Salt-losing nephritis

Introduction to salt-losing nephritis Loss of salt nephritis is a renal tubular dysfunction caused by various causes. It was first reported by Thorn in 1944, so it is also called Thorn syndrome. It is a special type of certain kidney diseases characterized by severe renal salt loss, most commonly seen in chronic pyelonephritis, followed by renal medullary cystic disease, polycystic kidney disease and renal calcification. basic knowledge The proportion of the disease: the disease is rare, the incidence rate is about 0.0001% - 0.0002% Susceptible people: no special people Mode of infection: non-infectious Complications: uremia, edema, high blood pressure, heart failure

Cause of salt-losing nephritis

(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, making it less reactive to aldosterone, reducing renal tubular reabsorption of sodium chloride, and a large amount of sodium chloride is excreted from the urine, resulting in hyponatremia, The special feature is that the reabsorption of sodium chloride in renal tubular loss is far more serious than the glomerular dysfunction. When the condition is severe, a large number of nephron damage may occur, and the residual person must be subjected to excessive load of solute in plasma, resulting in osmotic diuresis. The effect is that excessive loss of salt and moisture occurs.

Loss of salt nephritis prevention

The prevention of this disease is mainly to actively treat various primary chronic kidney diseases that cause the disease, and to actively treat the affected patients, to control the progress of the disease, to delay and prevent the occurrence of complications.

Loss of salt glomerulonephritis Complications uremia edema hypertensive heart failure

Easy to have low blood pressure, uremia acidosis, severe mental disorders such as mental disorders, late patients lose salt tolerance, salt loss can be reduced, can be complicated by complications such as edema, hypertension and heart failure.

Salt-loss nephritis symptoms Common symptoms Nitrogenemia Loss of salt Skin pigmentation is bronze nausea, weakness, loss of appetite, hypotension, coma, polyurina

The prominent clinical manifestation of this disease is hyponatremia, which can lead to circulatory failure, rapid pulse rate, decreased blood pressure or orthostatic hypotension, fainting, peripheral vein collapse, etc. Patients are often accompanied by dehydration, poor skin elasticity, and depressed eyeballs. 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.

The clinical features of this syndrome are:

1. Mostly adult males, especially young people.

2. There are symptoms similar to Addison disease, 50% of patients have polyuria and nocturia, skin pigmentation is bronze, evenly distributed, but buccal mucosal pigmentation is less common, which is different from Addison disease, acute attack Frequently obvious weakness, loss of appetite, nausea and vomiting, physical examination found weight loss, weak pulse, low blood pressure, prone to orthostatic hypotension, collapse and syncope, dehydration and tendon, severe mental confusion, paralysis, coma and uremia Symptoms and acidosis.

3. Have a history of chronic kidney disease.

4. Ingestion of large amounts of salt (10 ~ 20g / d) can alleviate symptoms, 30% of patients have gastritis and a long history of taking a lot of basic drugs.

5. Deoxycorticosterone treatment was ineffective, adrenal cortical function test was normal, and urinary aldosterone was increased.

Examination of salt-loss nephritis

1. Blood examination of blood sodium, blood chlorine is reduced, blood potassium is increased (occasionally reduced), creatinine urea nitrogen can increase azotemia and metabolic acidosis, blood bicarbonate and pH value are reduced.

2. Urine examination increased urine sodium, urine specific gravity, albuminuria, urinary aldosterone increased significantly, often more than primary aldosteronism.

3. Other 17 ketosteroids, 17-hydroxycortisol and other excretions are normal or slightly increased, and do not respond to deoxycorticosterone treatment (DOCA).

4. Regular B-ultrasound, X-ray film or CT examination.

5. Pathological examination of renal biopsy can confirm the diagnosis of primary disease.

Diagnosis and identification of salt-losing nephritis

Diagnostic criteria

1. There are typical clinical manifestations of 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, Deficiency and syncope, dehydration, tendon, severe mental confusion, paralysis, coma and uremia acidosis.

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

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

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

The patient's skin pigmentation is uneven, with wrinkles, scars, more common compression sites, and deeper mucosal pigmentation. The following points can be identified:

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

(2) Corticosteroid treatment is effective.

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