Water and sodium retention in the body

Introduction Sodium sulphate retention is mainly a lesion of glomerular filtration rate, imbalance of fluid exchange between the body and the outside, resulting in imbalance of water and liquid metabolism. Under normal circumstances, the intake and discharge of sodium and water are in a dynamic equilibrium state, so the body fluid volume of the body can be maintained relatively constant, and the kidney plays an important role in regulating the dynamic balance of sodium water, so the basic cause of sodium water retention is caused. The reason is that this regulation of the kidneys is impeded, so that the kidneys discharge sodium and water and cause systemic edema.

Cause

The intake and discharge of sodium in normal people are in a state of dynamic equilibrium, so the amount of body fluid remains constant. Sodium water is discharged mainly through the kidneys, so the basic mechanism of sodium water retention is renal regulation dysfunction. Normal glomerular filtration of sodium, if the water is 100%, the final discharge only accounts for 0.5-1% of the total, 99-99.5% of which are reabsorbed by the renal tubules, and the proximal convoluted tubules actively absorb 60-70%. The small tube and the collecting tube are regulated by the hormone for reabsorption of sodium water, maintaining the above state as the balance of the tube, and the imbalance of the kidney is the imbalance of the tube.

1, glomerular filtration rate decreased

The glomerular filtration rate is mainly determined by the effective filtration pressure, the permeability of the filtration membrane and the filtration area, and any occurrence of the disorder can lead to a decrease in glomerular filtration rate. In the case of heart failure, cirrhosis, ascites and other effective circulating blood volume decline, on the one hand, arterial blood pressure drops, reflex excitatory sympathetic nerve; on the other hand, due to renal vasoconstriction, renal blood flow reduction, activation of renin-angiotensin - ketoketene system, further contraction into the small arterioles, so that glomerular capillary blood pressure decreased, effective filtration pressure drop; acute glomerulonephritis, due to inflammatory exudate and glomerular capillary endothelial swelling, kidney The permeability of the ball filtration membrane is reduced; in chronic glomerulonephritis, a large number of renal units are destroyed, and the glomerular filtration area is reduced. These factors all lead to a decrease in glomerular filtration rate and retention of sodium water.

2, near-curved tubules reabsorbed sodium water increased

It is currently believed that in the reduction of effective circulating blood volume, in addition to renal blood flow reduction, sympathetic excitation, renin-angiotensin-aldosterone activation, increased vascular tone II causes glomerular outcocci small artery contraction than the small artery contraction More obvious, glomerular capillary blood pressure increased, the result is a decrease in renal plasma flow, more significant than the decline in glomerular filtration rate, that is, the glomerular filtration rate is relatively increased, and the filtration fraction is increased. Thus, the blood flowing out of the glomerulus is increased in the small sphere, the hydrostatic pressure is decreased, and the colloid osmotic pressure is increased (the blood is thick), and the blood having the above characteristics is distributed in the proximal convoluted tube, so that the proximal curve The small tube reabsorbs sodium water.

3, far-curved tubules, collecting tubes reabsorbed sodium water increased

The ability of the distal convoluted tubule and collecting tube to reabsorb sodium water is regulated by ADH and aldosterone. The effective circulating blood volume caused by various reasons is reduced, and the blood volume is reduced, which is the main reason for the increase of ADH and aldosterone secretion. Aldosterone and ADH are inactivated in the liver, and when liver dysfunction, the inactivation of both hormones is reduced. The content of ADH and aldosterone in the blood increased, resulting in distal convoluted tubules, increased absorption of sodium in the collecting tube, and retention of sodium water.

an examination

Related inspection

Serum sodium (Na+, Na) glomerular filtration fraction (GFF), general examination of glomerular filtration score

Long-term water and sodium retention in the kidney causes hypertension

Sodium chloride excretion disorder is the core link in the pathological mechanism of hypertension. If the renal sodium retention tendency is not corrected, then blood pressure elevation is inevitable.

The normality of blood pressure depends mainly on the amount of blood discharged from the heart, the resistance of the surrounding blood vessels, and the blood volume. Normal kidneys play an important role in regulating blood volume in blood vessels. It is assumed that certain factors, such as intravenous infusion, cause an increase in blood volume, and an increase in blood perfusion pressure in the kidney leads to an increase in sodium excretion, an increase in urination, a decrease in the amount of blood vessels, and a stable blood pressure at a normal level. The kidneys of patients with hypertension have a tendency to retain water and sodium, and a higher perfusion pressure is required to produce the same effect of sodium and water, so blood pressure needs to be maintained at a high level.

The significance of this mechanism is to increase blood pressure as a means of compensation for the normal water-sodium balance in the body. If the renal sodium retention tendency is not corrected, then the increase in blood pressure is inevitable and necessary for the body. If the kidney in this condition is transplanted to a person with normal blood pressure, the recipient will also become a hypertensive patient. Therefore, the disorder of water and sodium excretion is the core link in the pathological mechanism of hypertension. In addition, if the kidney is in a state of high perfusion pressure for a long time, structural changes will occur, causing renal vascular degeneration, narrowing or even occlusion of the lumen, leading to renal parenchymal ischemia, glomerular fibrosis, and tubular atrophy until Renal Failure.

Differential diagnosis

The difference between water poisoning and sodium retention:

Extracellular fluid hypotonic water is too much, more than the body's extraordinary ability to compensate for the kidneys, resulting in excessive intracellular water (intracellular edema) and a series of symptoms called water poisoning. The sodium retention of water can be hypertonic, isotonic, and hypotonic. Because the ratio of water to sodium is random. Inconsistent. Although water poisoning is produced on the basis of hypotonic edema, it is significantly different from hypotonic edema. In acute attacks, there are often induced factors such as stress stimulation, renal excretion dysfunction and excessive water intake.

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