It has been known for many years that the kidneys play a major role in the pathogenesis of congestive heart failure (CHF) and that most of the symptoms and signs that occur in this disease state result from renal sodium and water retention. 1 While the congestion of the circulation which characterizes CHF was initially thought to be merely a mechanical phenomenon, later workers realized that a more complex series of events is involved and that the kidneys play a key role in this process. Indeed, since failure of the heart to perform adequately its pumping action has potentially disastrous consequences for the whole organism, it is not surprising that a large number of compensatory hemodynamic and neurohumoral mechanisms are brought into play to minimize the impact of pump failure. The kidney is significantly involved in this compensatory process and acts to restore the adequacy of the circulation by retaining salt and water which expands the extracellular fluid volume (ECFV). Continued retention eventually leads to overcompensation and what is recognized clinically as edema. It is clear that regardless of the initial changes in cardiac or systemic hemodynamics which occur in CHF, expansion of the ECFV requires the participation of the kidney in reducing sodium excretion and that an inability to excrete ingested sodium is a fundamental component of this disease process. Studies have shown that the ability of the kidney to excrete sodium and water diminishes as the pumping function of the heart declines. While patients with mild heart failure may not be edematous, a reduced ability to excrete a sodium load can still be demonstrated. In advanced heart failure, marked renal sodium retention is present and only a small fraction of an infused or ingested salt load can be excreted. 2