Renal Plasma Flow and Sodium Reabsorption and Excretion in Congestive Heart Failure 1

Abstract

Warren and Stead's (1) contention that disturbed renal function secondary to a diminished cardiac output is responsible for the following series of events-salt and water retention, increased blood and extracellular fluid volume, rise in venous pressure, edema-seemed to offer a rational explanation for some of the clinically observed phenomena. We therefore initiated a series of studies on patients with chronic congestive heart failure, using the clearance techniques of Smith and associates (2), in order to evaluate the relationship between the decreased sodium excretion in heart failure (3, 4) and renal blood flow, to determine the nature of the disturbance in renal function and the relationship, if any, between the altered renal dynamics and sodium retention. We later attempted to define some of the variables involved in the tubular transfer system for sodium as it obtains in the normal and in the cardiac patient. Since our studies began, Merrill (5) reported that the renal plasma flow was reduced to as little as 20 per cent and the filtration rate to 33 per cent of normal in chronic congestive failure. We have been able to confirm his findings of a decreased sodium excretion rate due to a diminished load presented to the tubules for reabsorption, and not to enhanced tubular reabsorption as suggested by earlier workers (3). EXPERIMENTAL PROCEDUREPatients with advanced chronic congestive failure due predominantly to rheumatic heart disease were the subjects. All had variable amounts of edema at rest. Members of the resident house staff and patients without heart failure or renal disease served as controls.The subjects were brought to the laboratory in a postabsorptive state. Each patient was given 300 to 600 cc. of water about 30 to 60 minutes before the test period.' This study was aided by a grant from the Martha M. Hall Foundation and the Committee on Scientific Research of the American Medical Association.2 Martha M. Hall Foundation Fellow in Medicine.Five controls were maintained on a special cardiac saltpoor diet (about 1.3 grams of sodium chloride daily), for 4 to 5 days before the studies were made. Most of the patients with congestive heart failure were maintained on the same diet (strict metabolic control was not attempted) and, in addition, all were taking digitalis.

Some Effects of Variation in Sodium Intake and of Different Sodium Salts in Normal Subjects 1

“…In another paper (1) we have suggested that the increased glomerular filtration rate following sodium chloride administration is a nonspecific response secondary to the resulting increased vascular volume. One certainly is not justified in interpreting it as a specific adjustment of the kidney for the purpose of increasing sodium excretion as has been postulated recently (18). Our findings in normal subjects are similar to those of Briggs et al (19) who found no relation between glomerular filtration rates and sodium excretion in patients with congestive heart failure.…”

“…Glomerular filtration, tubular reabsorption and the excretion of sodium There has been considerable discussion in the current literature regarding the possible roles played by change in glomerular filtration rate and tubular reabsorption of sodium in the formation of edema (17)(18)(19). Because our studies involved very low and very high rates of sodium and chloride excretion resulting from the marked variations in sodium intake, observations were made to determine, if possible, how glomerular filtration and tubular reabsorption of sodium affected the excretion of sodium by normal subjects.…”

“…Mokotoff et al (18) have claimed that the tubular reabsorption of sodium is constant per unit of glomerular filtrate volume ("13.3 mM per 100 cc. of glomerular filtrate") and therefore varies directly with the glomerular filtration rate.…”

“…Thus as some 97% of the filtered sodium was always reabsorbed, the relatively large shift in urinary sodium must have occurred as a result of variations within this remaining 3% of the filtered sodium. In edematous cardiac and nephritic patients the glomerular filtration rate, though somewhat reduced (17)(18)(19), remains sufficiently large to still make the quantity of sodium excreted only a very small percentage of that filtered. Accordingly, the answer to the whole problem of the manner in which renal function is altered in certain cardiac and nephritic subjects making them unable to rid themselves of the usual daily sodium intake is hidden in the manner in which this very small fraction of the total filtered sodium is handled.…”

The Effect of Spinal Anesthesia on the Renal Ischemia in Congestive Heart Failure 1

“…We have calculated the renal fraction of the cardiac output to be reduced to about two-fifths of normal and have shown that there is marked efferent arteriolar constriction with increased intraglomerular filtration pressure in congestive heart failure (1). Although Merrill and co-workers (2) have demonstrated that renin is present in increased amounts in the renal venous blood of some patients with congestive failure, we wondered if renal vasoconstriction might also result from neurogenic stimulation when the cardiac output falls; in which case, hyperemia should be produced by blocking the reflex pathways.…”