Re-examination of salt and water retention in congestive heart failure: significance of renal filtration fraction.

S INCE the work of Starr [7] who concluded that the increase in venous pressure observed in congestive heart failure is due to an increased plasma volume, the “forward” theory of heart failure has been the subject of much research attempting to describe the precise mechanisms by which the extracellular volume is expanded during cardiac decompensation. Warren and Stead [Z] emphasized the diminished renal excretion of sodium and water as the cause of fluid retention in patients in whom edema forms. The cause of this renal salt and water retention was investigated by Merrill [3], who found that in patients in severe cardiac failure, filtration rates were reduced to onethird or one-half of normal, and renal blood flow was reduced to an even greater degree. Similar decreases in glomerular filtration rate had been observed by Seymour et al. [4], and Merrill theorized that renal ischemia leads to a decreased glomerular filtrate which is almost completely reabsorbed by normally functioning transport systems. Decreases in glomerular filtration rate (GFR) and renal blood flow (RBF) have been confirmed by numerous investigators [5-g]. However, much evidence has been reported which does not substantiate this theory: (1) Cases of cardiac failure in man have been reported in which GFR is within normal limits [79-E?]. (2) Diuresis (spontaneous or induced by bedrest or therapeutics other than diuretics) occurring in cardiac compensation is often not accompanied by an increase in glomerular filtration rate [4,70,72,73]. (3) Renal retention of salt in experimental heart failure in the dog takes place before any decrease in filtration rate is observed and may continue for long periods of time without any reduction in filtration rate [74-761. These experiments demonstrated that the decreased renal sodium and water excretion in heart failure showed no constant relationship to filtered load. Moreover, since the clinical symptoms of heart failure (edema, venous distention, basilar pulmonary rales, etc.) are quite gross, the work on experimental animals indicates that the earliest stages of salt retention in most patients may occur before any decrease in filtration rate. It seemed evident, therefore, that the primary cause of salt retention was an increased tubular reabsorption of electrolytes and water. It has been shown that in patients with congestive heart failure and edema, the production as well as excretion of aldosterone are much greater than normal [77-201. On the basis of these observations it is concluded that