Edema with Normal or Low ECF Volume
In certain settings such as hypoalbuminemia due to liver disease or in the nephrotic syndrome (see Chapter 24 Clinical Note), abundant evidence may point to generalized edema without venous distension. To explain this apparent contradiction, it is important to remember that the ECF encompasses both the interstitial fluid and the blood plasma, and that the Starling forces across the capillary walls determine the distribution of fluid between these two compartments. When the plasma albumin concentration and thus the plasma colloid osmotic pressure is decreased by liver disease or renal losses, a shift can be seen in ECF from the vascular to the interstitial compartment. Edema reflects the increased interstitial fluid volume, whereas the vascular volume is diminished. The same shift of fluid out of the vascular compartment into the interstitial compartment also occurs in burn patients. In these patients, the permeability of the capillaries in the traumatized tissue is increased, causing loss of plasma proteins together with fluid to the interstitial space. In each of these settings, the loss of fluid from the vascular compartment causes extracellular volume receptors to respond as if total extracellular volume were decreased, resulting in the retention of Na+ and water and a further expansion of ECF volume in an attempt to restore plasma volume. However, as will be discussed in the next Clinical Note, salt and water retention are also driven by other mechanisms in disease states such as these and can persist even when both the plasma and interstitial fluid compartments are expanded.
and the distal segments of the nephron. Figure 1 shows schematically the major locations of Na+ reabsorption and the relation to amounts filtered and excreted on a daily basis. In this example, the glomerular filtration rate (GFR) is 180 L/day and the plasma Na+ concentration is 139 mmol/L. This gives a daily rate of Na+
filtration of (139x180) = 25,000 mmol/day. To maintain Na+ balance, the kidney must excrete only as much Na+ as ingested, or 150 to 250 mmol/day. Thus the amount of Na+ excreted is ranges at most from 0.01-5% of the filtered load, meaning that 95-99.99% is reabsorbed. With normal dietary intake of Na+, the reabsorption
of Na+ must be finely regulated in the range of 99-99.99%. The processes involved in this delicate balancing process are considered in the subsequent sections of this chapter.
The Na+ concentration in the urine reveals little about the rate of Na+ excretion. As for any solute, the rate of excretion is equal to the product of the urine flow rate and the solute concentration, UF • UNa. Consequently, the Na+ concentration in the urine will depend on the urine osmolality and can vary from 5-200 mmol/L, depending on the rate of Na+ excretion relative to water excretion.
When considered on a day-to-day basis, the renal Na+ excretory system responds relatively slowly to changes in Na+ input in the diet. This is illustrated in Fig. 2, which shows the responses of urinary Na+ output and body weight to changes in the dietary intake of Na+. The human subject for whom the data are given in Fig. 2 has been ingesting an extremely low Na+ diet of about 15 mmol/day. If that rate of Na+ intake is abruptly increased 10-fold to 150 mmol/day, Na+ excretion also begins to rise, but not as rapidly as the sudden increase in Na+ intake. Because Na+ excretion does not rise as rapidly as Na+ intake, a transient period of positive sodium balance results. In other words, the total amount of Na+ in the body increases until a new steady state is established in which Na+ output is equal to Na+ input. As a consequence of the positive Na+ balance, this subject experienced an increase in ECF
Total Body Weight
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