Beach R E, Walden C, Boudreaux J P, DuBose T D
Department of Internal Medicine, University of Texas Medical Branch, Galveston 77550.
Am J Med Sci. 1989 Jun;297(6):339-42. doi: 10.1097/00000441-198906000-00001.
Recent studies have supported the possibility that mechanisms other than alterations in transcapillary oncotic pressure may contribute to edema formation in nephrotic syndrome. In a patient with a discrete, partial obstruction to lymphatic flow in the left upper extremity, the authors determined the transcapillary oncotic pressure differential in the obstructed, more edematous extremity and the contralateral, unobstructed extremity. The results demonstrate a normal transcapillary oncotic pressure gradient in the unobstructed extremity, while in contrast, the gradient in the obstructed extremity was reduced. Clinically, the edema resolved completely in conjunction with resolution of the nephrotic syndrome. The authors conclude, therefore, that the obstructed extremity may be more susceptible to edema formation because of inability to increase lymphatic flow during periods of hypoalbuminemia to levels sufficient to reduce the interstitial oncotic pressure gradient. Furthermore, the normal gradient in the unobstructed extremity supports the view that other mechanisms, such as intrinsic alterations in renal sodium reabsorption, may be involved in edema formation because edema was present without demonstrable alterations in the transcapillary oncotic pressure differential and plasma volume was increased in this patient.
