Renal regulation of fluid volume, sodium and potassium balance

The most important function of the kidneys is to ensure the constancy of the body's water spaces (the volume of circulating blood, extracellular and intracellular fluid) and to maintain homeostasis of sodium, potassium and other electrolytes. This chapter is devoted to the role of the kidneys in regulating the balance of two important electrolytes - sodium and potassium.

In the human body, water makes up 45 to 75% of body weight. It is distributed in two major water spaces - intracellular and extracellular, which are separated from each other by a cell membrane. Intracellular fluid accounts for about 60% of the total amount of water in the body. Extracellular fluid is distributed in plasma, interstitium (interstitial fluid and lymph), bone and cartilage tissue, and is also represented by transcellular fluid (urine, gastrointestinal water, cerebrospinal fluid, etc.). Transcellular fluid by volume makes up about half of the total amount of extracellular fluid.

Sodium is the main cation of the extracellular fluid, chlorine and bicarbonates are the main anions. The main cation of the intracellular fluid is potassium, the main anions are inorganic and organic phosphates and proteins.

Renal regulation of sodium balance and fluid volume

Normally, the sodium concentration in plasma and interstitial fluid ranges from 136 to 145 mmol/L. An increase in the sodium concentration in the blood above 145 mmol/L is called hypernatremia, while the concentration of the electrolyte in the blood, close to 160 mmol/L, is considered an emergency. A decrease in the sodium concentration in the blood below 135 mmol/L is called hyponatremia. A decrease in the sodium concentration below 115 mmol/L is life-threatening. The sodium content in the intracellular fluid is only 10% compared to the extracellular fluid, the concentration of chlorides and bicarbonates in it is low. The osmotic concentration of plasma, interstitial fluid and intracellular fluid do not differ.

The daily consumption of table salt (sodium chloride) by a healthy person in Ukraine is approximately 160-170 mmol/day. Of this amount, 165 mmol is excreted in the urine and approximately 5 mmol in the feces.

Sodium balance is regulated by the kidneys. Sodium transport in the nephron includes glomerular filtration and electrolyte reabsorption in the tubules. Sodium is completely filtered in the glomerulus. About 70% of the filtered sodium is reabsorbed in the proximal tubules. Further electrolyte reabsorption occurs in the descending thin segment, ascending thin segment, distal straight tubule of the loop of Henle, which plays an important role in creating an osmotic gradient in the renal interstitium. Combined reabsorption of sodium and chlorides occurs in the distal tubules and cortical collecting duct. Energy for this process is provided by Na ⁺, K ⁺ -ATPase.

Regulation of sodium balance is closely related to regulation of fluid volumes. Thus, with a sharp increase in the intake of table salt in the body, its excretion with urine increases, but a stable state is established only after 3-5 days. In the initial period, there is a positive sodium balance - electrolyte retention in the body. It is characterized by an increase in the volume of extracellular fluid, its retention and an increase in body weight. Then, in response to an increase in the volume of extracellular fluid, sodium excretion increases and the sodium balance is restored. Accordingly, when the consumption of table salt decreases sharply, the opposite effect occurs. Sodium excretion decreases within approximately 3 days. During this short period of negative sodium balance, the total amount of water in the body and, accordingly, body weight decrease. Thus, under physiological conditions, natriuresis develops in response to an increase in the volume of extracellular fluid, and with a decrease in it - sodium retention. Under pathological conditions, the relationship between the volume of extracellular fluid and the excretion of sodium by the kidneys is disrupted, which is clinically manifested by the development of edema or a state of dehydration.

The mechanisms by which the kidneys regulate the constant sodium content, and therefore the water content, in the body are complex and multifaceted. Sodium excretion in urine is determined by the difference between the amount of sodium filtered in the glomeruli and the amount of its reabsorption.

Since the concentration of sodium in the blood is usually a value that changes little, the regulation of renal excretion of sodium is considered from the standpoint of the regulation of SCF and electrolyte reabsorption.

