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APSN Thrombotic Not Immune Complex Lupus — ESENeph MCQ

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HardGlomerulonephritisAPSN Thrombotic Not Immune Complex LupusESENeph

A 40-year-old woman with SLE develops AKI and is found to have renal biopsy findings of intraluminal fibrin thrombi in glomerular capillaries, arteriolar thrombosis, and endothelial swelling without significant proliferative lupus nephritis. Complement C3 and C4 are normal. ADAMTS13 is normal. Antiphospholipid antibodies (lupus anticoagulant, anti-cardiolipin, anti-beta-2-glycoprotein I) are all strongly positive. What is the diagnosis?

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Correct answer: A — Antiphospholipid syndrome nephropathy (APSN)

Antiphospholipid syndrome nephropathy (APSN) is characterised by thrombotic microangiopathy affecting renal arterioles and glomerular capillaries, caused by antiphospholipid antibodies promoting endothelial activation and thrombosis. Unlike lupus nephritis (which is immune complex-mediated with proliferative/membranous changes and complement consumption), APSN shows predominantly THROMBOTIC injury: fibrin thrombi, fibrous intimal hyperplasia, and focal cortical atrophy from ischaemia. Complement and ADAMTS13 are normal (distinguishing from aHUS and TTP). The strongly positive triple-antiphospholipid profile confirms high-risk APS. Treatment is anticoagulation (therapeutic heparin then warfarin/LMWH long-term) rather than immunosuppression. Hydroxychloroquine has additional antithrombotic benefit.

Reference: Tektonidou et al 2014 – APSN Classification; KDIGO 2024 – LN; EULAR 2019 – APS