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Published on: June 23, 2014
Anti-cardiolipin antibody and renal disease: a report three cases
V D'Agati1, C Kunis, G Williams
1Department of Pathology, College of Physicians and Surgeons of Columbia University, New York, NY 10032.
Insights
Anti-cardiolipin antibodies can cause recurrent thrombosis. This study documents thrombotic renal disease in three patients linked to these antibodies, highlighting a distinct kidney injury mechanism.
Area of Science:
- Nephrology
- Immunology
- Rheumatology
Background:
- Anti-cardiolipin antibodies are associated with recurrent arterial and venous thrombosis across multiple organs.
- Thrombotic events are a significant concern in patients with anti-cardiolipin syndrome and systemic lupus erythematosus (SLE).
Observation:
- A biopsy-documented case series of thrombotic renal disease attributed to anti-cardiolipin antibodies.
- Patients presented with primary anti-cardiolipin syndrome, mild SLE, or a lupus-like syndrome.
- Clinical courses were characterized by recurrent multi-organ system thrombosis.
Findings:
- Renal biopsy revealed thrombosis in glomerular capillaries, arterioles, and interlobular arteries.
- Thrombosis occurred independently of active endocapillary proliferative lupus nephritis.
- Renal manifestations varied, including proteinuria, renal insufficiency, and hypertension.
Implications:
- Circulating anti-cardiolipin antibodies can cause significant renal thrombotic disease.
- This suggests a pathogenic mechanism for renal thrombosis separate from immune deposit injury in lupus.
- Highlights the importance of considering anti-cardiolipin antibodies in unexplained thrombotic events affecting the kidneys.
Abstract:
Anti-cardiolipin antibodies have been linked to recurrent arterial and venous thrombosis in multiple organs. We present a biopsy-documented report of thrombotic renal disease apparently attributable to circulating anti-cardiolipin antibodies. One patient had primary anti-cardiolipin syndrome, one had mild SLE, and the third had a mild lupus-like syndrome. All three patients had a clinical course dominated by repeated multi-organ system thrombosis. Renal biopsy disclosed thrombosis at the level of the glomerular capillaries, arterioles, and interlobular arteries--similar to that described in other thrombotic microangiopathies. Renal thrombosis was not associated with active endocapillary proliferative lupus nephritis, suggesting a mechanism independent of subendothelial immune deposit injury. Renal presentation was variable, ranging from asymptomatic mild proteinuria to nephrotic-range proteinuria, renal insufficiency, and hypertension.
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