A TEN-YEAR EXPERIENCE OF ATYPICAL HEMOLYTIC UREMIC SYNDROME: A MONOCENTRIC PROSPECTIVE EXPERIENCE.

https://storage.unitedwebnetwork.com/files/1099/588704dd89c28ed86c98fcaa77e253ab.pdf
A TEN-YEAR EXPERIENCE OF ATYPICAL HEMOLYTIC UREMIC SYNDROME: A MONOCENTRIC PROSPECTIVE EXPERIENCE.
Mariana
Ursino
Trimarchi Hernán htrimarchi@hotmail.com Hospital Británico de Buenos Aires Buenos Aires Buenos Aires
Mariano Forrester marianoforrester@hotmail.com Hospital Británico de Buenos Aires Buenos Aires Buenos Aires
Romina Iriarte romiriarte@gmail.com Hospital Británico de Buenos Aires Buenos Aires Buenos Aires
Fernando Lombi fernandolombi@gmail.com Hospital Británico de Buenos Aires Buenos Aires Buenos Aires
Eugenia Flores eugenia.mflores@gmail.com Hospital Británico de Buenos Aires Buenos Aires Buenos Aires
Matias Monkowski matias.mnk@gmail.com Hospital Británico de Buenos Aires Buenos Aires Buenos Aires
Mauro Lampo mglampo@gmail.com Hospital Británico de Buenos Aires Buenos Aires Buenos Aires
José Diaz jhdiaz@hbritanico.com.ar Hospital Británico de Buenos Aires Buenos Aires Buenos Aires
Liliana Borda sborda@hbritanico.com.ar Hospital Británico de Buenos Aires Buenos Aires Buenos Aires
 
 
 
 
 
 

Atypical hemolytic uremic syndrome (aHUS) is an entity characterized by microangiopathic hemolytic anemia, thrombocytopenia, and multisystemic organ dysfunction. Histologically, it is characterized by endothelial damage, widening and edema of the subendothelial space due to cell lysis material, and the subsequent presence of thrombi obstructing capillary lumen. It presents with a prevalence of 0.5 -1% per million population and approximately 50% of subjects develop end-stage kidney disease.

Prospective study performed at the British Hospital of Buenos Aires including clinical data, laboratory results, genetic studies and the respective treatment from time of diagnosis to the present time.

We report 10 cases of aHUS from 2014 to 2024, with 60% (n=6) of female gender, median age 40.7(18–64). At the time of diagnosis 30% (n=3) of patients presented systemic infections; 20% (n=2) with pregnancy; 20% (n=2) in the post-transplant period and 30% (n=3) with nephritic syndrome. All presented low haptoglobin levels, hypocomplementemia, thrombocytopenia, ADAMTS13 within normal limits, Shiga toxin stool test were negative, microangiopathy hemolytic anemia and renal damage, with 70% (n=7) requiring acute dialysis. All patients had hypertension. A renal biopsy was performed in all patients with a diagnosis of thrombotic microangiopathy (TMA) in 90% of them.

Initial approach consisted on plasmapheresis with plasma replacement and corticosteroid.  Eculizumab was started as per availability in all cases. Currently 100% continue with eculizumab therapy. Mortality rate:  30%(n=3) and 20% (n=2) continue on chronic dialysis and 2 received a kidney transplant. In 50% (n= 5) of cases genetic mutations were identified:  MCP; CFH; CFHR3 and CFHR1

aHUS is a rare syndrome cause by dysregulation with over-activation of the alternative complement pathway.  The diagnosis is made on clinical grounds and must lead to prompt therapeutic intervention. An early diagnosis leads to patient’s stabilization and eculizumab is a safe therapy that’s leads to plasmapheresis discontinuation.

E-Poster Format Requirements
  • PDF file
  • Layout: Portrait (vertical orientation)
  • One page only (Dim A4: 210 x 297mm or PPT)
  • E-Poster can be prepared in PowerPoint (one (1) PowerPoint slide) but must be saved and submitted as PDF file.
  • File Size: Maximum file size is 2 Megabytes (2 MB)
  • No hyperlinks, animated images, animations, and slide transitions
  • Language: English
  • Include your abstract number
  • E-posters can include QR codes, tables and photos