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cases of retroperitoneal fibrosis are secondary to specific causes, namely: drugs, infection, retroperitoneal haemorrhage and malignancy, while the other two-thirds of cases are considered idiopathic, as no specific causes can be identified. The histological lesions of retroperitoneal fibrosis in patients with and without inflammatory aneurysm are not different and the suggested pathogenesis for the disease does not differentiate between the two forms. In fact, inflammation and autoimmunity have been advocated as the pathogenetic processes leading to idiopathic retroperitoneal fibrosis. Inflammation is well documented by the rise of inflammatory tests and by the presence of inflammatory cells sometimes associated with frank vasculitic lesions in the fibrotic tissue. The reported association of the disease with other autoimmune disorders suggests that idiopathic retroperitoneal fibrosis could be an immunemediated disorder with marked inflammatory vascular traits. Parums et al. [1] postulated that the disease may be due to an immune reaction to some components of atherosclerothic plaques, i.e. ceroids, which are a complex of proteins and oxidized LDL. This hypothesis has been partially confirmed by the finding of antibodies directed against ceroid in the sera of patients with retroperitoneal fibrosis. However, the same antibodies have also been detected in the sera of healthy elderly subjects and in patients with atherosclerosis [1]. In fact, no clear differences in the severity of atherosclerosis have been demonstrated between patients with chronic periaortitis and controls [2] and this theory would not explain retroperitoneal fibrosis occurring in children and young people, who have no atheromatous arterial disease. Another possible pathogenetic hypothesis for chronic periaortitis suggests that vasa vasorum vasculitis of the aortic adventitia could be the ‘primum movens’ of chronic periaortitis, as demonstrated for other inflammatory aorta disorders and its main branches such as Takayasu arteritis, Behcet’s disease and aortitis associated with spondyloarthropaties [3]. As hypothesized by Numano et al .[ 4], regarding the above-mentioned diseases, vasa vasorum vasculitis of the aortic adventitia may trigger the recruitment of inflammatory cells in the aortic adventitia and in the retroperitoneum. The inflammatory process may progress from the adventitia to the media and the intima with consequent infiltration of lipids, blood cells and other blood material causing intimal changes similar to typical atherosclerotic lesions or inflammatory aneurysms. Our recent demonstration, that patients with active retroperitoneal fibrosis had a significantly increased number of circulating endothelial cells of microvascular origin with an activated phenotype (as evidenced by the surface expression of E-selectin), in comparison to healthy subjects and patients with diffuse atherosclerosis, would indicate that endothelial injury, as a part of immune-mediated inflammatory vascular damage, may play a key role in the pathogenesis of chronic periaortitis [5] and may support the above-mentioned pathogenetic hypothesis. In conclusion, in our opinion, the retroperitoneal fibrosis observed in patients with and without inflammatory aneurysm could however be considered idiopathic.

Association of low-grade urinary albumin excretion with left ventricular hypertrophy in the general population: a reply