الفهرس 
Introduction
Evaluation of living donorOnly 14 pages are availabe for public view
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Abstract
Renal transplantation is the best form of renal replacement therapy for patients with end-stage renal failure (ESRF), in comparison to dialysis, as it is associated with higher patient survivals, lower hospitalization rates and a superior quality of life. However, the ever-increasing numbers of new patients with ESRF and limited supply of donor kidneys for transplant mandate that every renal transplant be optimized to achieve long-term patient and allograft survival.
Immunological risk factors such as human leukocyte antigen (HLA) mismatching and pre-sensitization contribute to higher risks for graft loss from both acute rejection and chronic rejection. Apart from surgical causes, there are many pre-transplant donor and recipient factors leading to allograft failure by non-immunological mechanisms. Donor factors such as older age, cause of death due to cerebro-vascular accident, history of hypertension and recipient factors such as older age, male gender, increased body mass index and diabetic status all contribute to an excess risk for renal transplant failure.
The major mechanisms of transplant failure can be broadly classified into clearly immunological mechanisms such as acute rejection or chronic rejection and clearly non-immunological mechanisms such as surgical problems, reno-vascular thrombosis, nephron injury due to various causes including ischaemia-reperfusion and nephrotoxicity from Calcineurin inhibitors (CNI).
In addition, a significant proportion of allograft failures can be attributed to recurrence of original disease or chronic allograft nephropathy, which is likely mediated by multiple mechanisms including immunological, non-immunological, haemodynamic and other factors.
The causes of allograft dysfunction depend on the time period after transplantation, allowing a rational diagnostic and therapeutic approach in many cases. It can be divided into immediately post-transplant, early (1 – 12 weeks) post-transplant and late (more than 3 – 6 months) post-transplant but there is obviously some overlap in causes between these periods.
In the immediate post-transplant period, delayed graft function (DGF) is defined as failure of the renal allograft to function immediately, with the need for one or more dialysis sessions within one week. Acute tubular necrosis (ATN) is the most common cause of DGF in addition to other surgical complications as urinary tract obstruction. Hyperacute rejection is considered a devastating cause of DGF.
There is obviously some overlap in the causes of delayed and early allograft dysfunction. However, acute rejection is the common and most feared complication in this period. The use of Calcineurin inhibitors is a double edged weapon; in one hand it is one of the effective measures that maintain graft survival. But in the other hand, they may cause many complications as hypertension, nephrotoxicity and thrombotic microangiopathy.
Despite major improvements in one-year graft survival since the introduction of CsA in the 1980s, chronic allograft dysfunction remains a major clinical problem. The most important cause of chronic allograft dysfunction and failure is chronic rejection/chronic allograft nephropathy. Of note, death with a functioning graft is the second most common cause of graft loss and it is responsible for about40% of cases. Death may occur due to cardiovascular diseases, infection or malignancy.
There are many strategies to optimize graft survival as all kidney transplant recipients require life-long immunosuppression to prevent transplant rejection. Strategies to reduce immunological graft loss include the use of Calcineurin inhibitors, Mycophenolate and other immunosuppressive agents as Polyclonal antibodies. On the other hand, several methods have been suggested to reduce the risk of non-immunological graft loss as reducing organ ischaemia and ischaemia-reperfusion injury, mitigating Calcineurin inhibitors nephrotoxicity and using anti-hypertensive drugs.