Mechanisms of edema in experimental nephrosis

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Abstract
In a study of nephrosis induced experimentally by antiserum or by the aminonucleoside of puromycin, it was demonstrated that edema in the former type was transitory, was not associated with endogenous hyperaldosteronism, and could be induced in adrenalectomized animals. The onset of sodium retention, leading to the edema, preceded marked proteinuria. It was associated with a profound reduction in inulin clearance, inability to excrete a sodium load, and an increase in plasma volume. The disappearance of edema was associated with recovery of ability to excrete a sodium load and with a return of inulin clearance almost to normal. It is concluded that the edema was primarily due to temporary renal impairment of Na excretion. In aminonucleoside nephrosis, edema was normally dependent on increased aldosterone production. High Na intake, however, led to edema in the absence of aldosterone, probably because of the presence of a relatively mild degree of impairment of Na excretion, which alone was insufficient to result in edema when Na intake was at a normal level.