Acute tubular necrosis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Ischemic ATN=== | ===Ischemic ATN=== | ||
[[File:ATN_Pathophysiology.png|center|600px]] | |||
'''Intrarenal Vasoconstriction'''<br> | '''Intrarenal Vasoconstriction'''<br> | ||
Many studies have demonstrated that following ischemia, the renal vasculature has increased sensitivity to vasoconstrictive stimuli particularly endothelin. Endothelin (ET-1) is a vasoactive substance release by endothelial cells and one of the most potent vasoconstrictors identified. The ET-1 gene has also been shown to be upregulated during ischemic injuries.<ref name="pmid11251028">{{cite journal| author=Lameire N, Vanholder R| title=Pathophysiologic features and prevention of human and experimental acute tubular necrosis. | journal=J Am Soc Nephrol | year= 2001 | volume= 12 Suppl 17 | issue= | pages= S20-32 | pmid=11251028 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11251028 }} </ref> In parallel, the initial insult following renal ischemia is endothelial dysfunction which contributes to the exacerbation of tissue hypoxia via several mechanisms. Endothelial injury disrupts normal vascular function and impairs reactivity and permeability of renal vessels causing maladaptive vasoconstriction and increased leukocyte recruitment. This is further exacerbated by an increase in vasoconstrictor substances, adhesion molecules, and inflammatory mediators.<ref name="Fogo">Fogo A, Cohen AH, Colvin RB et al. Fundamentals of Renal Pathology. Springer 2013. Acute Tubular Necrosis. http://dx.doi.org/10.1007/978-3-642-39080-7_15 </ref> | Many studies have demonstrated that following ischemia, the renal vasculature has increased sensitivity to vasoconstrictive stimuli particularly endothelin. Endothelin (ET-1) is a vasoactive substance release by endothelial cells and one of the most potent vasoconstrictors identified. The ET-1 gene has also been shown to be upregulated during ischemic injuries.<ref name="pmid11251028">{{cite journal| author=Lameire N, Vanholder R| title=Pathophysiologic features and prevention of human and experimental acute tubular necrosis. | journal=J Am Soc Nephrol | year= 2001 | volume= 12 Suppl 17 | issue= | pages= S20-32 | pmid=11251028 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11251028 }} </ref> In parallel, the initial insult following renal ischemia is endothelial dysfunction which contributes to the exacerbation of tissue hypoxia via several mechanisms. Endothelial injury disrupts normal vascular function and impairs reactivity and permeability of renal vessels causing maladaptive vasoconstriction and increased leukocyte recruitment. This is further exacerbated by an increase in vasoconstrictor substances, adhesion molecules, and inflammatory mediators.<ref name="Fogo">Fogo A, Cohen AH, Colvin RB et al. Fundamentals of Renal Pathology. Springer 2013. Acute Tubular Necrosis. http://dx.doi.org/10.1007/978-3-642-39080-7_15 </ref> | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Serge Korjian, Yazan Daaboul
Overview
Pathophysiology
Ischemic ATN
Intrarenal Vasoconstriction
Many studies have demonstrated that following ischemia, the renal vasculature has increased sensitivity to vasoconstrictive stimuli particularly endothelin. Endothelin (ET-1) is a vasoactive substance release by endothelial cells and one of the most potent vasoconstrictors identified. The ET-1 gene has also been shown to be upregulated during ischemic injuries.[1] In parallel, the initial insult following renal ischemia is endothelial dysfunction which contributes to the exacerbation of tissue hypoxia via several mechanisms. Endothelial injury disrupts normal vascular function and impairs reactivity and permeability of renal vessels causing maladaptive vasoconstriction and increased leukocyte recruitment. This is further exacerbated by an increase in vasoconstrictor substances, adhesion molecules, and inflammatory mediators.[2]
Obstruction by Casts
Tubular Backleak
Interstitial Inflammation
Toxic ATN
References
- ↑ Lameire N, Vanholder R (2001). "Pathophysiologic features and prevention of human and experimental acute tubular necrosis". J Am Soc Nephrol. 12 Suppl 17: S20–32. PMID 11251028.
- ↑ Fogo A, Cohen AH, Colvin RB et al. Fundamentals of Renal Pathology. Springer 2013. Acute Tubular Necrosis. http://dx.doi.org/10.1007/978-3-642-39080-7_15