Neutrophil gelatinase-associated lipocalin (NGAL) is a protein that was initially thought to be associated with human neutrophil gelatinase, which is secreted by activated neutrophils. Many clinical studies have followed these observations . Numerous reports have proved that NGAL is synthesized in kidney tissue following several mechanisms of kidney injury, such as ischemic, nephrotoxic like contrast material injection for radiological purposes, or septic. It is nowadays known that NGAL is a marker of renal tubular damage as it is released from the distal tube. It is filtered through the glomerular membrane and is reabsorbed in the proximal tubule of the kidney. Kidney injury molecule-1 (KIM-1) is a marker for proximal tubular injury, the hallmark of virtually all proteinuric, toxic and ischaemic renal diseases. The selective KIM-1 expression by injured proximal tubular cells provides a strong evidence for using KIM-1 as a biomarker of damage. When renal epithelial cells die, a soluble KIM-1 together with the fluid may be entrained to the interstitium and enter therefrom the bloodstream . Higher KIM-1 concentration in blood together with its increased contents in urine can also reflect injury of the kidney tubular apparatus. Findings of several studies have shown that urinary KIM-1 is an early marker of AKI induced by the administration of the contrast agent to the patients who undergo coronary or peripheral angiography. Monocyte chemoattractant protein-1 (MCP-1), also referred to as chemokine ligand 2 (CCL2), belongs to the CC subfamily of cytokines. Increased glomerular synthesis of CC chemokines, including MCP-1, has been shown to correlate with monocyte/macrophage infiltration in experimental models of antibody and immune complex–mediated glomerulonephritis