Renal regulation of fluid volume, sodium and potassium balance
Last reviewed: 23.04.2024
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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 fluids) and the maintenance of the homeostasis of sodium, potassium and other electrolytes. The present chapter is devoted to the role of kidneys in the regulation of the balance of the two most important electrolytes, sodium and potassium.
In the human body water is from 45 to 75% of body weight. It is distributed in two important water spaces - intracellular and extracellular, which are separated from each other by the 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 cartilaginous tissue, and is represented by a transcellular fluid (urine, water of the contents of the gastrointestinal tract, cerebrospinal fluid and so on). Transcellular fluid by volume is approximately half the total amount of extracellular fluid.
Sodium acts as the main cation of the extracellular fluid, chlorine and bicarbonates are the main anions. The main cation of intracellular fluid is potassium, the main anions are inorganic and organic phosphates and proteins.
Renal regulation of sodium balance and volume of fluid
Normally, the concentration of sodium in plasma and interstitial fluid is between 136 and 145 mmol / l. An increase in the concentration of sodium in the blood of more than 145 mmol / l is called hypernatremia, while the electrolyte concentration in the blood, close to 160 mmol / l, is considered an emergency situation. Reducing the concentration of sodium in the blood less than 135 mmol / l is called hyponatremia. Reducing the concentration of sodium below 115 mmol / l poses a threat to life. In the intracellular fluid, the sodium content is only 10% compared to the extracellular fluid, the concentration of chlorides and bicarbonates in it is low. The osmotic concentration of plasma, fluid interstitium and intracellular fluid do not differ.
The daily intake of table salt (sodium chloride) by a healthy person in Ukraine is about 160-170 mmol / day. Of this amount, 165 mmol is excreted in the urine and approximately 5 mmol with feces.
Sodium balance regulates the kidneys. The sodium transport in the nephron includes glomerular filtration and reabsorption of the electrolyte in the tubules. In the glomerulus, sodium is completely filtered. About 70% of the filtered sodium is reabsorbed in the proximal tubules. Further reabsorption of the electrolyte occurs in the descending thin segment, the ascending thin segment, the distal straight tubule of the Henle loop, which plays an important role in creating the osmotic gradient of renal interstitium. In the distal tubules and the cortical collecting tube there is a combined reabsorption of sodium and chlorides. Energy for this process is provided by Na +, K + -ATPase.
The regulation of the sodium balance is closely related to the regulation of liquid volumes. So, with a sharp increase in the intake of table salt in the body, excretion of it with urine increases, but the stable state is established only after 3-5 days. In the initial period there is a positive balance of sodium - the retention of electrolyte in the body. It is characterized simultaneously by an increase in the volume of extracellular fluid, its delay and 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 consumption of table salt sharply decreases, the opposite effect occurs. For about 3 days, sodium excretion decreases. During this short period of negative sodium balance, the total amount of water in the body decreases and, correspondingly, the body weight. Thus, under physiological conditions, in response to an increase in the volume of extracellular fluid, sodium nares develop, and when it decreases, sodium retention develops. In pathological conditions, the relationship between extracellular fluid volume and sodium kidney excretion is impaired, which is clinically manifested by the development of edema or a state of dehydration.
The mechanisms by which the kidneys regulate the constant content of sodium, and consequently, the water in the body, are complex and multifaceted. The excretion of sodium in urine is determined by the difference between the amount of sodium filtered in the glomerulus and the amount of its reabsorption.
Since the concentration of sodium in the blood, as a rule, is small, the regulation of renal sodium excretion is considered from the position of regulation of GFR and reabsorption of the electrolyte.
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 insufficiency), as a rule, do not disturb the balance of sodium in the body. Reduced GFR, as the determining factor of water-electrolyte disorders, is rarely detected: in acute nephritic syndrome, in the oliguric stage of acute renal failure, in the phase of swelling in nephrotic syndrome; also observed in acute circulatory disorders (acute heart failure, cardiogenic shock), after acute blood loss.
Tuberculosis reabsorption
This is the main factor in the regulation of sodium balance. The process is under the control of hormones, the most important of which is considered aldosterone, as well as the physical factors acting in the proximal tubule and the redistribution of the intrarenal blood flow.
Aldosterone
Among the factors controlling the balance of sodium, this hormone is of the greatest importance. It is characterized as the second factor controlling sodium excretion. The main physiological effects of aldosterone are the regulation of the volume of extracellular fluid and the homeostasis of potassium. The volume of extracellular fluid is regulated by aldosterone indirectly through the effect on sodium transport. The hormone exerts its influence mainly in the cortical collecting tubes and certain segments of the distal nephron, where, through complex intracellular transformations, aldosterone enhances sodium reabsorption and increases the secretion of potassium into the lumen of the renal tubule. Clinical observations confirm the important role of aldosterone in the regulation of sodium homeostasis. Thus, in patients with adrenal insufficiency, a significant sodium naresis is detected; in patients with a low volume of extracellular fluid, there is an active stimulation of aldosterone secretion, and in hypervolemia, the secretion of aldosterone, on the contrary, decreases.
"The third factor"
Other factors of regulation of the sodium balance are united under the general name "third factor". These factors include hormonal factors (atrial natriuretic hormone, catecholamines, kinins and prostaglandins), physical, acting through the wall of the renal tubules (hydrostatic pressure and oncotic pressure in the renal capillaries); and hemodynamic (strengthening of medullary renal blood flow, redistribution of intrarenal blood flow).
Atrial natriuretic peptide promotes the development of diuresis, increases the release of sodium, chlorine and potassium in the urine. The mechanism of natriuretic action of the hormone is complicated. A large role in the development of natriuresis is attributed to the increase in glomerular filtration and filtration fraction, the direct action of the hormone on the renal tubules with a decrease in sodium reabsorption, mainly in the region of cortical collection tubes; a certain role in the development of natriuresis is played by the blockade of the hormone production of aldosterone.
The role of catecholamines in the regulation of sodium excretion is associated with exposure to Starling forces in peripheral capillaries and changes in renal hemodynamics.
The natriuretic effect of kinins and prostaglandins is associated with their vasodilating properties, redistribution of the intrarenal blood flow and changes in the osmotic gradient in the renal brain substance. Do not rule out the direct action of kinins and prostaglandins on sodium transport in the distal sections of the nephron and the proximal tubules.
Among the physical factors affecting the excretion of sodium, Starling's forces, acting through the capillary wall in the proximal tubule area, play an important role. Reduction of the oncotic pressure in the near-capillary capillaries and / or an increase in the hydrostatic pressure in them is accompanied by a decrease in sodium reabsorption and increased sodium naresus, and vice versa: as the oncotic pressure in the capillaries increases, sodium reabsorption in the proximal nephron increases. Low oncotic pressure in the outgoing glomerular arteriol is detected with hypoproteinemia, including in HC, as well as in conditions with a high volume of extracellular fluid, which explains the decrease in proximal reabsorption of sodium. An increase in the oncotic pressure due to the perfusion of the near-capillary capillaries with a solution with a high albumin content leads to a normalization of sodium reabsorption.
Redistribution of renal blood flow
The role of this factor in the mechanisms of sodium excretion regulation remains to the end not established and requires specification. Most likely, it has an insignificant effect on the regulation of the water-salt balance.
Thus, the kidneys maintain water-sodium homeostasis through complex mechanisms. In this case, the leading role in them is played by the hormonal system of the kidneys and adrenal glands. These mechanisms provide high efficiency of maintaining the constancy of sodium in the body. Violations of the water-electrolyte balance of the body develop with a disruption in its regulation systems and can be associated with extrarenal causes and kidney damage.