Abstract: PO1466
Limited Therapeutic Arsenal for the Thrombotic Microangiopathy Spectrum
Session Information
- Glomerular Diseases: Immunology and Inflammation in IgANP, C3GP, TMA, and Nephrotic Diseases
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1202 Glomerular Diseases: Immunology and Inflammation
Authors
- Diaz Correa, Jesse E., Baylor University Medical Center at Dallas, Dallas, Texas, United States
- Schuller, Joris M., Dallas Nephrology Associates, Dallas, Texas, United States
- Szerlip, Harold M., Baylor University Medical Center at Dallas, Dallas, Texas, United States
Introduction
Thrombotic microangiopathy (TMA) is a common renal pathologic finding with an associated broad spectrum of clinical diseases. Complement-mediated TMA (C-TMA) is a frequently recognized cause of TMA due to uncontrolled complement activation. Terminal complement inhibitors such as Eculizumab have been shown to improve renal function in C-TMA. Multiple case reports have demonstrated a benefit in patients without identifiable complement disorder.
Case Description
41-year-old Ethiopian female with a history of metastatic ovarian cancer treated with omentectomy, partial hepatectomy, salpingo-oophorectomy, splenectomy one year before admission was admitted for renal biopsy for evaluation of an increasing creatinine and proteinuria. Following her surgery she had been treated initially with paclitaxel and carboplatin and subsequently she had received bevacizumab and doxorubicin; the last doses of these latter agents were six months before admission. Four months prior to admission she developed new onset hypertension and her creatinine began to increase with subsequent development of nephrotic range proteinuria. All serologies were negative. Kidney biopsy demonstrated TMA. Despite the discontinuation of all chemotherapeutic agents and adequate blood pressure control, her creatinine continued to increase, peaking at 6.8 mg/dl 2 months after the biopsy She was started on Eculizumab with an improvement in creatinine to 3.49 mg/dL 2 months later.
Discussion
There are no randomized trials evaluating terminal complement inhibitors for c-TMA. The indication for these medications becomes even more unclear when we factor in drug-induced TMA, cancer-associated TMA, malignant hypertension, and other TMAs without readily identifiable complement disorders. More research on the use of genetic testing and complement inhibition is warranted for the entire spectrum of TMA.