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* {{Cite journal |last=Moschcowitz |first=Eli |author-mask=2 |date=1952 |title=An Acute Febrile Pleiochromic Anemia with Hyaline Thrombosis of the Terminal Arterioles and Capillaries: An Undescribed Disease |url=https://www.sciencedirect.com/science/article/abs/pii/0002934352900223 |journal=The American Journal of Medicine |volume=13 |issue=5 |pages=567–569 |doi=10.1016/0002-9343(52)90022-3 |issn=0002-9343 |pmid=12996533}}
* {{Cite journal |last=Moschcowitz |first=Eli |author-mask=2 |date=1978 |title=An Acute Febrile Pleiochromic Anemia with Hyaline Thrombosis of the Terminal Arterioles and Capillaries: An Undescribed Disease |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0039-1681113 |journal=Thrombosis and Haemostasis |language=en |volume=40 |issue=04 |pages=004–008 |doi=10.1055/s-0039-1681113 |issn=0340-6245 |pmid=725850}}
* {{Cite journal |last=Moschcowitz |first=Eli |author-mask=2 |date=2003 |title=An Acute Febrile Pleiochromic Anemia with Hyaline Thrombosis of the Terminal Arterioles and Capillaries: An Undescribed Disease |url=https://archive.org/details/sim_mount-sinai-journal-of-medicine_2003-10_70_5/page/352/mode/2up |journal=The Mount Sinai Journal of Medicine |volume=70 |issue=5 |pages=352–355 |pmid=14631522}}</ref><ref>{{Citation |title=Commentary on and reprint of Moschcowitz E, An acute febrile pleiochromic anemia with hyaline thrombosis of the terminal arterioles and capillaries: An undescribed disease, in ''Archives of Internal Medicine'' (1925) 36:89–93 |date=2000 |url=https://www.sciencedirect.com/science/article/pii/B9780124485105501059 |work=Hematology |pages=119–125 |editor-last=Lichtman |editor-first=Marshall A. |publisher=Academic Press |doi=10.1016/b978-012448510-5.50105-9 |isbn=978-0-12-448510-5 |editor2-last=Spivak |editor2-first=Jerry L. |editor3-last=Boxer |editor3-first=Laurence A. |editor4-last=Shattil |editor4-first=Sanford J.}}</ref> Moreover, Moschcowitz was among the first to work in psychosomatic medicine, and he presented a paper in 1935 on the psychological origins of physical disease. HUS was first described by Conrad Gasser in 1955, and the systemic character of HUS was subsequently defined.<ref>{{Citation |last=Gianantonio |first=Carlos A. |title=Hemolytic Uremic Syndrome |date=1984 |url=http://dx.doi.org/10.1007/978-1-4613-2841-4_16 |work=Acute Renal Failure |pages=327–339 |access-date=2023-08-21 |place=Boston, MA |publisher=Springer US |isbn=978-1-4612-9794-9}}</ref> Bernard Kaplan identified several distinct entities that can manifest as HUS and emphasized that HUS was a syndrome with a common pathologic outcome. Kaplan is a Canadian professor and director of Pediatric Nephrology. He has an international reputation for his studies, over the past 34 years, on the hemolytic uremic syndromes.<ref>{{Cite journal |last=Kaplan |first=Bernard S. |last2=Drummond |first2=Keith N. |date=1978-04-27 |title=The Hemolytic-Uremic Syndrome Is a Syndrome |url=http://dx.doi.org/10.1056/nejm197804272981710 |journal=New England Journal of Medicine |volume=298 |issue=17 |pages=964–966 |doi=10.1056/nejm197804272981710 |issn=0028-4793}}</ref> The discovery that endothelial cell injury underlies this broad spectrum of TMA disorders has come into focus during the last two decades. In the 1980s, Mohamed Karmali (1945-2016) was the first to make the association between Stx, diarrheal E. coli infection and the idiopathic hemolytic uremic syndrome of infancy and childhood. Karmali’s work showed that the hemolytic uremic syndrome the children in Canada was caused by this particular bacteria. Karmali also developed the system of classifying strains of E.coli and determining which cause disease in humans. He defined the presence of microvascular injury in diarrhea-associated HUS and the critical role of a verotoxin produced by specific strains of Escherichia coli.<ref>{{Cite web |last=ovcweb@uoguelph.ca |first=OVC Communications- |title=Dr. Mohamed Karmali – Solving the Mystery of the Haemolytic-Uremic Syndrome - June 10 |url=https://bulletin.ovc.uoguelph.ca/post/120469569400/dr-mohamed-karmali-solving-the-mystery-of-the |access-date=2023-08-21 |website=Tumblr |language=en-CA}}</ref> This verotoxin was subsequently found to be a member of a family of toxins first identified with Shigella and known as Shiga toxin (Stx).<ref>{{Cite journal |last=Karmali |first=M. A. |last2=Petric |first2=M. |last3=Lim |first3=C. |last4=Fleming |first4=P. C. |last5=Arbus |first5=G. S. |last6=Lior |first6=H. |date=1985-05-01 |title=The Association Between Idiopathic Hemolytic Uremic Syndrome and Infection by Verotoxin-Producing Escherichia coli |url=http://dx.doi.org/10.1093/infdis/151.5.775 |journal=Journal of Infectious Diseases |volume=151 |issue=5 |pages=775–782 |doi=10.1093/infdis/151.5.775 |issn=0022-1899}}</ref> This relationship and the eventual link of TTP to abnormally high levels of ultra-large Von Willebrand factor (vWF) multimers caused by congenital or acquired reductions in ADAMTS13 activity was established at approximately the same time. In 1924, a Finnish physician [[Erik Adolf von Willebrand]] (1870-1949) was consulted about a young girl with a bleeding disorder. Von Willebrand<ref>{{Citation |title=Erik Adolf von Willebrand |date=2023-01-12 |url=https://en.wikipedia.org/w/index.php?title=Erik_Adolf_von_Willebrand&oldid=1133137677 |work=Wikipedia |access-date=2023-08-21 |language=en}}</ref> described this disorder in 1926, distinguishing it from hemophilia. The disorder was named after him, becoming known as von Willebrand disease. The cause of the disease was later discovered to be a deficiency of a protein, now known as von Willebrand factor, that enables hemostasis.
==Epidemiology==
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