Does obesity play a role in the pathogenesis of calcific uraemic arteriolopathy?

Calcific uremic arteriolopathy (CUA) [1] refers to calcification of the media of small terminal arteries and arterioles and associated fibrotic intimal thickening and lumen narrowing, thereby increasing the risk of ischaemic necrosis. As the term suggests, CUA is reported in patients with chronic kidney disease (CKD) ‘nearly exclusively’ [2]. Identical clinical and pathologic features have developed with hyperphosphataemia from other causes [3–7]. CUA develops silently [1,5,8], sometime presenting only with subcutaneous plaques and/or nodules. But with ischaemic complications it presents acutely with foci with discoloured skin progressing to necrosis and deep ulcers; hereafter designated complicated CUA. Once mistakenly likened to an allergic reaction by Selye (and therefore inappropriately termed ‘calciphylaxis’ [9]), complicated CUA is uncommon but is recognized increasingly in dialysis patients and renal transplant patients [3,8]. The lesions have appeared in ‘proximal’ body areas – abdominal wall, thighs, flanks, buttocks and breasts – and are generally more devastating than ‘distal’ ones localizing mainly in the lower legs [1,5,9–12]. Both may coexist [5].