Atypical Hemolytic Uremic Syndrome: New Challenges in the Complement Blockage Era


Por: Avila Bernabeu AI, Cavero Escribano T and Cao Vilarino M

Publicada: 1 nov 2020 Ahead of Print: 18 sep 2020
Resumen:
Atypical hemolytic uremic syndrome (aHUS) is a rare cause of thrombotic microangiopathy (TMA), characterized by microangiopathic hemolytic anemia, consumptive thrombocytopenia, and multisystem end organ involvement, most commonly affecting the kidney. Diagnosis is clinical, after exclusion of other TMA causes. Primary aHUS arises from genetic abnormalities, resulting in uncontrolled complement activity, while a variety of clinical scenarios cause secondary aHUS, including infection, pregnancy, malignancy, autoimmune disease, and medications. They can also induce a temporary complement deregulation with an overlap between both scenarios, which can make differential diagnosis difficult. Primary aHUS can be sporadic or familial and is associated with a high rate of progression to ESRD. Many aHUS patients relapse in the native or transplanted kidneys, leading to kidney failure. The introduction of eculizumab has changed the prognosis of aHUS, by inducing hematologic remission, improving or stabilizing kidney functions, and preventing graft failure. The early institution of appropriate therapy can prevent multiorgan damage, so is essential to recognize and differentiate the TMA syndromes. Eculizumab is considered now the first-line treatment, and it is recommended lifelong therapy. However, the high cost of therapy has led to make efforts to develop precise complement functional and genetic studies that help physicians to determine the appropriate duration of eculizumab therapy. Nowadays, more studies are needed to select candidates to adjustment of therapy.

Filiaciones:
:
 Department of Nephrology, Hospital Universitario Dr Peset, Valencia, Spain,

Cavero Escribano T:
 Department of Nephrology, Hospital Universitario Doce de Octubre, Madrid, Spain

Cao Vilarino M:
 Department of Nephrology, Hospital Universitario A Coruña, A Coruña, Spain
ISSN: 16608151





NEPHRON
Editorial
S. Karger AG, Switzerland, Suiza
Tipo de documento: Review
Volumen: 144 Número: 11
Páginas: 537-549
WOS Id: 000587465300001
ID de PubMed: 32950988
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