Abstract: TH-PO630

Eculizumab, a Novel Treatment for Acute Kidney Failure Associated with Severe Preeclampsia

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports

Authors

  • Elabd, Hatem, Jacobi Medical Center/Albert Einstein College of Medicine, Bronx, New York, United States
  • Nayak, Rushi K., Jacobi Medical Center/Albert Einstein College of Medicine, Bronx, New York, United States
  • Jim, Belinda, Jacobi Medical Center/Albert Einstein College of Medicine, Bronx, New York, United States
  • Anis, Kisra, Jacobi Medical Center/Albert Einstein College of Medicine, Bronx, New York, United States
  • Acharya, Anjali, Jacobi Medical Center/Albert Einstein College of Medicine, Bronx, New York, United States
Background

Preeclampsia is a leading cause of maternal and neonatal morbidity and mortality. It is the most common cause of AKI during pregnancy. Preeclampsia complicates approximately 5% of all pregnancies, making it perhaps the most common glomerular disease in the world. The complement system is a key mediator of systemic inflammation and is excessively activated in preeclampsia. As alloantibodies commonly develop against the semi-allogeneic fetal tissues, the placenta is potentially a target for complement-mediated immune attack.

Methods

A 29-year-old female multiparous at 40 weeks of gestation admitted to surgical ICU post emergent cesarean section for severe preeclampsia complicated with rupture membrane and fetal heart deceleration. Peri-operatively course complicated with bleeding, shock and acute kidney injury, for which patient needed resuscitation, and mechanical ventilation. She remained anuric with progressive kidney failure and continuous renal replacement therapy was started. We performed extensive workup to rule out acute fatty liver of pregnancy, TTP, atypical HUS, SLE, or antiphospholipid syndrome. Also complement gene mutation studies associated with atypical HUS were checked, which later turned out to be negative. Therefore, she was diagnosed with severe preeclampsia with multi-organ dysfunction. We decided to give Eculizumab 900mg/dose, a C5 inibitor, on day 4 post admission. One week later, patient had marked clinical improvement, and dialysis was discontinued. Furthermore, there was complete normalization of all laboratory abnormalities and complement activation markers.

Conclusion

To our knowledge this is the first case describing the use of Eculizumab in acute kidney injury (AKI) in setting of severe preeclampsia. The use of Eculizumab was previously described in a women with HELLP syndrome which led to improved liver function tests and pregnancy prolongation for 17 days. As opposed to our case, Eculizumab was given intrapartum and their patient had no evidence of kidney failure. The use of Eculizumab in this report supports a possible benefit of C5 inhibition for the treatment of severe preeclampsia and AKI. Its use may be particularly helpful among women with mutations in complement regulatory proteins. Further research is warranted to validate our findings.