Colour duplex US with calculation of the RI and delta RI of intrarenal arteries is a valuable non-invasive test assessing the haemodynamic effects of a RAS. Low costs and safety support the use of the Doppler technique in screening for renovascular disease.

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Inflammatory systemic disorders with renal tissue damage require the adherence of polymorphonuclear leukocytes to the endothelium, which is mediated by cell surface adhesion molecules. This study measured the serum concentrations of circulating adhesion molecules [intercellular adhesion molecule 1 (cICAM-1), vascular cell adhesion molecule 1 (cVCAM-1), cE-selectin] by sandwich enzyme-linked immunosorbent assay in Wegener's granulomatosis (n = 25) and systemic lupus erythematosus (n = 50). Active Wegener's granulomatosis with cellular crescent formation was associated with significantly raised cICAM-1 levels, an elevated histological activity index, and a high rate of hemodialysis in comparison to Wegener's granulomatosis with fibrocellular crescents or lupus nephritis. The activity index and cICAM-1 levels can be used as parameters to predict renal outcome in Wegener's granulomatosis. cVCAM-1 levels in Wegener's granulomatosis were significantly higher in patients with hemodialysis compared to those without hemodialysis. In lupus nephritis only cVCAM-1, not cICAM-1 or cE-selectin, were significantly higher (P < 0.01) than controls. cVCAM-1 levels in both diseases were significantly higher than in controls. Only in Wegener's granulomatosis did cICAM-1 and cVCAM-1 levels decrease with clinical remission; in systemic lupus erythematosus the levels remained unchanged. cE-selectin levels were not significantly elevated in systemic vasculitis or collagen disease although individual patients revealed high serum concentrations. These data suggest that levels of circulating adhesion molecules reflect different pathophysiological processes in systemic vasculitis and collagen disease and may be used as markers of disease activity and renal outcome.

The present study provides evidence that interferons are important regulators of beta2M expression. It also shows that proinflammatory monocytic cytokines do not modulate directly the expression of beta2M in cells of hepatic, monocytic and T-lymphocytic origin. Whether they influence beta2M synthesis and secretion indirectly by modulating interferon synthesis needs to be elucidated.