ICAM-1 expression and leukocyte accumulation in inner stripe of outer medulla in early phase of ischemic compared to HgCl2-induced ARF

Greef, Kathleen E. De; Ysebaert, Dirk; Persy, Veerle P.; Vercauteren, Sven R.; Broe, Marc E. De

doi:10.1046/j.1523-1755.2003.00909.x

Cited by 51 publications

(46 citation statements)

References 31 publications

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“…Secondary inflammation plays a major role during ischemic AKI, 2 and ICAM-1 expression is known to increase and to contribute to progressive tissue damage. 24,37 Changes of ICAM-1 were detected in many of the cases despite the short time frame of the study. Cell necrosis and apoptosis were not expected because they develop only after a delay.…”

Section: Discussionmentioning

confidence: 92%

Tolerance of the Human Kidney to Isolated Controlled Ischemia

Parekh¹,

Weinberg²,

Ercole

et al. 2013

Journal of the American Society of Nephrology

183

149

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Tolerance of the human kidney to ischemia is controversial. Here, we prospectively studied the renal response to clamp ischemia and reperfusion in humans, including changes in putative biomarkers of AKI. We performed renal biopsies before, during, and after surgically induced renal clamp ischemia in 40 patients undergoing partial nephrectomy. Ischemia duration was .30 minutes in 82.5% of patients. There was a mild, transient increase in serum creatinine, but serum cystatin C remained stable. Renal functional changes did not correlate with ischemia duration. Renal structural changes were much less severe than observed in animal models that used similar durations of ischemia. Other biomarkers were only mildly elevated and did not correlate with renal function or ischemia duration. In summary, these data suggest that human kidneys can safely tolerate 30-60 minutes of controlled clamp ischemia with only mild structural changes and no acute functional loss.

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Section: Discussionmentioning

confidence: 92%

Tolerance of the Human Kidney to Isolated Controlled Ischemia

Parekh¹,

Weinberg²,

Ercole

et al. 2013

Journal of the American Society of Nephrology

183

149

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“…Therefore, it could be concluded that the level of these chemoattractants was not responsible for the diminished PMN/MO infiltration in uPAR Ϫ/Ϫ allografts. Adhesion molecules are rapidly up-regulated early after transplantation (55) and after induction of IR injury (56). Therefore, we analyzed expression of ICAM-1 in WT2 and uPAR Ϫ/Ϫ allografts given the facts that, being the major counterreceptor for leukocyte ␤2-integrins, this adhesion molecule is rapidly up-regulated within the first 2-3 h after transplantation (57) and the blockade of ICAM-1 strongly attenuated PMN infiltration in some experimental models of renal ischemia (58 -60).…”

Section: Discussionmentioning

confidence: 99%

Renal Urokinase-Type Plasminogen Activator (uPA) Receptor but not uPA Deficiency Strongly Attenuates Ischemia Reperfusion Injury and Acute Kidney Allograft Rejection

Gueler

Rong

Mengel

et al. 2008

The Journal of Immunology

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Central mechanisms leading to ischemia induced allograft rejection are apoptosis and inflammation, processes highly regulated by the urokinase-type plasminogen activator (uPA) and its specific receptor (uPAR). Recently, up-regulation of uPA and uPAR has been shown to correlate with allograft rejection in human biopsies. However, the causal connection of uPA/uPAR in mediating transplant rejection and underlying molecular mechanisms remain poorly understood. In this study, we evaluated the role of uPA/uPAR in a mice model for kidney ischemia reperfusion (IR) injury and for acute kidney allograft rejection. uPAR but not uPA deficiency protected from IR injury. In the allogenic kidney transplant model, uPAR but not uPA deficiency of the allograft caused superior recipient survival and strongly attenuated loss of renal function. uPAR-deficient allografts showed reduced generation of reactive oxygen species and apoptosis. Moreover, neutrophil and monocyte/macrophage infiltration was strongly attenuated and up-regulation of the adhesion molecule ICAM-1 was completely abrogated in uPAR-deficient allografts. Inadequate ICAM-1 up-regulation in uPAR−/− primary aortic endothelial cells after C5a and TNF-α stimulation was confirmed by in vitro experiments. Our results demonstrate that the local renal uPAR plays an important role in the apoptotic and inflammatory responses mediating IR-injury and transplant rejection.

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“…TLR expression was highest in outer medullary cells, the area with the greatest amount of inflammation after ischemic AKI (97). The time course of TLR4 expression following injury was highest at 4 hours, the same point at which the microvasculature begins to show dysfunction (75).…”

Section: Endotheliummentioning

confidence: 98%