Kidney swelling on the legs

Edema of the kidney origin in mostcases are very characteristic and easily distinguishable from edema of another origin, in particular cardiac. They first of all arise not on the legs, but in places where the most loose fiber is, on the eyelids, on the face. Renal edema can quickly arise and increase and also disappear quickly; in severe cases they are usually more evenly distributed along the trunk and extremities (such common swelling of the body is called anasarka). Not only the skin and subcutaneous tissue swell, but also internal organs. Usually, the liver swells and grows, but with kidney diseases, the increase in the liver is proportional to the increase in other organs and is never as significant as with cardiac edema. A larger or smaller amount of fluid accumulates in the serous cavities: the pleural, the abdominal, in the pericardium. You can determine the swelling by palpation. The presence of edema is also confirmed by the McClure-Aldrich blister test: after intradermal injection of 0.2 ml of isotonic sodium chloride solution into the inner forearm area of ​​the forearm, a blister forms, which quickly dissolves, the more pronounced "swelling readiness" of the tissue. In a healthy person, the resorption of the blister occurs within an hour.

With pronounced edematous syndrome, tracethe dynamics of edema in the course of treatment is helped by repeated, with an interval of several days, measuring the circumference of the extremities and abdomen at the same level, determining the height of the fluid level in the pleural and abdominal cavities, measuring the patient's body weight, and determining the daily diuresis and body water balance (the ratio of the amount drunk and the liquid isolated per day). The causes of edema in kidney disease are different.

1. In many renal diseases that occur with nephrotic syndrome, an increase in the permeability of the capillary wall plays an important role in the origin of edema. Of great importance in recent times is the increase in the hyaluronidase activity of blood serum, which, as a rule, is observed in many renal diseases. Hyaluronidase enhances the depolymerization of hyaluronic complexes of mucopolysaccharides, which form an intercellular substance (interendothelial "cement") and the basic basal membrane of the capillary wall, as a result of which the porosity of this wall increases. There is a significant reduction in calcium in the blood serum (since the intercellular substance includes its compounds with protein in the form of calcium proteinate), as well as the change in blood pH (acidosis). A generalized increase in the permeability of capillaries leads to the fact that not only water with substances dissolved in it begins to intensively pass through the bloodstream, but also a fairly large amount of protein. In addition, the depolymerization of mucopolysaccharides of the intercellular substance of tissues leads to an increase in the number of molecules in the intercellular fluid and an increase in its colloid-osmotic pressure.

Consequently, with nephrotic syndrome, notonly an increase in the permeability of the capillary wall is observed, which facilitates the passage of fluid into the tissues, but also creates conditions for its retention in the tissues, since the increased colloid-osmotic pressure of the intercellular fluid determines its hydrophilicity, the intercellular fluid absorbs and diffuses water more easily. A relatively high protein content in the edematous fluid accounts for the greater density and less edema displacement when capillary permeability is impaired compared to edema of hypoproteinemic origin.

Ointment fluid with increased capillarypermeability accumulates both in the subcutaneous tissue and in other tissues, especially those rich in blood vessels. In the serous cavities of fluid usually accumulates little. Edema of this type is observed not only in diseases of the kidneys, but also in some other diseases (for example, allergic, angioneurotic - Quincke edema origin), with bee stings, etc.

2. Colloid osmotic (hypoproteinemic) edema is observed with nephrotic syndrome and amyloidosis of the kidneys. They are caused by a decrease in the oncotic pressure of the blood plasma (depending on the degree of hypoproteinemia) due to the high proteinuria usually present in such patients, as well as the transition of the protein through the porous wall of the capillaries to the tissue. The formation of edemas mainly colloid-osmotic nature occurs according to the laws of hydrologic growth. These swelling occurs primarily on the feet of walking patients and on the waist in the recumbent. Usually hypoproteinemic edema occurs with a blood content of less than 3.5-4.0 g of protein and up to 1.0-1.5% of albumins. Of great importance is the change in the qualitative composition of plasma proteins. In nephritis, mostly fine proteins, albumins, are lost in the urine; The number of globulins decreases to a lesser extent. Osmotic pressure is determined by the number of molecules per unit volume of plasma, and not by their molecular mass. Therefore, the loss of finely dispersed albumins, the specific colloid-osmotic pressure of which is approximately 3 times higher than in coarsely dispersed globulins, significantly reduces the oncotic blood pressure. Hypoproteinemic edema occurs not only with nephrotic syndrome and amyloidosis of the kidneys. They can appear with prolonged starvation ("hunger edema"), malabsorption in the small intestine, cancer cachexia and some other diseases, accompanied by a decrease in the protein content in the plasma.

3. Sodium edema is caused by a delay in blood and tissues of sodium ions. Sodium ions have a high hydrophilicity, and with their excess in the body, edema develops (osmotic equilibrium is disturbed). So, when ingesting a large amount of sodium chloride (table salt), there may be swelling. Hypernatremia in kidney diseases is an additional factor that enhances the effect of increased capillary permeability and hypoproteinemia. In the mechanism of accumulation of sodium ions in a number of diseases, hormonal factors are of great importance, especially the excessive release into the blood of the hormone of the adrenal cortex-aldosterone and the posterior lobe of the pituitary-antidiuretic hormone.

Any edema, regardless of its cause, in that orto a different degree reflects the violation of osmoregulation of the organism, in which the hormonal link plays the main role: the aldosterone system is an antidiuretic hormone. The activity of this system is primarily aimed at maintaining the constancy of the volume and ionic composition of the blood. In the case of a slight decrease in the volume of blood (which, with kidney disease, can occur when a part of the fluid flows from the bloodstream into the tissue due to an increase in the porosity of the capillary wall or a decrease in the oncotic blood pressure), volumetric receptors, located mainly in the walls of the right atrium and common carotid arteries. In response to this irritation, protective mechanisms to maintain the intravascular volume are included. The production of aldosterone increases with the adrenal cortex, which leads to an increase in sodium reabsorption by the wall of the renal tubules, an increase in its concentration in the blood and accumulation in the tissues. Thus, the amount of aldosterone released per day with urine, with nephrotic edema increases from 2-10 to 25-200 μg or more; At the same time, the excretion of sodium in the urine decreases significantly. The increase in aldosterone production, which occurs again as a compensatory reaction, for example, with edema or sudden loss of water by the body, is called secondary hyperaldosteronism, in contrast to the primary adrenal cortex observed in tumors or hypertrophy. After the increase in the reabsorption of sodium by renal tubules, reabsorption of water increases. Increase in the concentration of sodium ions in the blood (due to increased reabsorption in the renal tubules) causes irritation of the osmoreceptors and increased pituitary gland antidiuretic hormone, which further increases the facultative reabsorption of water in the distal tubules. If the original cause of edema (increased porosity of capillaries, hyponionism of plasma) persists, fluid does not stay in the bloodstream and continues to pass into the tissues, increasing edema.

4. Edema can occur with acute cessation or a sharp decrease in the formation of urine by the kidneys (anuria), observed in patients with some acute poisoning (poisoning with fuels), and also in the terminal stage of some chronic kidney diseases (retention edema). The delay of sodium and water can occur, for example, in chronic glomerulonephritis due to a significant lesion of the glomeruli and a decrease in glomerular filtration, as well as in hypovolemic blood circulation in the kidneys (severe blood loss, shock). However, the decrease in glomerular filtration becomes important only if there are other prerequisites for the development of edema, and not as an independent factor. Thus, with severe renal failure with a sharp violation of filtration edemas are often absent or even disappear, if there were before.