Objectives To review derangements of pathways of fibrin turnover that promote pathologic
fibrin deposition in the acute respiratory distress syndrome and to review the contribution of
the endothelium and parenchymal lung cells to the derangements. In addition, to review how
these pathways can be exploited in specific clinical circumstances, including sepsis and
acute lung injury. Lastly, to review newly recognized posttranscriptional and urokinase-
dependent pathways by which the fibrinolytic system is regulated in the lung.