In several conditions, extracellular fluid volume becomes markedly increased but blood volume remains normal or even slightly reduced. These conditions are usually initiated by leakage of fluid and protein into the interstitium, which tends to decrease the blood volume. The kidneys’ response to these conditions is similar to the response after hemorrhage—that is, the kidneys retain salt and water in an attempt to restore blood volume toward normal. Much of the extra fluid, however, leaks into the interstitium, causing further edema.

NEPHROTIC SYNDROME—LOSS OF PLASMA PROTEINS IN URINE AND SODIUM RETENTION BY THE KIDNEYS

The general mechanisms that lead to extracellular edema are reviewed in Chapter 25. One of the most important clinical causes of edema is the so-called nephrotic syn drome. In nephrotic syndrome, the glomerular capillaries leak large amounts of protein into the filtrate and the urine because of increased glomerular capillary permeability. Thirty to 50 grams of plasma protein may be lost in the urine each day, sometimes causing the plasma protein concentration to fall to less than one-third normal. As a consequence of the decreased plasma protein concentration, the plasma colloid osmotic pressure falls to low levels. This action causes the capillaries all over the body to filter large amounts of fluid into the various tissues, which in turn causes edema and decreases the plasma volume.

Renal sodium retention in nephrotic syndrome occurs through multiple mechanisms activated by leakage of protein and fluid from the plasma into the interstitial fluid, including stimulation of various sodium-retaining systems such as the renin-angiotensin system, aldosterone, and the sympathetic nervous system. The kidneys continue to retain sodium and water until plasma volume is restored nearly to normal. However, because of the large amount of sodium and water retention, the plasma protein concentration becomes further diluted, causing still more fluid to leak into the tissues of the body. The net result is massive fluid retention by the kidneys until tremendous extracellular edema occurs unless treatment is instituted to restore the plasma proteins.

LIVER CIRRHOSIS—DECREASED SYNTHESIS OF PLASMA PROTEINS BY THE LIVER AND SODIUM RETENTION BY THE KIDNEYS

A similar sequence of events occurs in cirrhosis of the liver as in nephrotic syndrome, except that in liver cirrhosis, the reduction in plasma protein concentration results from destruction of liver cells, thus reducing the ability of the liver to synthesize enough plasma proteins. Cirrhosis is also associated with large amounts of fibrous tissue in the liver structure, which greatly impedes the f low of portal blood through the liver. This impedance in turn raises capillary pressure throughout the portal vascular bed, which also contributes to the leakage of fluid and proteins into the peritoneal cavity, a condition called ascites.

Once fluid and protein are lost from the circulation, the renal responses are similar to those observed in other conditions associated with decreased plasma volume. That is, the kidneys continue to retain salt and water until plasma volume and arterial pressure are restored to normal. In some cases, plasma volume may actually increase above normal because of increased vascular capacity in cirrhosis; the high pressures in the portal circulation can greatly distend veins and therefore increase vascular capacity.

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مواضيع ذات صلة

kidney Diseases

Diuretics and Their Mechanisms of Action

Conditions That Cause Large Increases in Blood Volume and Extracellular Fluid Volume

Integrated Responses to Changes in Sodium Intake

Role of Atrial Natriuretic Peptide in Controlling Renal Excretion

Role of Aldosterone in Controlling Renal Excretion

Role of Ang II in Controlling Renal Excretion

Sympathetic Nervous System Control of Renal Excretion: Arterial Baroreceptor and Low-Pressure Stretch Receptor Reflexes

Importance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid Balance

Integration of Renal Mechanisms for Control of Extracellular Fluid

Osmoreceptor-ADH Feedback System

Urine Specific Gravity