Causes of hyperchloremic renal acidosis

Hyperchloremic renal acidosis It is caused by the loss of too much sodium bicarbonate from the body. In addition, the kidneys do not remove acid from the body in sufficient quantity.

It is characterized by decreased capacity of the proximal tubules to reabsorb the bicarbonate of the glomerular filtrate, which causes hyperchloremic metabolic acidosis.

Its prevalence is unknown. However, proximal renal tubular acidosis (pRTA) induced by drugs is relatively frequent. However, hereditary isolated hereditary renal hydrochloride acidosis is very rare.

Symptoms of hyperchloremic renal acidosis

Symptoms of hyperchloremic renal acidosis depend on the disease or underlying condition. This condition causes rapid breathing, lethargy, or confusion. In addition, it can lead to shock and even death.

Initially, it is revealed with a very basic urine because of the bicarbonate not reabsorbed. There is also a delay in growth and a reduction in bone mineral density due to hyperchloremic renal acidosis.

In some cases, hypokalemia may appear and, occasionally, symptoms of periodic paralysis may be revealed. However, rickets and osteomalacia are due to vitamin D deficiency and lack of phosphate reabsorption.


Hyperchloremic renal acidosis It can be caused by kidney diseases, such as distal renal acidosis and proximal renal tubular acidosis.

As well It can appear in cases of poisoning with acetylsalicylic acid, ethylene glycol or methanol. In addition, it can appear if there is intense dehydration.

Hyperchloremic renal acidosis it can be acquired or inherited recessively, in most cases, or dominant. Acquired renal acidosis is caused by a mutation in the SLC4A4 gene (4q13.3).

But nevertheless, The dominant acidosis is caused by mutations in a gene not yet identified. The proximal mound reabsorbs around 80% of the bicarbonate filtrate, but a defect in it causes the loss of bicarbonate.

As well some drugs may be the cause of the development of acquired renal acidosis.

Read also: Management of chronic kidney disease

Diagnosis of hyperchloremic renal acidosis

Unlike patients with distal renal acidosis, those affected by the proximal renal retain the ability to lower the pH of the urine below 5.5

To diagnose the disease it is necessary to demonstrate the lack of bicarbonate reabsorption. The diagnosis is confirmed with a bicarbonate titration test.

In the valuation test, an exaggerated increase in urinary bicarbonate excretion will be observed and the pH of the urine as the plasma bicarbonate increases above the renal threshold.

It is also necessary to exclude other inherited proximal tubulopathies, such as the oculo-cerebro-renal syndrome, Dent's disease and glycogen storage disease due to GLUT2 deficiency.

As laboratory tests you can request an arterial blood gas analysis and an electrolyte analysis to confirm hyperchloremic renal acidosis.

In addition, a basic metabolic panel can be ordered, consisting of a group of blood tests that measure sodium and potassium levels, kidney function and other chemical substances. In turn, the pH of the urine, the ketones in blood and urine and the levels of lactic acid are evaluated.

This set of tests can also help determine if the cause of the acidosis is a problem of respiratory origin or a metabolic problem.

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The treatment of hyperchloremic renal acidosis depends on the cause of the disease. Inherited proximal renal acidosis requires bicarbonate replacement therapy throughout life.

To carry out that treatment, you need a lot of baking to be able to normalize the bicarbonate in serum.

Diuretics of the thiazide family are used in some cases in doses of 25-50 mg daily. For example, hydrochlorothiazide. This is done in order to improve the bicarbonate reabsorption and, in this way, the amount of bicarbonate needed can be reduced.

As well it is necessary to monitor the plasma potassium level, so in some cases it is necessary to administer a mixture of sodium and potassium bicarbonate salts.

Normally, drug-induced hyperchloremic proximal renal acidosis is reversible upon cessation of drug administration. With the proper treatment, the prognosis of this condition is good.