Initial ischemia/reperfusion injury influences late functional and structural changes in the kidney

Azuma, Haruhito; Nadeau, Kari; Takada, Moriatsu; Tilney, N. L.

doi:10.1016/s0041-1345(96)00662-8

Cited by 18 publications

(13 citation statements)

References 6 publications

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“…Initial cardiac function after transplantation is probably influenced by the clinical condition and management of the organ donor (28), as well as the effect of organ preservation (29). Data from kidney transplantation have shown that ischemia-reperfusion injury is related to the development of chronic allograft rejection (6,7), also a vascular process in the kidney. Due to ischemia-induced activation, endothelial cells release growth factors responsible for migration of smooth muscle cells into the intima of arteries (6).…”

Section: Discussionmentioning

confidence: 99%

Impaired Left Ventricular Systolic Function Early After Heart Transplantation is Associated with Cardiac Allograft Vasculopathy

Bolad

Robinson

Webb

et al. 2006

American Journal of Transplantation

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Cardiac allograft vasculopathy (CAV) is a major cause of death more than 1 year after heart transplantation. We evaluated the role and possible predictive value of different etiological factors on development of CAV as diagnosed by quantitative coronary angiography (QCA). A total of 121 patients were studied with baseline QCA and 117 had a follow-up study at 1 year to assess the relationship of mean lumen diameter loss (MLDL) in main coronary arteries to immunological and non-immunological factors potentially affecting long-term survival. Out of them, 103 patients were males (85%), 114 (94%) patients were Caucasians and mean age was 48.5 ± 10 years. Univariate analysis showed that MLDL at 1 year was inversely related to echocardiographic fractional shortening (FS) measured within the first week after transplantation (p = 0.0098) and to intracranial hemorrhage as cause of donor death (p = 0.04) and was directly related to male donors (p = 0.0008), domino transplants (p = 0.037) and donor negative cytomegalovirus (CMV) status (p = 0.022). Multivariate analysis showed that initial FS (p = 0.006) and donor intracranial hemorrhage as a cause of death (p = 0.042) were inversely related to MLDL whereas donor male sex (p = 0.003) and prednisolone treatment throughout the first year (p = 0.012) were directly related. Thus, left ventricular systolic dysfunction early after heart transplantation was associated with subsequent development of CAV.

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Section: Discussionmentioning

confidence: 99%

Impaired Left Ventricular Systolic Function Early After Heart Transplantation is Associated with Cardiac Allograft Vasculopathy

Bolad

Robinson

Webb

et al. 2006

American Journal of Transplantation

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“…TGF-ß2 and TGF-ß3 have similar staining patterns [7]. The study by Azuma et al [14] additionally investigated the effects of mycophenolate mofetil in this model. In contrast to the chronically rejecting animals, those receiving drug treatment had decrements in renal TGF-ß1 immunostaining to the same level as that observed in isografts with associated marked improvement in the histologic changes.…”

Section: Chronic Rejectionmentioning

confidence: 97%

“…Immunohistochemical studies have examined the expression of the various TGF-ß isoforms in this model of chronic rejection [7,14]. At 12 and 16 weeks when chronic rejection is in an early stage, there is increased TGF-ß1 in glomeruli and vascular walls, with a smaller increment in the interstitium.…”

Section: Chronic Rejectionmentioning

confidence: 99%

TGF-β in Renal Allograft Rejection

Cohen

Nast²

1998

Mineral Electrolyte Metab

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The role of TGF-β in pathological processes in the transplanted kidney is beginning to be investigated both in animal models and in humans. In both settings in acute cell-mediated rejection, TGF-β, receptor, and message have all been documented to be elevated in the tubulointerstitium, likely a reflection of TGF-β’s role in recruiting leukocytes to areas of injury and downregulation of the inflammatory response. In chronic rejection, expression of TGF-β, message, and induced proteins is elevated, especially in cortex. TGF-β mRNA, unlike other inflammatory cytokine mRNAs, correlated very well with interstitial fibrosis, a hallmark of chronic rejection. Thus, a relationship between renal scarring and TGF-β has been documented by most studies of transplant kidneys. Additionally, this growth factor also appears to have a role in the renal fibrosis associated with cyclosporine administration and perhaps in augmenting this drug’s immunosuppressive effects.

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“…Initial I/RI is a main course of DGF which exerts a direct negative impact on short- and long-term graft survival [63]. In experimental animals, both renal isografts and kidneys exposed to transient ischemia showed a long-term course of progressive proteinuria and gradual renal failure in a same, albeit delayed fashion compared with allografts [64, 65]. Thus, initial damage appears to foster a subsequent decline, even if immunologic mechanisms of rejection are not involved.…”

Section: Antisense Strategy For the Prevention Of I/ri In Renal Transmentioning

confidence: 99%

Diapedesis of Leukocytes: Antisense Oligonucleotides for Rescue

Dragun

Haller²

1999

Nephron Exp Nephrol

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Ischemia-reperfusion injury is an acute inflammatory process during which leukocytes are intimately involved. In this review, we summarize the current data on the leukocyte cell adhesion cascade in ischemia-reperfusion injury, focus upon studies which have demonstrated specific cell adhesion molecule interactions which mediate the leukocyte involvement in ischemia-reperfusion injury, and suggest future avenues of therapeutic interventions. The increased adhesion between activated vascular endothelium and peripheral blood leukocytes is central to the structural and the functional impairment in ischemia-reperfusion injury. Several families of adhesion molecules, namely the selectins, the intercellular adhesion molecules (ICAMs), and the integrins expressed either on the endothelium or on the leukocytes, are involved the cascade of events. Sequential and overlapping cellular interactions between the members of the three gene families of adhesion receptors result in adhesion of the leukocytes to the endothelium and extravasation at the site of ischemia. The functional importance of ICAM-1 and its β₂ integrin ligands in ischemia-reperfusion of the kidney has been demonstrated by monoclonal antibody blockade studies, in knockout mice and by treatment with antisense oligodeoxynulceotides (ODN). We have shown that antisense ODN for ICAM-1 protected the kidney against ischemic renal failure. In addition, in transplanted kidneys, ICAM-1 inhibition by antisense ODN ameliorates ischemia-reperfusion injury and prevents delayed graft function. Recent developments in antisense ODN technology make this a promising therapeutic approach, and antisense ODN treatment of donors or donor organs for ICAM-1 may be useful for the prevention of reperfusion injury in human renal transplantation and could influence acute and chronic graft function.

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Initial ischemia/reperfusion injury influences late functional and structural changes in the kidney

Cited by 18 publications

References 6 publications

Impaired Left Ventricular Systolic Function Early After Heart Transplantation is Associated with Cardiac Allograft Vasculopathy

Impaired Left Ventricular Systolic Function Early After Heart Transplantation is Associated with Cardiac Allograft Vasculopathy

TGF-β in Renal Allograft Rejection

Diapedesis of Leukocytes: Antisense Oligonucleotides for Rescue

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