Alveolar edema results from an imbalance between fluid filtration into the alveolar space and its removal by reabsorption. Increased filtration is caused by increased pulmonary capillary pressure (high pressures can rupture the alveolar wall), and by increased endothelial and epithelial permeability e.g. subsequent to inflammation. Both processes allow fluid and, with massive ruptures of the alveolar wall, even blood cells to access the alveolar space. Fluid reabsorption from the alveolar space is driven by active, transepithelial Na-transport. Na-uptake from alveolar fluid is mediated mainly by epithelial Na-channels (ENaC) in the apical membrane; Na is extruded by basolateral Na/K-ATPase. Transport is activated by beta-adrenergics, glucocorticoids and other hormones and mediators but is inhibited by alveolar hypoxia, a direct consequence of alveolar edema. Lack of ENaC causes death early after birth due to impaired clearance of alveolar fluid. A (genetically determined) low activity of alveolar reabsorption might cause alveolar edema since reabsorption may not keep pace with filtration. Na-reabsorption might prove totally inefficient in the presence of large leaks of the alveolar barrier. In contrast, the clinical outcome of patients with alveolar edema is dramatically improved when the integrity of the alveolar wall and reabsorption are restored.