We thank Dr. Kopterides and colleagues for their comments on our study of edema fluid-to-plasma protein ratios in patients with postobstructive pulmonary edema. The authors question whether the use of medications known to increase the rate of alveolar fluid clearance (β-agonists and corticosteroids)1–2 has led to misclassification of the etiology of postobstructive pulmonary edema in our study.3We agree that alveolar epithelial fluid transport can increase the edema fluid-to-plasma protein ratio through the more rapid clearance of fluid and solute compared to protein.4 Misclassification would be most likely to occur if substantial time had elapsed between the onset of acute pulmonary edema and sampling of the edema fluid and plasma. In our study, the median time to fluid collection was very short, 1.5 h (interquartile range, 0.5 to 5 h).3 Furthermore, rapid alveolar fluid clearance could only lead to misclassification of patients with underlying hydrostatic pulmonary edema, who might be misclassified as having increased permeability edema because of an elevated edema fluid-to-plasma protein ratio; patients with increased permeability pulmonary edema would not be misclassified. In our study, 7 of 10 patients had edema fluid-to-plasma protein ratios in the hydrostatic range (< 0.65). Two patients had levels that were slightly above this cutoff point at 0.66 and 0.69, still suggesting a predominant hydrostatic mechanism. One patient had an initial ratio of 0.80, suggesting either a nonhydrostatic mechanism or the possibility that sampling of the edema fluid took place after alveolar epithelial fluid transport had begun. Thus, among the 10 patients studied, only 1 patient had the potential to be misclassified. Furthermore, only a minority of patients received β-agonists or corticosteroids during the study period: one patient received albuterol, two patients received epinephrine, and four patients received corticosteroids. In summary, the available evidence including the low edema fluid-to-plasma protein ratio in the majority of the patients despite intact alveolar fluid clearance strongly supports a hydrostatic mechanism of edema fluid formation in postobstructive pulmonary edema.