[Skip to Content]
[Skip to Content Landing]
October 25, 1985


JAMA. 1985;254(16):2273-2276. doi:10.1001/jama.1985.03360160105023

Advances in our understanding of nephrologic matters have been occurring at an increasing pace and along several fronts. Regulation of body sodium and fluid economy have always been of particular interest to nephrologists. For many years it has been clear that changes in glomerular filtration rate and aldosterone secretion and/or action cannot entirely account for changes in the way renal sodium is handled in health and disease. Among the additional factors postulated is a natriuretic hormone, but the identity and source of this hormone(s) have proven remarkably elusive. Recent studies, however, have settled on two excellent candidates.1 One of these is called endoxin, which behaves in a fashion resembling an endogenous digoxin.2,3 This substance has a molecular weight of less than 500 daltons, is not a peptide, and antigenically cross-reacts with antibodies to the digoxin molecule.4 The organ or tissue source of endoxin remains unknown, as does