Nowadays, recondition. Few well described molecules are; Serine plasma

kidneys from non-heart beating donors are more
commonly being used.  An additional risk
to the one of suboptimal donor background (aged, pre-existing comorbidities) is
the prolonged exposure of them to warm ischemia and prolonged anoxia/hypoxia.  Subsequently they are at a greater risk of
delayed graft function (DGF) and more importantly – of primary non-function. As
a result, this raised the awareness of the significance of looking after the
quality and functional status of the grafts and has led to further research in
methods of optimisation while offering pre-transplant graft preservation of
those marginal kidneys. A new challenge was therefore created, that of
Recondition. Recondition includes all innovative methods used
to improve the condition of the parenchyma of those organs aiming to boost transplantation


Medical reconditioning of machine-perfused kidneys can be
performed during perfusion through medications administered into the perfusate
and modification of flow parameters. Machine perfusion itself other than organ
preservation can be broadly considered as a more of recondition. Few well
described molecules are; Serine plasma proteases, Heparin,
Thrombalexin, siRNA Cocktail solution and other Pharmacological manoeuvres. Another interesting chapter is the ischaemic
Pre-Conditioning and use of trophic factors in organ preservation. Gene
transfer is also a promising therapeutic option in reconditioning grafts.  Along with gene therapy, cell transplantation
methods are in theory novel and promising techniques to improve organ

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Ischaemic Pre-Conditioning and Organ


has been a considerable amount of research on potential exposure of organs or
other body parts of the donor to a periodic short-term hypoxia and then
re-perfusion prior to their retrieval as a mode of cyto-protection. This effect
can be explained by activation of molecular signalling pathways as a result of
subjecting the organ to ischaemia, as they extort appropriate stress response
and protective effects on cellular level in cases of ischaemia 95. The above
signalling cascades include anti-apoptotic pathways, adenosine-related
cytoprotection, nitric oxide synthases and haeme-oxygenase 96. Interestingly
enough, this protection can be remotely activated i.e. limb ischaemia / hypoxia
with subsequent re-perfusion to protect the liver 97. The expectation to use
the described method with aim to boost outcomes in organ preservation has not
been fully met 97, 98. There is need to clarify further how brain death is
associated with cellular stress response and study the impact of hypothermia on
signalling cascade and stress response prior to this becoming established clinical
practice 99. 


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