The term
Acute Renal Failure (ARF) has been replaced by the term
Acute Kidney Injury (AKI). AKI indicates an abrupt (within 24-48h) decrease in Glomerular Filtraton Rate, due to renal damage, that causes fluid and metabolic waste retention and alteration of
electrolyte and acid-base balance. The renal
biomarkers of AKI are substances or processes that are indicators of normal or impaired function of the kidney. The most used renal
biomarker is still serum
creatinine that is inadequate for several reasons, one of which is its inability to differentiate between hemodynamic changes of renal function ("prerenal
azotemia") from intrinsic
renal failure or obstructive nephropathy.
Cystatin C is no better in this respect. After the description of the pathophysiology of "prerenal
azotemia" and of
Acute Kidney Injury (AKI) due to
ischemia or nephrotoxicity, the renal
biomarkers are listed and described: urinary NAG, urinary and serum KIM-1, serum and urinary NGAL, urinary
IL-18, urinary L-FABP, serum
Midkine, urinary IGFBP7 and TIMP2, urinary α-GST and π-GST, urinary ɣGT and AP, urinary β2M, urinary RBP, serum and urinary
miRNA. All have been shown to appear much earlier than the rise of serum
Creatinine. Some of them have been demonstrated to predict the clinical outcomes of AKI, such as the need for initiation of dialysis and mortality.