What Is Renal Tubular Acidosis?

Renal tubular acidosis (RTA) is a clinical syndrome caused by various causes of renal acidification dysfunction, which is mainly manifested by hyperchloric metabolic acidosis with normal plasma anion gap, and at the same time glomeruli The filtration rate is relatively normal. In the past, when glomerular filtration was impaired, acid radicals such as H ₂ PO ₄ -and SO ₄ [sup] 2 [/ sup]-were retained in the body, replacing HCO ₃ -and causing metabolic acidosis. In fact, the essence of acidosis caused by renal causes is renal tubular hydrogen dysfunction or renal tubular bicarbonate reabsorption.

Basic Information

nickname

Renal tubular acidosis

English name

renaltubularacidosis; RTA

Visiting department

Nephrology

Common causes

Impairment of renal tubular hydrogen secretion or renal bicarbonate reabsorption

Common symptoms

Growth retardation, polyuria, metabolic acidosis

Causes of renal tubular acidosis

1. Type I (distal) renal tubular acidosis

(1) The primary renal tubular function often has congenital defects and can be sporadic, but most of them are autosomal dominant, and there are also recessive and sporadic cases.

(2) Secondary tubule damage, tubulointerstitial disease, chronic pyelonephritis, obstructive kidney disease, high oxalate urine, Kidney transplantation and other diseases.

2. Type II (proximal) renal tubular acidosis

The etiology of proximal tubular acidosis is more complex. All primary diseases involving renal tubular function can lead to proximal RTA. Such as multiple myeloma, Wilson disease, hyperparathyroidism and so on. In addition, some drug poisons can also induce the disease by damaging tubulointerstitial.

3. Mixed renal tubular acidosis (type III RTA)

It is characterized by clinical manifestations of both type and type tubular acidosis. Hyperchloric metabolic acidosis is obvious, a large amount of bicarbonate is lost in the urine, the excretion of titratable acid and ammonium ions in the urine is reduced, and the treatment is the same as that of type I and type II.

4. Type IV renal tubular acidosis

The main causes of hyperkalemia-type renal tubular acidosis: aldosterone deficiency accompanied by glucocorticoid deficiency; simple aldosterone deficiency; aldosterone tolerance. This type of RTA is mostly acquired in adults. Absolute aldosterone deficiency can be due to primary adrenal dysfunction or secondary to hyporeninemia caused by various mild and moderate renal insufficiency; relatively insufficient aldosterone is related to obstructive kidney disease, transplant rejection and drugs Damage caused by chronic interstitial kidney disease.

Clinical manifestations of renal tubular acidosis

It varies depending on the location and severity of renal tubule damage, but the common manifestations have varying degrees of metabolic acidosis.

1. Type I

In addition to acidosis, there are obvious clinical signs of stunted growth and polyuria. In the recessive inherited distal renal tubular acidosis, there is also neurological deafness, and the time of onset of deafness varies from birth to older children. .

2. Type II

Except for hyperchlorine metabolic acidosis with normal anion gap, the incidence of bone disease is about 20%, mainly osteomalacia or osteoporosis, and children may have rickets. Urinary stones and renal calcification are rare. Due to the occult nature of RTA's disease, such patients often seek treatment for other combined symptoms, such as stunting in early childhood, eye disease, and mental retardation.

3. Type III (mixed type)

Mixed renal tubular acidosis, hyperchloremic metabolic acidosis, obvious loss of bicarbonate in urine, reduced titratable acid and ammonium ion excretion in urine, the same treatment as type I and type II.

4. Type IV

In addition to patients with hyperchloric metabolic acidosis, the main clinical features are hyperkalemia and decreased serum sodium. Due to decreased blood volume, some patients may develop orthostatic hypotension.

In addition to the above clinical manifestations of various types of renal tubular acidosis, there are also clinical manifestations of primary diseases in secondary patients.

Renal tubular acidosis test

Blood biochemistry

All patients have decreased blood pH. Only incomplete type I patients have blood pH values within the normal range. Type and blood potassium decreased, type was normal, and type increased. There may be secondary hyperammonia in severe distal renal tubular acidosis.

