Risk Factors for Delayed Graft Function in Cadaveric Kidney Transplantation

Koning, Ohj; Ploeg, Rutger J.; Vanbockel, Jh; Vanderwoude, F; Gg, Persijn; Hermans, J.

doi:10.1097/00007890-199706150-00015

Cited by 206 publications

(35 citation statements)

References 18 publications

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“…Although the cold storage of cadaveric donor organs adversely impacts short-term graft function (30,31) it is unavoidable in the process of organ allocation. A syngeneic murine renal transplant model characterised by prolonged cold ischemia was developed to examine the effect of hCD39 transgene expression in a setting that simulated aspects of clinical renal transplantation.…”

Section: Resultsmentioning

confidence: 99%

Transgenic Overexpression of CD39 Protects Against Renal Ischemia-Reperfusion and Transplant Vascular Injury

Crikis

Lü

Murray‐Segal

et al. 2010

American Journal of Transplantation

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The vascular ectonucleotidases CD39 [ENTPD1 (ec-tonucleoside triphosphate diphosphohydrolase-1), EC 3.6.1.5] and CD73 [EC 3.1.3.5] generate adenosine from extracellular nucleotides. CD39 activity is critical in determining the response to ischemia-reperfusion injury (IRI), and CD39 null mice exhibit heightened sensitivity to renal IRI. Adenosine has multiple mechanisms of action in the vasculature including direct endothelial protection, antiinflammatory and antithrombotic effects and is protective in several models of IRI. Mice transgenic for human CD39 (hCD39) have increased capacity to generate adenosine. We therefore hypothesized that hCD39 transgenic mice would be protected from renal IRI. The overexpression of hCD39 conferred protection in a model of warm renal IRI, with reduced histological injury, less apoptosis and preserved serum creatinine and urea levels. Benefit was abrogated by pretreatment with an adenosine A2A receptor antagonist. Adoptive transfer experiments showed that expression of hCD39 on either the vasculature or circulating cells mitigated IRI. Furthermore, hCD39 transgenic kidneys transplanted into syngeneic recipients after prolonged cold storage performed significantly better and exhibited less histological injury than wild-type control grafts. Thus, systemic or local strategies to promote adenosine generation and signaling may have beneficial effects on warm and cold renal IRI, with implications for therapeutic application in clinical renal transplantation.

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Section: Resultsmentioning

confidence: 99%

Transgenic Overexpression of CD39 Protects Against Renal Ischemia-Reperfusion and Transplant Vascular Injury

Crikis

Lü

Murray‐Segal

et al. 2010

American Journal of Transplantation

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“…The cohort was 43.5% female, 56.5% Caucasian, 39.1% African American and 4.3 % Asian. Nearly 48% had delayed graft function (DGF) defined as the need for dialysis within the first week post transplantation (1,6). Patients who did not have sufficient graft dysfunction to be classified as having DGF were defined to have slow graft function (23).…”

Section: Study Cohortsmentioning

confidence: 99%

“…There is an increasing incidence of delayed graft function (DGF) (8-50%) after deceased donor kidney transplantation (1)(2)(3)(4)(5)(6). This is due, in part, to the need to use kidneys from donors with risk factors for acute tubular necrosis which is driven by the increasing numbers of patients wait listed for transplantation with little increase of the donor pool (7).…”

Section: Introductionmentioning

confidence: 99%

Quantitative Detection of Promoter Hypermethylation as a Biomarker of Acute Kidney Injury During Transplantation

Mehta

Hoque

Ugarte

et al. 2006

Transplantation Proceedings

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Aberrant promoter hypermethylation, also known as epigenetics, is thought to be a promising biomarker approach to diagnose malignancies. Kidney repair after injury is a recapitulation of normal morphogenesis, with similarities to malignant transformation. We hypothesized that changes in urine epigenetics could be a biomarker approach during early kidney transplant injury and repair. We examined urine DNA for aberrant methylation of 2 gene promoters (DAPK CALCA) by quantitative methylation specific PCR from 13 deceased and 10 living donor kidney transplant recipients on postoperative day 2 and 65 healthy controls. Results were compared with clinical outcomes and to results of the kidney biopsy. Transplant recipients were significantly more likely to have aberrant hypermethylation of the CALCA gene promoter in urine than healthy controls (100% vs. 31%, p<0.0001). There was increased CALCA hypermethylation in the urine of deceased vs. living donor transplants (21.60 +/− 12.5 vs. 12.19 +/− 4.7 P=0.04). Furthermore, there was a trend towards increased aberrant hypermethylation of urine CALCA in patients with biopsy-proven acute tubular necrosis vs. acute rejection and slow or prompt graft function (mean: 20.40 +/− 6.9, 13.87 +/− 6.49, 17.17 +/− 13.4, P=0.67). However, there was no difference of CALCA hypermethylation in urine of patients with delayed graft function vs. those with slow or prompt graft function (16.9 +/− 6.2 vs. 18.5 +/− 13.7, respectively; P=0.5). There was no aberrant hypermethylation of DAPK in the urine of transplant patients. Urine epigenetics is a promising biomarker approach for acute ischemic injury in transplantation that merits future study.

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“…Several definitions of DGF are applied in the current literature, thus influencing the reported incidences. Many studies define DGF as the need for any or more than one dialysis session in a specified postoperative period [12,16,17,25, 261, a definition that is easy to apply especially for aquisition of data in large registries. However, there are undoubtedly forms of early impairment of allograft function that do not require postoperative dialysis.…”

Section: Discussionmentioning

confidence: 99%

Risk factors for delayed graft function after renal transplantation and their significance for long-term clinical outcome

Hetzel¹,

Klein²,

Brause³

et al. 2002

Transplant International

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Risk Factors for Delayed Graft Function in Cadaveric Kidney Transplantation

Abstract: DGF results in an approximately 10% higher rate of graft failure. DGF incidence can be reduced by the administration of mannitol during transplantation, which minimizes CIT and optimizes donor management. Grafts from multi-organ donors and kidney-only donors appear to be of equal quality.

Cited by 206 publications

References 18 publications

Transgenic Overexpression of CD39 Protects Against Renal Ischemia-Reperfusion and Transplant Vascular Injury

Transgenic Overexpression of CD39 Protects Against Renal Ischemia-Reperfusion and Transplant Vascular Injury

Quantitative Detection of Promoter Hypermethylation as a Biomarker of Acute Kidney Injury During Transplantation

Risk factors for delayed graft function after renal transplantation and their significance for long-term clinical outcome

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