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Ann Transplant 2011; 16(1): 90-98
Acute graft dysfunction can be caused by ischaemic damage or immunological injury leading to serious consequences both in the short and long term. We are in a desperate need for biomarkers of immune and nonimmune injury at different time points of the transplantation time course, beginning from a potential kidney donors where acute kidney damage can pass unnoticed, during the early post-transplant periods to predict acute transplant dysfunction due to various causes and during long term follow up to predict chronic histological changes. The implementation of these novel biomarkers could increase the sensitivity of diagnosis and monitoring of kidney injury in kidney transplant recipients. Traditionally acute graft dysfunction is diagnosed by measuring serum creatinine concentrations. Unfortunately rise in serum creatinine is a late sign of kidney damage. It indicates rather predicts the damage. The treatment, in order to be effective, must be instituted very early after the initiating insult, well before the serum creatinine even begins to rise. Fortunately, emerging technologies such as functional genomics and proteomics have uncovered novel candidates that are emerging as potentially useful biomarkers of acute kidney injury (AKI). The most promising of biomarkers in AKI for clinical use include a plasma panel consisting of Neutrophil Gelatinase-Associated Lipocalin (NGAL) and Cystatin C and a urine panel including NGAL, Il-18 and Kidney Injury Molecule 1 (KIM-1). Most of these biomarkers were developed in non-transplant AKI, yet their role in clinical transplantation has to be identified.