الفهرس 
Acute kidney injuryOnly 14 pages are availabe for public view
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Abstract
Acute kidney injury (AKI) is a protean syndrome of varied
severity. It is characterized by a rapid decline in the glomerular filtration
rate (GFR) and retention of nitrogenous waste products such as blood
urea nitrogen (BUN) and creatinine.
AKI is diagnosed using blood urea, and serum creatinine levels,
but serum creatinine is an unreliable indicator of kidney function during
acute changes, as serum creatinine level can vary widely with age,
gender, muscle mass, muscle metabolism, medications, and hydration
status, another cause is that its concentration may not change until about
50% of kidney function has already been lost, at lower rates of
glomerular filtration the amount of tubular secretion of creatinine results
in overestimation of renal function, during acute changes in renal
filtration, serum creatinine does not accurately depict kidney function
until steady state equilibrium has been reached, which may require
several days.
The application of innovative technologies such as functional
genomics and proteomics to human and animal models of AKI had
uncovered several novel biomarkers, such as; neutrophil gelatinase
associated lipocalin (NGAL) which can be measured in blood and urine
and was found to diagnose AKI 1-3days before serum creatinine is
elevated. Urinary interleukin 18 (IL-18) was found to detect contrast
induced nephropathy 24 hours before serum creatinine elevation. Kidney
injury molecule 1 (KIM-1) level in renal transplant patients was found to
correlate with the incidence of graft loss. Growth related oncogene alpha
(GRO-α) was found to be elevated in renal transplant patients whose
renal biopsy showed acute tubular necrosis. Alpha-1 microglobulin was
found to predict the need for renal replacement therapy in non-oliguric
acute renal failure.
Key words: AKI, biomarkers, NGAL, IL-18, KIM-1, GRO-α,
Alpha-1 microglobulin,, cystatin C, Fetuin-A, Meprin.