ArticleCEN case reports2022
Thrombotic microangiopathy in a patient with systemic lupus erythematosus and anti-factor H autoantibodies.
Article in CEN case reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Reversal of refractory systemic lupus erythematosus-associated immune thrombotic thrombocytopenic purpura and cerebritis via optimized lymphoplasmapheresis: a case report and literature review.Frontiers in immunology · 2026Review
- Treatment of thrombotic microangiopathy associated with systemic lupus erythematosus with low-dose rituximab as an induction agent and belimumab as a maintenance agent.BMC pediatrics · 2025Article
- Pregnancy-Induced Thrombotic Microangiopathy in Systematic Lupus Erythematosus: A Case Report.Cureus · 2024Article
- Case report: Rituximab combined with plasma exchange treatment for systemic lupus erythematosus complicated with thrombotic microangiopathy and non-cirrhotic portal hypertension.Frontiers in immunology · 2024Article
- Renal Thrombotic Microangiopathy: A Complication of Paediatric Systemic Lupus Erythematosus That Requires Attention.Cureus · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
Thrombotic microangiopathy (TMA) is a serious complication that may occur in patients with systemic lupus erythematosus (SLE), adversely affecting the prognosis and increasing mortality. The pathogenesis of TMA in these patients may be multifactorial and overlap between different entities may exist. We present a case of a 24-year-old man, previously diagnosed with SLE, class IV lupus nephritis, and antiphospholipid antibody syndrome, who was admitted with acute kidney injury, severe pancytopenia, and other features consistent with lupus flare. A clinical TMA diagnosis was made and the patient was treated with plasmapheresis, rituximab and immunoglobulin endovenous (EV) infusions. Hemodialysis was initiated during hospitalization and, despite the hematological recovery, the patient remained dialysis dependent. The complementary study revealed high levels of anti-factor H (fH) autoantibodies with no pathogenic mutations on complement genes (namely CFHR1 and CFHR3). Initially, the most likely cause of TMA seemed to be secondary to SLE, but the presence of anti-fH antibodies in our patient may suggest a concomitant complement-mediated TMA.
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