In addition, we followed proper biorepository procedures including validated and blinded biomarker measurements from sample aliquots that had not undergone MEK162 buy prior freeze thaw cycles. The use of a dichotomous cutoff value for a continuous measure ment can be considered a limitation, however, the value of 5 ng ml for YKL 40 was pre specified based on our previ ous findings in a separate patient cohort. In addition, sam ple size limited our ability to evaluate multiple biomarker combinations and comparisons. We therefore controlled for the same confounders and evaluated a simple, repre sentative combination of YKL 40 with the best injury bio marker based on our prior analyses. Lastly, this study was limited by a lack of post hospitalization information and outcomes given IRB approval with waiver of consent to study the effects of AKI on inpatient outcomes only.

Conclusions In summary, YKL 40 is a repair phase protein that is de tectable in urine on the first day of clinically apparent AKI and provides only modest prognostic potential on its own. Our findings suggest that there may be utility in combining YKL 40 with other biomarkers like NGAL to refine AKI prognosis and better determine the relationship between injury severity and the degree of repair activation. Further studies are needed to validate the performance of YKL 40 in a large population of patients with AKI and, in particular, to follow trends in this marker of renal injury and repair over the course of disease progression and or recovery. The kidney is clearly an intricate organ with sev eral cell types that are responsible for multiple homeostatic functions.

As we continue to learn more about the com plex mechanisms that maintain and repair the renal urinary system following periods of stress and injury, we envision developing better clinical AKI biomarker panels that provide useful diagnostic and prognostic information relative to those mechanisms. With further insights into the renal selleck chemicals Tubacin responses to acute injury, novel biomarkers like YKL 40 may also begin to give us better information about overall kidney health and could suggest new therapeutic targets for study in humans. Background Factors contributing to anemia in ESRD patients include erythropoietin deficiency, blood loss, shortened red blood cell life span, vitamin deficiencies, iron deficiency, and chronic inflammation. The shortened RBC sur vival observed in uremic patients has been attributed mainly to uremic toxins. In patients with ESRD, there is growing evidence that increased oxidative stress may contribute to anemia, along with other factors such as erythropoietin stimulating agent resistance, malnu trition, and atherosclerosis. Erythrocyte G6PD is the key enzyme in the hexose monophosphate shunt.