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Abstract: TH-PO1021

Complement-Mediated Thrombotic Microangiopathy Following Removal of Retained Products of Conception

Session Information

Category: Women's Health and Kidney Diseases

  • 2200 Women's Health and Kidney Diseases

Authors

  • Panthappattu, Justin Joseph, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Toglia, Gianna C., University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Lawanto, Stephanie, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Geara, Abdallah Sassine, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Nader, Ralph, University of Pennsylvania, Philadelphia, Pennsylvania, United States
Introduction

Pregnancy-associated acute kidney injury (AKI) exists across a spectrum of disease states including thrombotic microangiopathy (TMA).

Case Description

A 34-year-old female with pre-eclampsia in prior pregnancy and miscarriage presented after surgical termination of pregnancy at 12 weeks gestation requiring dilation and evacuation of retained products of conception (POC). Labs showed uptrend in creatinine to 9.52 mg/dL from baseline 0.8 (Fig. 1) by post-procedure day four with UPCR 1.15 mg/mg and dysmorphic red blood cells with granular casts on urine microscopy, normal ADAMTS13 and consumed C4 suggestive of microangiopathic hemolytic anemia (MAHA) in the setting of suspected complement-mediated (CM) TMA incited by the POC and later removal. Severe thrombocytopenia prohibited renal biopsy. Kidney function and hemolysis markers began to improve without initiation of eculizumab though her injury did not resolve by the time of outpatient visit.

Discussion

Microangiopathy and endothelial injury must be considered in AKI during pregnancy and the peripartum phase. AKI with MAHA and thrombocytopenia can occur in pre-eclampsia with severe features or HELLP syndrome, developing, by definition, after 20 weeks gestation usually with milder kidney injury. By contrast, CM-TMA most commonly occurs in multigravid women immediately postpartum with more severe kidney injury, as in our patient. Importantly, thrombotic thrombocytopenic purpura, which tends to present in the second trimester of pregnancy due to decreased ADAMTS13 activity, must be ruled out as it warrants an urgent change of management, mobilization of significant resources, and the need for plasma exchange. Biopsy reveals endothelial injury, endotheliosis and microvascular obliteration by fibrin and platelet microthrombi. Treatment consists of treating the inciting factor, such as evacuation of POC in our patient, and can include eculizumab, an anti-C5 agent that blocks formation of the membrane attack complex and propagation of injury. This patient may benefit from genetic testing to identify complement gene variants predisposing her to AKI in future pregnancies.

Figure 1 - trend in selected lab work over hospitalization

Digital Object Identifier (DOI)