Nephritic edema results from the primary retention of salt. Acute glomerulonephritis is the prototypical form of the disorder. The stimulus for the salt retention arises within the kidney by an unknown mechanism. As effective arterial blood volume (EABV) was normal at the start of the disease process, it becomes expanded as salt and water are added to it. The pathophysiological sequelae of this process are compared with those which follow the salt retention of congestive heart failure (CHF). The latter is a syndrome in which salt retention is secondary, driven by the contraction of EABV which is at the heart of CHF. Finally, mechanisms responsible for the salt retention of nephrosis are considered. It is possible, and even likely, that most patients with nephrotic edema have primary salt retention, rather than secondary edema. If this view is correct, salt is retained not because of urinary protein loss and its consequent hypoalbuminemia, but rather because of the glomerulopathy which caused the syndrome in the first place.