CONCLUSION:This study demonstrated that the source of infection infl uenced the outcome of SA-AKI patients in an independent manner.Lung injury may influence renal function in an asyet undetermined manner as the recovery of kidney function was poorer in SA-AKI patients with a pulmonary source of infection.
文摘Background Animal models that demonstrate changes of renal function in response to acute lung injury （ALl） and mechanical ventilation （MV） are few. The present study was performed to examine the effect of ALl induced by oleic acid （OA） in combination with conventional MV strategy on renal function in piglets. Methods Twelve Chinese mini-piglets were randomly divided into two groups： the OA group （n=6）, animals were ventilated with a conventional MV strategy of 12 ml/kg and suffered an ALl induced by administration of OA, and the control group （n=6）, animals were ventilated with a protective MV strategy of 6 ml/kg and received the same amount of stedle saline. Results Six hours after OA injection a severe lung injury and a mild-moderate degree of renal histopathological injury were seen, while no apparent histological abnormalities were observed in the control group. Although we observed an increase in the plasma concentrations of creatinine and urea after ALl, there was no significant difference compared with the control group. Plasma concentrations of neutrophil gelatinase-associated lipocalin （NGAL） and cystatin C increased （5.6＋1.3） and （7.4＋1.5） times in the OA group compared to baseline values, and were significantly higher than the values in the control group. OA injection in combination with conventional MV strategy resulted in a dramatic aggravation of hemodynamic and blood gas exchange parameters, while these parameters remained stable during the experiment in the control group. The plasma expression of TNF-a and IL-6 in the OA group were significantly higher than that in the control group. Compared with high expression in the lung and renal tissue in the OA group, TNF-a and IL-6 were too low to be detected in the lung and renal tissue in the control group. Conclusions OA injection in combination with conventional MV strategy not only resulted in a severe lung injury but also an apparent renal injury. The potential mechanisms involved a cytokine response of TNF-a and
