Loss of salt

Introduction Loss of salt refers to a disease in which the body loses too much salt for various reasons. Loss of salt can cause salt-loss nephritis and pseudo-aldosterone reduction. Loss of salt nephritis, also known as Thorn syndrome, is currently considered to be a special type of kidney disease characterized by severe renal salt loss. The clinical manifestations are hyponatremia, which can lead to circulatory failure, rapid pulse rate, Blood pressure drop or orthostatic hypotension, fainting, peripheral vein collapse, etc., patients often accompanied by water loss, poor skin elasticity, eyeball depression, muscle weakness, loss of appetite, nausea and vomiting, weight loss and severe tendon. If the sodium salt is not replenished in time, the patient may die from uremia due to loss of water, loss of salt, and a sharp drop in glomerular filtration rate. The blood sodium and blood chlorine are reduced, but the blood potassium is slightly higher, the blood urea nitrogen can also be increased to varying degrees, and often there are metabolic acidosis, continuous increase of urinary sodium, increased urinary aldosterone output, etc. Go to the hospital for treatment and treatment. Pseudohypoaldosteronism, also known as Cheek-Perry syndrome, is a rare salt-loss syndrome. The age of onset is mostly in the neonatal period. Symptoms of repeated vomiting, diarrhea, thirst or loss of thirst, growth and development are the main symptoms (even idiots), and some cases are limited to salt or aldosterone antagonists. The symptoms are revealed and relieved with age. Clinically, the cause of this disease is the deficiency of aldosterone receptors in the target organs (tubules, salivary glands, sweat glands, and colons) of patients, or the combination of aldosterone and its receptors with reduced or no binding at all; molecular biology and molecular biochemistry Further studies have found that the etiology of pseudoaldosteronism is based on genetically determined sodium channel dysfunction on the cell membrane. The target organs in different patient receptors are not necessarily the same, and the degree of salt loss in clinical manifestations is also different. Since most patients can trace the family history of salt loss, it is reported that the disease is a hereditary disease, and its genetic pattern can be expressed as autosomal dominant inheritance or autosomal recessive inheritance.

Cause

(1) Causes of the disease

The disease is a clinically rare syndrome of chronic kidney disease. Common causes are:

1. Chronic interstitial nephritis, chronic pyelonephritis.

2. Renal medullary cystic lesions, such as polycystic kidney disease.

3. Kidney tuberculosis, renal calcification.

4. bilateral renal hypoplasia.

5. Obstructive nephropathy.

(two) pathogenesis

Renal tubular epithelial cell damage caused by renal interstitial disease makes it less responsive to aldosterone, renal tubular reabsorption of sodium chloride is reduced, and a large amount of sodium chloride is excreted from the urine, resulting in hyponatremia. Its particularity is that the reabsorption of sodium chloride by renal tubular loss is far more serious than that of glomerular function. In severe cases, a large number of nephrons may be damaged, and the survivors are subject to excessive loading of solute in the plasma, causing osmotic diuretic effects, i.e., excessive loss of salt and moisture.

an examination

Related inspection

Blood analyzer to check urine routine

1. Typical clinical manifestations: polyuria and nocturia, skin pigmentation is bronze, acute exacerbation is often weak, loss of appetite, nausea and vomiting, weight loss, weak pulse, low blood pressure, prone to orthostatic hypotension , collapse and fainting. Dehydration, tendon, severe mental confusion, paralysis, coma and uremia acidosis.

2. Laboratory tests have blood sodium, blood chlorine decreased, blood potassium increased (occasionally reduced), azotemia and metabolic acidosis changes.

3. In the case of ingestion of 10 g/d of salt, the normal sodium balance could not be maintained.

4. Deoxycorticosterone treatment is ineffective.

5. Adrenal cortical function is normal and urinary aldosterone content is increased.

A diagnosis can be made based on the above.

Differential diagnosis

The main diseases that should be identified are:

1. Pseudo aldosterone reduction or congenital renal salt loss syndrome

(1) is a hereditary disease.

(2) In neonates, there are many lesions in the renal interstitial, which generally resolves with age.

2. Chronic adrenal insufficiency patients with uneven skin pigmentation, wrinkles, scars, compression sites are more common, mucosal pigmentation is deeper. The following points can be identified:

(1) 17 ketosteroids, 17-hydroxycortisol excretion decreased.

(2) Corticosteroid treatment is effective.

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