Hemolytic-uremic syndrome pathophysiology: Difference between revisions

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Revision as of 19:54, 18 July 2018

@@ Line 1: / Line 1: @@
 __NOTOC__
 {{HUS}}
-{{CMG}}
-==Overview==
-==Pathophysiology==
-===Molecular Biology===
-:*[[Platelet]]-rich thrombi in affected organs (unclear etiology of tissue specificity CD36)
-:*[[vWF]] ([[endothelial]]ly 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).
-==References==
-{{reflist|2}}
-{{WH}}
-{{WS}}
 [[Category:Nephrology]]
 [[Category:Hematology]]