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AKT/mTORC pathway in antiphospholipid-related vasculopathy: a new player in the game

Since the early 1990s, it has become clear that the antiphospholipid syndrome (APS) is not only associated with vascular thrombosis but also with a severe intimal hyperplasia called ‘antiphospholipid arterial vasculopathy’. Such vasculopathy has been recognized as a major contributor to large artery occlusion rather than thrombosis or vasculitis. These lesions are described in many vascular territories, including the coronary, carotid or mesenteric arteries. However, their best morphological characterization was conducted in the kidneys, where these lesions have been called APS nephropathy (APSN). These lesions have been associated with a progressive decline of kidney function leading to end-stage renal failure. Interestingly, APSN recurs after kidney transplantation, sometimes quickly, and reduces the allograft survival rate. The molecular pathways that were involved in the development of such lesions were unknown, and therefore no specific treatment was offered to these patients.