Molecular differences in susceptibility of the kidney to sepsis-induced kidney injury
Author:
Funder
National Sustainability Program I
Publisher
Springer Science and Business Media LLC
Subject
Nephrology
Link
http://link.springer.com/content/pdf/10.1186/s12882-017-0602-x.pdf
Reference28 articles.
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2. Wan L, Bagshaw SM, Langenberg C, Saotome T, May C, Bellomo R. Pathophysiology of septic acute kidney injury: what do we really know? Crit Care Med. 2008;36(4 Suppl):S198–203.
3. Benes J, Chvojka J, Sykora R, Radej J, Krouzecky A, Novak I, et al. Searching for mechanisms that matter in early septic acute kidney injury: an experimental study. Crit Care. 2011;15:R256.
4. Zager RA, Johnson AC, Frostad KB. Acute hepatic ischemic-reperfusion injury induces a renal cortical “stress response,” renal “cytoresistance,” and an endotoxin hyperresponsive state. Am J Physiol Renal Physiol. 2014;307:F856–68.
5. El-Achkar TM, Huang X, Plotkin Z, Sandoval RM, Rhodes GJ, Dagher PC. Sepsis induces changes in the expression and distribution of Toll-like receptor 4 in the rat kidney. Am J Physiol Renal Physiol. 2006;290:F1034–43.
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