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-low-birth-weight infants from birth to 34-36 wk postmenstrual age. Pediatr Res. 2015; 77: 696. 5. Subramanian S, Agarwal R, Deorari AK, et al. Acute renal failure in neonates. Indian J Pediatr. 2008: 75(4): 385-91. 6. Askenazi D. Evaluation and management of critically ill children with acute kidney injury. Curr Opin Pediatr. 2011; 23(2): 201-207. 7. Libório AB, Branco CM, Bezerra CT. Аcute kidney injury in neonates: from urine output to new biomarkers. BioMed Research International. 2014, 2014: 601568. 8. Bezerra CT, Vaz Cunha LC, Libório AB. Defining reduced urine output in neonatal

References 1. Bellomo R, Ronco C, Kellum Ja, Mehta Rl, Palevsky P. (2004). Acute Dialysis Quality Initiative Workgroup:Acute Renal Failure- Definition, Outcome Measures, Animal Models, Fluid Therapy And Information Technology Needs:The Second International Consensus Conference Of The Acute Dialysis Quality Initiative (Adqi) Group. Crit Care , 8:R204-R212 2. Kdigo Clinical Practice Guideline For Acute Kidney Injury.(2012). Kidney International .2(1), 1-141. 3. Lopes J A, Fernandes P, Jorge S, Gonçalves S, Alvarez A, França C&Prata M.(2008).Acute Kidney Injury In

-related weight gain and subsequent mortality in acute renal failure patients treated with continuous renal replacement therapy. ASAIO J 2010;56:333-7. 15. Goldstein SL. Advances in pediatric renal replacement therapy for acute kidney injury. Semin Dial 2011;24:187-91. 16. Beierwaltes WH, Harrison-Bernard LM, Sullivan JC, Mattson DL. Assessment of renal function; clearance, the renal microcirculation, renal blood flow, and metabolic balance. Compr Physiol 2013;3:165-200. 17. Dewitte A, Coquin J, Meyssignac B, Joannès-Boyau O, Fleureau C, Roze H, et al. Doppler resistive index

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 acute kidney injury (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

Abstract

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.

References 1. Siew ED, Ware LB, Ikizler TA. Biological markers of acute kidney injury. J Am Soc Nephrol 2011; 22(5): 810-20. 2. Devarajan P. Neutrophil gelatinase-associated lipocalin - An emerging troponin for kidney injury. Nephrology Dialysis Transplantation 2008; 23(12): 3737-43. 3. Schrezenmeier E V, Barasch J, Budde K, Westhoff T, Schmidt-Ott KM. Biomarkers in acute kidney injury - pathophysiological basis and clinical performance. Acta Physiol (Oxf) 2016; 219(3): 554-72. 4. Niemann CU, Walia A, Waldman J, Davio M, Roberts JP, Hirose R, Feiner J. Acute

Introduction Acute kidney injury (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 acute kidney injury. 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 acute kidney injury in critically ill multiple trauma patients. Clin Chem Lab Med 2009; 47(1): 79-82.

Introduction Cardiac surgery carries a greater risk for perioperative acute kidney injury (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