Abstract
Recent studies have focused on the potential role of fibrocytes in the pathogenesis of nephrogenic systemic fibrosis (NSF). Advances in our understanding of the cellular and molecular biology of fibrocytes, which are reviewed herein, now allow for the exploration of specific hypothesis regarding fibrocyte function in NSF. We hypothesize that when the half-life of gadolinium-based MRI contrast agents (GBCA) is prolonged during renal insufficiency, these agents persist in tissues and trigger the recruitment or differentiation of fibrocytes. Ongoing experiments suggest that GBCA may promote fibrocyte differentiation by interfering with the physiologic inhibitory action of serum amyloid P (SAP) on circulating fibrocyte precursors. Further exploration of fibrocyte function in NSF may clarify not only the pathogenesis of this disorder but contribute to the explication of other idiopathic fibrosing diseases and lead to new therapeutic approaches.
Keywords: Gadolinium, interstitial lung disease, magnetic resonance imaging, scleroderma, serum amyloid P
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