Hemolytic-uremic syndrome pathophysiology: Difference between revisions
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[[Category:Nephrology]] | [[Category:Nephrology]] | ||
[[Category:Hematology]] | [[Category:Hematology]] | ||
Revision as of 17:12, 17 June 2016
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Hemolytic-uremic syndrome Microchapters |
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Differentiating Hemolytic-uremic syndrome from other Diseases |
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Hemolytic-uremic syndrome pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Molecular Biology
- Platelet-rich thrombi in affected organs (unclear etiology of tissue specificity CD36)
- vWF (endothelially synthesized) -> ULvWf multimers -> shear stress unfolds and causes massive platelet aggregation
- Normally, UlvWf digested by metalloprotease to “normal” size vWf multimers
- Familial forms of TTP lack metalloprotease activity
- Acquired forms of TTP have IgG antibody, which reduce metalloprotease activity during flares
Metalloprotease activity appears normal in HUS
- In HUS, and in cases of TTP without decreased metalloprotease activity, other etiologies of platelet activation have been proposed:
- Endothelial injury (esp. drug induced)
- Toxins (i.e. Shiga toxin)
- PAI – 1
- Other genetic factors (Factor H, Factor I deficiencies, complement derangements).