**4. Markers of inflammatory reaction connected with acute renal failure**

**Neutrophil gelatinase-associated lipocalin (NGAL)** is a glycoprotein expressed and secreted by immune cells, trachea, stomach, colon, and injured kidney epithelial cells as an monomer (22 kDa), dimer or trimer. NGAL may complex with collagenase type IV of human neutrophils named gelatinase B or metalloproteinase 9 (MMP-9) creating heterodimer (125 kDa) (Flower, 1996). NGAL binds and transports small lipophilic molecules e.g. free fatty acids, retinoids, arachidonic acid, and steroids (Mishra et al., 2003). NGAL is considered as provider iron to proximal renal tubules. Iron stimulates oxygenase synthesis which protects renal tubules cells. NGAL may be applied as a predictor of ischemic or toxic renal damage, before development of a full symptomatic renal insufficiency. Increase in urinary NGAL concentration is early, sensitive and non-invasive marker of renal damage correlating with intensity and time of ischemia and preceding increase in other markers such as hexosaminidase or β2-microglobu‐ lin. A strict correlation between NGAL concentration and degree of proteinuria was demon‐ strated (Flower, 1996). NGAL activated formation of nephrons in early step of renal development demonstrates a protective action in kidney (Mori & Nakao, 2007). Low molecular weight, resistant to degradation NGAL is easily excreted by cells of thick ascending arm of Henry loops and collective tubules into urine both free and in complex with MMP-9. Increase in urinary excretion of NGAL is observed several hours after stimuli of nephrotoxic factor. As concentration of urinary NGAL correlates with plasma NGAL concentration, NGAL may be an useful marker in diagnostics of renal diseases (Nickolas et al., 2008). There is an opinion that NGAL is the most promising biomarker for diagnosis of acute renal injury (AKI) in acute renal graft dysfunction (Halawa, 2011; Ting et al., 2012; Hollmen, 2011).

**Kidney injury molecule-1 (KIM-1)** is a transmembrane glycoprotein receptor (104 kDa) appearing as KIM-1a and KIM 1b. KIM-1 is produced in large quantities in renal proximal tubules after a toxic or ischemic damage. It is assumed that direct cause of KIM-1 induction is an increase of the protein concentration in glomerular ultrafiltration and presence of urinary protein casts favoring tubular obstruction, mechanical stress and an increase in glomerular pressure. An increase in urinary KIM-1 excretion is specific to the ischemic renal damage and is practically independent of chronic renal insufficiency or renal tract infection (Nickolas et al., 2008; Melnikov & Molitoris, 2008). It was reported that KIM-1 extracellular domain (fragment 90 kDa) reaches urine after cleavage by metalloproteinase (Han et al., 2002; Waanders et al., 2010). Urinary KIM-1 is particularly important in the diagnosis of the acute transplanted kidney insufficiency(AKI) (Halawa, 2011). As in renal graft recipients, contrary to urinary NGAL or IL-18, KIM determination gives better possibility for predicting a rate of the trans‐ planted kidney deterioration (Szeto et al., 2010), KIM-1 was proposed as an independent predictor of the long term renal graft survival (Ting et al., 2012).
