A Randomized Prospective Study of Cadaver Donor Pretreatment in Renal Transplantation

Jeffery,; Downs, Allan R.; Jw, Grahame; C, Lye; Ramsey, Ernest W.; Ae, Thomson

doi:10.1097/00007890-197806000-00001

Cited by 31 publications

(8 citation statements)

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“…Based on our findings on increased expression activity in the context of the functional groups immune response and inflammation along cadaveric donor organs we have started a multicenter, randomized placebo controlled trial performing immunosuppressive treatment of the cadaveric organ donor before graft harvesting. Previous trials on donor pretreatment were carried out in the late 1970s and early 1980s, but severe problems in the design and sample size of all three randomized studies performed so far preclude a clear cut answer [63–65].…”

Section: Discussionmentioning

confidence: 99%

Gene expression and biomarkers in renal transplant ischemia reperfusion injury

et al. 2007

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Summary The incidence of postischemic acute renal allograft failure (ARF) occurs in roughly 25% of cadaveric donor kidney recipients. This high rate remained virtually unchanged over the last decades despite modification in recipient management and modern immunosuppressive strategies. It has recently been shown that among other reasons, the systemic inflammation in the brain death cadaveric organ donor contributes to subsequent ARF in the recipient. This review focuses on the consequences of ischemia and reperfusion on the cellular level and offers potential solutions for the reduction of ARF. Genome‐wide gene expression analysis together with sophisticated biostatistical analysis made it possible to identify several candidate gene products and proteins that may act as specific and sensitive biomarker for renal inflammation and ischemia. These markers may be very helpful in the clinical management of patients with a high a priori risk of subsequent ARF such as recipients of marginal donor kidneys. Ongoing clinical trials will evaluate whether immunosuppression of the cadaveric organ donor before organ harvest will have the potential to reduce inflammation in the transplant kidney and subsequently lead to a reduction in the rate of ARF.

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Section: Discussionmentioning

confidence: 99%

Gene expression and biomarkers in renal transplant ischemia reperfusion injury

et al. 2007

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“…If the systemic inflammatory response elicited by brain death has a harmful effect on graft survival, steroid treatment of the BD donor may be beneficial. In early studies, steroid treatment of the BD donor did not improve post‐transplantation graft function or survival 93–95 . However, in more recent studies, steroids given to the donor led to a higher survival in the kidney‐transplanted rats 96 .…”

Section: Anti‐inflammatory Steroid Treatment Of the Bd Donormentioning

confidence: 99%

Systemic inflammation in the brain‐dead organ donor

Barklin

2009

Acta Anaesthesiol Scand

152

122

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Brain death itself impairs organ function in the potential donor, thereby limiting the number of suitable organs for transplantation. In addition, graft survival of kidneys obtained from brain-dead (BD) donors is inferior to that of kidneys obtained from living donors. Experimental studies confirm an inferior graft survival for the heart, liver and lungs from BD compared with living donors. The mechanism underlying the deteriorating effect of brain death on the organs has not yet been fully established. We know that brain death triggers massive circulatory, hormonal and metabolic changes. Moreover, the past 10 years have produced evidence that brain death is associated with a systemic inflammatory response. However, it remains uncertain whether the inflammation is induced by brain death itself or by events before and after becoming BD. The purpose of this study is to discuss the risk factors associated with brain death in general and the inflammatory response in the organs in particular. Special attention will be paid to the heart, lung, liver and kidney and evidence will be presented from clinical and experimental studies.

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“…First, compared to rat renal allografts, human renal allografts are far more difficult to enhance (French & Batchelor 1972, Wilson et al 1981, they respond much less satisfactorily to donor pretreatment ffl •? ( SO with cytotoxic drugs when critically assessed in randomized trials (Jeffery et al 1978, Zinke et al 1978, and the recipient must be immunosuppressed ad infinitum, also presumably after the 'dendritic' cells are replaced. Second, the number of Kupffer cells in the liver clearly exceeds the number of dendritic cells in the kidney; however, liver allografts (in man and especially in the pig) are less promptly rejected than (human) renal allografts (Calne 1969).…”

Section: Immunogenic Potential Of Isolated Allograft Componentsmentioning

confidence: 99%