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References 1. Chawla LS, Amdur RL, Shaw AD, Faselis C, Palant CE, Kimmel PL. Association between AKI and longterm renal and cardiovascular outcomes in united states veterans. Clin J Am Soc Nephrol. 2014;9(3):448-56. DOI: 10.2215/CJN.02440213 2. Bellomo R, Auriemma S, Fabbri A, D’Onofrio A, Katz N, McCullough PA, et al. The pathophysiology of cardiac surgery-associated acutekidneyinjury (CSAAKI). Vol. 31, International Journal of Artificial Organs. 2008. p. 166-78. 3. Nangaku M, Rosenberger C, Heyman SN, Eckardt KU. Regulation of hypoxia-inducible factor in
Apoptosis is an inborn process that has been preserved during evolution; it allows the cells to systematically inactivate, destroy and dispose of their own components thus leading to their death. This program can be activated by both intra and extracellular mechanisms. The intracellular components involve a genetically defined development program while the extracellular aspects regard endogenous proteins, cytokines and hormones as well as xenobiotics, radiations, oxidative stress and hypoxia. The ability of a cell to enter apoptosis as a response to a „death” signal depends on its proliferative status, the position in the cell cycle and also on the controlled expression of those genes that have the capacity of promoting and inhibiting cell death. The fine regulation of these parameters needs to be maintained in order to ensure the physiological environment required for the induction of apoptosis.
In this review, we first describe evidence for the role of apoptotic pathways in ischemic acute renal failure, and then consider the potential mechanisms that may participate in this model of acute renal tubular injury. Potential therapeutic interventions to prevent tubular apoptosis in renal disease include angiotensin system inhibition, whereby the angiotensin II AT2 receptor blockade seems more promising in apoptosis inhibition than the inhibition of other receptor subtypes. A better understanding of the mechanisms of apoptosis could lead to safer and more specific therapeutic interventions for acute kidney injury.
Introduction Acutekidneyinjury (AKI) that can occur after the surgery is characterized by rapid progressive complications and adverse outcomes, which are raising morbidity and mortality rates high above ordinary rates observed in major surgeries ( 1 , 2 , 3 ). Criteria for classification of AKI stages have evolved over the years, and recently the Kidney Disease Improving Global Outcomes (KDIGO) consensus conference on AKI recommended re-arrangement and harmonization of classification criteria for AKI by using new KDIGO criteria ( 4 ). Although classifications
References Akcan-Arikan, A., Zappitelli, M., Loftis, L. L, Washburn, K. K., Jefferson, L. S, Goldstein, S. L. (2007). Modified RIFLE criteria in critically ill children with acutekidneyinjury. Kidney Int., 71, 1028-1035. Akech, S., Gwer, S., Idro, R., Fegan, G., Eziefula, A. C., Newton, C. R. J., Levin, M., Maitland, K. (2006). Volume expansion with albumin compared to gelofusine in children with severe malaria: Results of a controlled trial. PLoSClin Trials, 1 (5): e21. Akech, S., Ledermann, H., Maitland, K. (2010). Choice of fluids for resuscitation in
biomarker for acute renal injury after cardiac surgery. Lancet 2005; 365(9466): 1231-1238. 5. Makris K, Markou N, Evodia E, et al. Urinary neutrophil gelatinase-associated lipocalin (NGAL) as an eary marker of acutekidneyinjury in critically ill multiple trauma patients. Clin Chem Lab Med 2009; 47(1): 79-82.
Introduction Cardiac surgery carries a greater risk for perioperative acutekidneyinjury (AKI) than any other type of surgery ( 1 ). Cardiac surgery-associated AKI (CSA-AKI) occurs in approximately 22% of cardiac surgery patients and is linked to a 5-fold increase in mortality ( 2 , 3 , 4 ). Given the limited prevention and treatment strategies, recognition of patients at risk for development of CSA-AKI is of paramount importance. Risk assessment has, so far, been restricted to risk scores, and, arguably, novel biomarkers of AKI. The best validated risk scores