The glomerular filtration rate is usually defined as the first factor controlling sodium excretion. However, as follows from clinical observations and experimental data, even significant changes in the filtration function of the kidneys (up to the state of chronic renal failure), as a rule, do not disrupt the sodium balance in the body. Reduced GFR, as a determining factor in water-electrolyte disorders, is rarely detected: in acute nephritic syndrome, in the oliguric stage of acute renal failure, in the phase of increasing edema in nephrotic syndrome; it is also observed in acute circulatory disorders (acute heart failure, cardiogenic shock), after acute blood loss.

Tubular reabsorption

This is the main factor regulating sodium balance. The process is controlled by hormones, the most important of which is aldosterone, as well as physical factors acting in the area of the proximal tubule and redistribution of intrarenal blood flow.

Aldosterone

Among the factors regulating sodium balance, this hormone is of the greatest importance. It is characterized as the second factor controlling sodium excretion. The main physiological effects of aldosterone are regulation of extracellular fluid volume and potassium homeostasis. Extracellular fluid volume is regulated by aldosterone indirectly through its effect on sodium transport. The hormone exerts its effect primarily in the cortical collecting ducts and certain segments of the distal nephron, where, through complex intracellular transformations, aldosterone enhances sodium reabsorption and increases potassium secretion into the lumen of the renal tubule. Clinical observations confirm the important role of aldosterone in regulating sodium homeostasis. Thus, significant natriuresis is detected in patients with adrenal insufficiency; active stimulation of aldosterone secretion occurs in patients with low extracellular fluid volume, and, conversely, aldosterone secretion decreases with hypervolemia.

"The Third Factor"

Other factors regulating sodium balance are combined under the general name of "the third factor". They include hormonal factors (atrial natriuretic hormone, catecholamines, kinins and prostaglandins), physical factors acting through the wall of the renal tubules (hydrostatic pressure and oncotic pressure in the renal capillaries); and hemodynamic factors (increased medullary renal blood flow, redistribution of intrarenal blood flow).

Atrial natriuretic peptide promotes diuresis, increases excretion of sodium, chlorine and potassium in urine. The mechanism of natriuretic action of the hormone is complex. A major role in the development of natriuresis is attributed to an increase in glomerular filtration and filtration fraction, direct action of the hormone on the renal tubules with a decrease in sodium reabsorption mainly in the area of the cortical collecting tubes; a certain role in the development of natriuresis is played by the blockade of aldosterone production by the hormone.

The role of catecholamines in the regulation of sodium excretion is associated with the effect on Starling forces in peripheral capillaries and changes in renal hemodynamics.

The natriuretic effect of kinins and prostaglandins is associated with their vasodilatory properties, redistribution of intrarenal blood flow and changes in the osmotic gradient in the renal medulla. The direct effect of kinins and prostaglandins on sodium transport in the distal parts of the nephron and proximal tubules is also not excluded.

Among the physical factors influencing sodium excretion, an important role is given to the Starling forces acting through the capillary wall in the area of the proximal tubules. A decrease in the oncotic pressure in the peri-tubular capillaries and/or an increase in the hydrostatic pressure in them is accompanied by a decrease in sodium reabsorption and an increase in natriuresis, and vice versa: with an increase in the oncotic pressure in the capillaries, sodium reabsorption in the proximal nephron increases. Low oncotic pressure in the efferent glomerular arteriole is detected in hypoproteinemia, including NS, as well as in conditions with a high volume of extracellular fluid, which explains the decrease in proximal sodium reabsorption. An increase in oncotic pressure due to perfusion of the peri-tubular capillaries with a solution with a high albumin content leads to normalization of sodium reabsorption.

Redistribution of renal blood flow

The role of this factor in the mechanisms of sodium excretion regulation remains unclear and requires clarification. Most likely, it has an insignificant effect on the regulation of water-salt balance.

Thus, the kidneys maintain water-sodium homeostasis through complex mechanisms. The leading role in them is played by the hormonal system of the kidneys and adrenal glands. These mechanisms ensure high efficiency of maintaining the constancy of sodium in the body. Disturbances in the water-electrolyte balance of the body develop when there is a breakdown in its regulation systems and can be associated with extrarenal causes and kidney damage.

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