Free radical-mediated injury releases proinflammatory cytokines and
activates innate immunity. It has been suggested that the early innate response
and the ischemic tissue damage play roles in the development of adaptive responses,
which may lead to acute kidney rejection. Various durations of hypothermic
kidney storage before transplantation add to ischemic tissue damage.
The final stage of ischemic injury occurs during reperfusion that develops hours
or days after the initial insult. Repair and regeneration processes occur together
with cellular apoptosis, autophagy and necrosis and a favorable outcome is expected
if regeneration prevails. Along the entire transplantation time course,
there is a great demand for novel immune and nonimmune injury biomarkers.
The use of these markers can be of great help in the monitoring of kidney injury in potential kidney
donors, where acute kidney damage can be overlooked, in predicting acute transplant dysfunction
during the early post-transplant periods, or in predicting chronic changes in long term
followup. Numerous investigations have demonstrated that biomarkers that have the highest predictive
value in acute kidney injury include NGAL, Cystatin C, KIM-1, IL-18, and L-FABP.
Most investigations show that the ideal biomarker to fulfill all the needs in renal transplant has
not been identified yet. Although, in many animal models, new biomarkers are emerging for predicting
acute and chronic allograft damage, in human allograft analysis they are still not routinely
accepted and renal biopsy still remains the gold standard.
Keywords: Acute Kidney Injury, Kidney transplantation, Acute renal failure, NGAL, Cystatin C, KIM-1, IL-18, LFABP.
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