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SLE-Associated TMA Classical Complement — ESENeph MCQ

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HardGlomerulonephritisSLE-Associated TMA Classical ComplementESENeph

A 40-year-old woman with SLE develops thrombotic microangiopathy. Her ADAMTS13 is 45% (normal). Complement studies show low C3, low C4, elevated anti-C1q antibodies, and normal factor H. What is the most likely type of TMA?

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Correct answer: E — SLE-associated TMA – driven by classical complement pathway activation (anti-C1q, low C4) and endothelial injury from lupus; treatment is immunosuppression for SLE (not Eculizumab unless complement-mediated aHUS is confirmed)

SLE can cause TMA through multiple mechanisms: (1) antiphospholipid antibody-mediated thrombosis; (2) immune complex-mediated endothelial injury (classical pathway – anti-C1q, low C4); (3) complement dysregulation (overlap with aHUS); (4) thrombotic microangiopathic HELLP in pregnancy. Low C3 AND C4 with elevated anti-C1q suggests classical pathway-mediated SLE TMA rather than alternative pathway (aHUS shows low C3, normal C4, low factor H). Treatment focuses on immunosuppression for SLE (glucocorticoids, plasma exchange, Rituximab). Eculizumab is reserved for cases where complement-mediated aHUS is confirmed.

Reference: KDIGO 2024 – LN; Sciascia et al 2017 – SLE TMA