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Antiphospholipid Syndrome and Renal Allograft Thrombosis

Morales, Jose Maria, PhD, MD1; Serrano, Manuel, MD1; Martinez-Flores, Jose Angel, PhD1; Perez, Dolores1; Serrano, Antonio, MD, PhD1

doi: 10.1097/TP.0000000000002510

Renal allograft thrombosis is the most frequent and devastating complication in the early postrenal transplantation period. Several risk factors to develop graft thrombosis depending on donors and recipients are well known. Antiphospholipid syndrome (APS) is well recognized as an important cause of kidney injury, with specific clinical and histological features that may lead to renal injury caused by thrombosis at any location within the renal vasculature. There are 3 forms of APS, primary (the most common form), associated to other systemic autoimmune diseases (SAD-APS), and catastrophic. Nevertheless, patients with SAD-APS and renal failure only represent 2% to 5% in hemodialysis or transplantation. The presence of pretransplant antiphospholipid antibodies increases risk of graft thrombosis. A new form of APS based on IgA anti–β-2-glycoprotein-I (B2GPI) antibodies, representing up to 30% of patients in end-stage renal disease and renal transplantation, is the main independent risk factor for graft thrombosis and early graft loss after renal transplantation. In addition, B2GP1 bound to IgA aB2GP1 immunocomplexes have been described as a marker to predict thrombosis after renal transplantation in patients with antiphospholipid antibodies. Anticoagulation remains the main treatment to prevent renal allograft thrombosis, although new preventive strategies are coming. Future studies may help to identify better therapeutic targets.

1Immunology Department, Healthcare Research Institute, Hospital 12 de Octubre, Madrid, Spain.

Received 2 March 2018. Revision received 15 September 2018.

Accepted 19 October 2018.

This work was supported by grant PI17-00147 from Spanish “Fondo de Investigaciones Sanitarias” (Institute of Health Carlos III, cofunded with European Regional Development Funds).

J.M.M. and M.S. collaborated equally to this work.

The authors declare no conflict of interest.

J.M.M., M.S., and A.S. designed the structure of the review, discussed the relevant literature and wrote the article. J.A.M.F. and D.P. worked in the pathophysiology of renal allograft thrombosis. Finally, all authors discussed the complete article and all agree with the final text.

Correspondence: Jose M Morales, PhD, MD, Healthcare Research Institute, Hospital 12 de Octubre, 28041 Madrid, Spain. (

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