Type II renal tubular acidosis

Introduction to type II renal tubular acidosis Intrinsic is the proximal renal tubular reabsorption of sodium carbonate function, resulting in decreased blood in the blood, showing high chloride acidosis. As the proximal tubule reabsorbs sodium carbonate, the amount of sodium carbonate reaching the distal renal tubule increases. If the absorption threshold is exceeded, the urinary sodium carbonate increases and the urine pH increases. If the blood sodium carbonate drops to a certain extent, the kidney When the tubule can completely absorb the sodium carbonate in the glomerular filtrate, the urine can be restored to acidity, and the urine pH can be lowered. In addition, proximal renal tubules can also reduce glucose, phosphate, uric acid, amino acid reabsorption, and manifest as Fanconi syndrome. If the primary DRTA can be diagnosed and treated early, the HCO-3 can be maintained at a normal level, the acidosis can be completely corrected, the clinical symptoms can disappear, the growth and development can reach the normal standard within 2 years, and the prognosis is good, such as kidney calcification at the time of diagnosis. More residual kidney dysfunction. basic knowledge Sickness ratio: 0.0001% Susceptible people: no specific population. Mode of infection: non-infectious Complications: renal failure

Causes of type II renal tubular acidosis

First, the primary: family or sporadic.

Second, other hereditary diseases: Wilson's disease, carbonic anhydrase deficiency, cystine disease and lowe syndrome (brain-eye-kidney syndrome).

Third, drugs and poisons: such as lead, cadmium, mercury, copper and other poisoning, long-term application of carbonic anhydrase inhibitors, expired tetracycline, injection of arginine, lysine and so on.

Fourth, other diseases: such as hyperparathyroidism, multiple myeloma, Sjogren's syndrome, autoimmune hepatitis, transplanted kidney rejection, excessive vitamin D and so on.

Type II renal tubular acidosis prevention

1. Prevention:

If the primary DRTA can be diagnosed and treated early, the HCO-3 can be maintained at a normal level, the acidosis can be completely corrected, and the clinical symptoms can disappear and the growth and development reach the normal standard within 2 years. The prognosis is good. If kidney calcification is present at the time of diagnosis, kidney dysfunction is left.

2. Other notes:

1) If renal calcification is present at the time of diagnosis, kidney dysfunction is left.

2) Typical patients may have increased glucose, amino acid, uric acid and phosphate excretion in the urine, and manifested as Fanconi syndrome.

Complications of type II renal tubular acidosis Complications, renal failure

Typical patients may have glucose, amino acid, uric acid and phosphate excretion in the urine, and the performance is Fanconi syndrome.

Type II renal tubular acidosis symptoms Common symptoms Weak appetite loss nausea and vomiting Dehydration Polyuria kidney area dull pain Kidney calcification constipation bone pain

First, there is high chlorine acidosis, urine PH value can be reduced to below 5.5, may have fatigue, anorexia, nausea, vomiting and other symptoms.

Second, the intrinsic acidosis, urine can be acidic, ammonium ion formation is not affected, can reduce the loss of sodium, potassium, calcium, although acidosis can cause bone decalcification, urinary calcium excretion, but cause bone damage and Patients with nephrolithiasis are rare; because of the increase in ions reaching the distal renal tubules, and the exchange of potassium increases, hypokalemia can still occur.

Third, typical patients may still have glucose, amino acid, uric acid and phosphate excretion in the urine, and the performance is Fanconi syndrome.

Examination of type II renal tubular acidosis

First, the urine PH value.

Second, X-ray examination found osteoporosis, pathological fractures or urinary tract stones.

Third, the diagnosis needs to be urine H2CO3-excretion rate determination (sodium carbonate load test) oral method: daily oral sodium bicarbonate 1-10mEq / kg, once every 3 days, until the plasma CO2 binding is normal, then determine the plasma And urine H2CO3- and creatinine (Cr).

Diagnosis and diagnosis of type II renal tubular acidosis

Identification of type I renal tubular acidosis and type II renal tubular acidosis

Type I renal tubular acidosis is a defect in distal renal tubular function that does not establish an effective pH gradient between renal tubular fluid and pericardial fluid. Hydrogen secretion and ammonia production are reduced, causing hydrogen ion retention in the body to cause acidosis. The family sex is more common in adult women, and the infant type rarely recurs after a short-term improvement.

Type II renal tubular acidosis is caused by decreased proximal renal tubular reabsorption of sodium carbonate, which causes a decrease in the blood, which is characterized by hyperchloric acidosis, and increased sodium carbonate reaching the distal renal tubule due to proximal tubule reabsorption of sodium carbonate. If the absorption threshold is exceeded, the sodium urate increases the urine pH; if the sodium carbonate in the blood drops to a certain extent, the renal tubule can completely absorb the sodium carbonate in the glomerular filtrate, then the urine can be restored to acidity. The urine pH can be lowered. In addition, the proximal renal tubules can also decrease in glucose phosphate, uric acid, and amino acid reabsorption, and manifest as Fanconi syndrome.

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