- Reduction in Incidence of Chronic Dialysis was also Observed in Patients Initiating Soliris Treatment Prior to Transplant -
- Reduction in Dialysis was Sustained Post-Transplant with Ongoing Treatment -
"Patients suffering from the devastating effects of aHUS are at a high risk of graft loss following kidney transplant due to the ongoing, unpredictable risk of complement-mediated thrombotic microangiopathy," said Martin Mackay, Ph.D., Executive Vice President and Global Head of R&D at
aHUS is a genetic, chronic, and progressive ultra-rare disease associated with vital organ failure and premature death.2,3,4 Soliris is approved in nearly 40 countries as a treatment for patients with aHUS and in nearly 50 countries as a treatment for patients with paroxysmal nocturnal hemoglobinuria (PNH), a debilitating, ultra-rare and life-threatening blood disorder characterized by complement-mediated hemolysis (destruction of red blood cells). Both aHUS and PNH are caused by chronic uncontrolled complement activation.
Researchers at ASN will also present an update on renal survival characteristics of patients enrolled in the Global aHUS Registry in a poster presentation at ASN on
Timing of Eculizumab Treatment and the Need for Dialysis in Patients with aHUS Who Receive a Kidney Transplant (TH-OR095)1
In an oral session,
- Six out of 69 patients who started on Soliris therapy before transplant required dialysis, compared to 28 out of 78 who initiated Soliris treatment post-transplant. The adjusted hazard ratio was 3.0 (95% CI 1.2-7.7) comparing dialysis events in the two populations, indicating a three-fold increase in the likelihood of dialysis in the patients who initiated Soliris treatment post-transplant.
- In the sub-analysis of patients receiving labeled dosing, 4 out of 53 patients who started Soliris therapy before transplant required dialysis, compared to 23 out of 65 patients who initiated Soliris treatment post-transplant, indicating a nearly three-fold increase in likelihood of dialysis in the patients initiating Soliris treatment post-transplant. In addition, 1 out of 53 patients who started on Soliris therapy before transplant required chronic dialysis, compared to 9 out of 65 patients who initiated Soliris treatment post-transplant, indicating a four-fold increase in the likelihood of chronic dialysis in patients initiating Soliris treatment post-transplant.
"The aim of this analysis was to evaluate the timing of eculizumab treatment and the need for dialysis in patients with aHUS who receive a kidney transplant," said lead study investigator,
The Global aHUS Registry is dedicated to increasing the knowledge of the natural history of aHUS, irrespective of management strategy, to help optimize care and improve quality of life for patients. Data from the registry serve to enhance the understanding of aHUS, as well as the use of Soliris as a treatment for patients with aHUS.
About Atypical Hemolytic Uremic Syndrome (aHUS)
aHUS is a chronic, ultra-rare, and life-threatening disease in which a life-long and permanent genetic deficiency in one or more complement regulatory genes causes chronic uncontrolled complement activation, resulting in complement-mediated thrombotic microangiopathy (TMA), the formation of blood clots in small blood vessels throughout the body.6,7 Permanent, uncontrolled complement activation in aHUS causes a life-long risk for TMA, which leads to sudden, catastrophic, and life-threatening damage to the kidney, brain, heart, and other vital organs, and premature death.7,8 Seventy-nine percent of all patients with aHUS die, require kidney dialysis or have permanent kidney damage within three years after diagnosis despite plasma exchange or plasma infusion (PE/PI).9 Moreover, 33-40 percent of patients die or progress to end-stage renal disease with the first clinical manifestation of aHUS despite PE/PI.9,10 The majority of patients with aHUS who receive a kidney transplant commonly experience subsequent systemic TMA, resulting in a 90 percent transplant failure rate in these TMA patients.11
aHUS affects both children and adults. Complement-mediated TMA also causes reduction in platelet count (thrombocytopenia) and red blood cell destruction (hemolysis). While mutations have been identified in at least ten different complement regulatory genes, mutations are not identified in 40-50 percent of patients with a confirmed diagnosis of aHUS.9,11,12
About Soliris® (eculizumab)
Soliris is a first-in-class terminal complement inhibitor developed from the laboratory through regulatory approval and commercialization by
More information on Soliris, including the full
IMPORTANT SAFETY INFORMATION:
The
In patients with PNH, the most frequently reported adverse events observed with Soliris treatment in clinical studies were headache, nasopharyngitis (runny nose), back pain and nausea. Soliris treatment of patients with PNH should not alter anticoagulant management because the effect of withdrawal of anticoagulant therapy during Soliris treatment has not been established. In patients with aHUS, the most frequently reported adverse events observed with Soliris treatment in clinical studies were headache, diarrhea, hypertension, upper respiratory infection, abdominal pain, vomiting, nasopharyngitis, anemia, cough, peripheral edema, nausea, urinary tract infections, and pyrexia. Soliris is not indicated for the treatment of patients with Shiga-toxin E. coli-related hemolytic uremic syndrome (STEC-HUS). Please see full prescribing information for Soliris, including BOXED WARNING regarding risk of serious meningococcal infection.
About
[ALXN-G]
Forward-Looking Statements
This news release contains forward-looking statements, including statements related to potential medical benefits of Soliris® (eculizumab) for the treatment of atypical hemolytic uremic syndrome (aHUS). Forward-looking statements are subject to factors that may cause
References
1. Siedlecki A, Isbel N,
2. Benz K, Amann K. Thrombotic microangiopathy: new insights. Curr Opin Nephrol Hypertens. 2010;19(3):242-247.
3. Ariceta G, Besbas N, Johnson S, et al. Guideline for the investigation and initial therapy of diarrhea-negative hemolytic uremic syndrome. Pediatr Nephrol. 2009;24:687-696.
4. Tsai HM. The molecular biology of thrombotic microangiopathy. Kidney Int. 2006;70(1):16-23.
5. Schaefer F, Fakhouri F, Kupelian V, et al. Age at Onset, Complement Abnormality and Renal Survival in Patients with aHUS Enrolled in a Global Registry. Poster presentation at the
6. Benz K, Amann K. Thrombotic microangiopathy: new insights. Curr
7. Ariceta G, Besbas N, Johnson S, et al. Guideline for the investigation and initial therapy of diarrhea-negative hemolytic uremic syndrome. Pediatr Nephrol. 2009;24:687-96.
8. Tsai HM. The molecular biology of thrombotic microangiopathy. Kidney Int. 2006;70(1):16-23.
9. Noris M, Caprioli J, Bresin E, et al. Relative Role of genetic complement abnormalities in sporadic and familial aHUS and their impact on clinical phenotype. Clin J Am Soc Nephrol. 2010;5:1844-59.
10. Caprioli J, Noris M, Brioschi S, et al; for the International Registry of Recurrent and Familial HUS/TTP. Genetics of HUS: the impact of MCP, CFH, and IF mutations on clinical presentation, response to treatment, and outcome. Blood. 2006;108:1267-1279.
11. Bresin E, et al. Combined Complement Gene Mutations in Atypical Hemolytic Uremic Syndrome Influence Clinical Phenotype. J Am Soc Nephrol. 2013;24: 475-486.
12. Fremeaux-Bacchi, et al. Genetics and Outcome of Atypical Hemolytic Uremic Syndrome: A Nationwide French Series Comparing Children and Adults. Clin J Am Soc Nephrol. 2013
View source version on businesswire.com: http://www.businesswire.com/news/home/20161117006414/en/
Media
Senior Vice President, Corporate Communications
or
Associate Director, Corporate Communications
or
Investors
Vice President, Investor Relations
Source:
News Provided by Acquire Media