2. Load test

For incomplete type 1 renal tubular acidosis, ammonium chloride load test can be used to help confirm the diagnosis. The test method is that after fasting acidic or alkaline drugs, oral ammonium chloride 0.1g / kg, 3 times / d, for 5 consecutive days, when the blood pH value drops, the urine pH value can not fall below 5.5. The diagnosis was incomplete type 1 renal tubular acidosis. Oral calcium chloride 0.2g / kg, after 5 hours, the urine pH value can not fall below 5.5, indicating that there is a disorder in uric acidification, which can be diagnosed as incomplete renal tubular acidosis. For suspected cases of type II RTA, a bicarbonate reabsorption test is available. Patients are instructed to orally or intravenously inject sodium bicarbonate. If the excretion fraction of bicarbonate is> 15%, the diagnosis can be confirmed.

3. ECG examination

In patients with hypokalemia, the ST segment moves downward, the T wave is inverted, and the U wave appears.

4.X-ray and bone density

People with rickets or osteomalacia can take X-ray pictures and bone density measurements.

Diagnosis of renal tubular acidosis

Typing diagnosis

2. Etiology diagnosis

Hereditary renal tubular acidosis can be diagnosed with molecular biology techniques. However, renal tubules make uric acidification complicated. H-ATPase has been mentioned previously. Some patients have not detected this enzyme by immunohistochemistry in renal tubule cells. However, the gene that expresses this enzyme has not been identified, therefore, genes related to uric acid function need to be further searched. There are many causes of secondary tubular acidosis, and relevant examinations should be performed to confirm the diagnosis based on the suspected disease.

Complications of renal tubular acidosis

1. Patients with rickets or osteomalacia without kidney stone disease or renal calcium deposits supplement vitamin D and calcium to correct rickets or osteomalacia. Ban acetazolamide, because it can aggravate renal tubular secretion.

2. Patients with concurrent fractures or bone pain can use analgesics or calcitonin.

Renal tubular acidosis treatment

For secondary tubular acidosis caused by other diseases, the primary disease should be treated first. If the primary disease can be cured, renal tubular acidosis can also be cured. For those who cannot cure the primary disease, they can only take the following symptomatic treatments as with hereditary tubular acidosis.

1. Type renal tubular acidosis treatment

First, add an alkaline agent to correct acidosis. Unlike the proximal RTA, the amount of alkali supplement is small, but it is still necessary to supplement enough alkali to balance the production of acid. Potassium citrate is commonly used, and sodium bicarbonate can also be used, but the sodium salt may exacerbate hypokalemia. Supplement potassium to correct hypokalemia. Such as potassium chloride tablets, potassium chloride sustained release capsules, potassium citrate and so on. Third, prevent kidney stones, kidney calcification and bone disease.

2.Treatment of type 2 renal tubular acidosis

For those who can perform causal treatment, the causal treatment should be performed first. Patients lose more bicarbonate, so the amount of alkali needed to be supplemented is also large (about 10 to 20 mmol / Kg for 24 hours). At present, it is recommended to use a mixture of sodium citrate and potassium citrate, because citrate metabolism can produce bicarbonate. It should be noted that the daily dose should be taken in multiples to maintain the day and night compound balance as much as possible. However, the dosage of alkali supplement therapy is large and the taste is poor, so the patient's long-term compliance is poor. Combining thiazide diuretics can reduce the amount of alkali, but the disadvantage is that it may make hypokalemia worse.

Because bicarbonate reabsorption in the proximal tubule is linked to reabsorption of sodium ions through NBC, patients need a salt-restricted diet to reduce extracellular volume and promote renal bicarbonate reabsorption.

To control bone disease, some patients, especially children, can be given active vitamin preparations.

3. Type IV renal tubular acidosis treatment

Treatment and prognosis depend on the underlying cause, and the patient's medical history, especially the drug history, should be understood. In addition, it is important to control blood potassium and avoid any potassium-containing drugs and high potassium diets. Mineralocorticoid supplementation can not only correct hyperchloride metabolic acidosis, but also correct hyperkalemia. A commonly used drug is fludrocortisone. Furosemide can increase the excretion of sodium sodium, Cl-, K and H in urine, so it can also be used to treat patients with type IV renal tubular acidosis. Combined with fludrocortisone can enhance the efficacy.

4. The treatment of mixed renal tubular acidosis type is similar to the treatment of proximal and distal renal tubular acidosis.

Prognosis of renal tubular acidosis

Long-term acidosis in chronic renal insufficiency can affect the metabolism of vitamin D and PTH, and aggravate renal bone disease.

Prevention of renal tubular acidosis

Active treatment of primary disease and complications, such as bone disease or severe calcium deficiency can be given calcium and active vitamin D preparations.