Causes of Hyperuricemia

Hyperuricemia is a symptom that is not very common clinically. Its pathogenesis is mainly due to a disorder in the metabolism of purine in the body, which leads to an increase in the content of uric acid in the blood. Since many people do not understand the causes of hyperuricemia, this article specifically explains the causes of hyperuricemia as follows.

Generally speaking, when preventing a disease, if you can take timely precautions against some of the causes of its onset, it will play a certain role in preventing the onset and deterioration of the disease. Therefore, I hope that this article about the causes of hyperuricemia can help everyone.

1. The metabolism of purine substances in the body is disrupted, resulting in an increase in the synthesis of uric acid.

1. Excessive intake of exogenous purine: High uric acid content is proportional to the purine content in food. 50% of RNA and 25% of DNA in the food you eat are excreted in your urine.

Purine is excreted in the form of uric acid. Strictly limiting purine intake can reduce serum uric acid levels to 60 μmol/L (1.0 mg/dL) and urinary uric acid secretion to 1.2 mmol/d (200 mg/d).

2. Excessive production of endogenous purine: Endogenous purine metabolism disorders are more important than exogenous factors. The de novo synthesis of purine from non-cyclic to cyclic forms requires 11 steps, during which abnormalities in the enzymes can lead to excessive purine synthesis. The ones that have been discovered are:

1) Increased phosphoribosyl-pyrophosphate synthetase activity.

2) Hypoxanthine-guanine phosphoribosyltransferase deficiency.

3) Glucose 6-phosphatase deficiency.

3. Increased purine metabolism: High uric acid levels may occur in chronic hemolytic anemia, rhabdomyolysis, polycythemia, myeloproliferative diseases, chemotherapy or radiotherapy. Excessive exercise, epileptic status, and glycogen storage disease types III, V, and VII can all accelerate the degradation of muscle ATP. Myocardial infarction, smoking, and acute respiratory failure are also associated with accelerated degradation of APT.

2. The metabolic disorder of purine substances in the body leads to reduced uric acid excretion. 90% of patients with persistently high uric acid levels have abnormalities in the kidney's ability to process uric acid.

In patients with hyperuricemia and gout, when given different uric acid loads, the ratio of urate clearance to glomerular filtration rate is lower than that in normal people. The decrease in uric acid secretion may be related to a decrease in glomerular filtration rate, decreased tubular secretion, or tubular reabsorption. Although high uric acid levels are always present in chronic kidney disease, the relationship between uric acid concentration and serum creatinine and blood urea nitrogen is still unclear.

As renal function declines, the amount of uric acid secreted per unit glomerulus increases, but the secretion capacity of the renal tubules remains basically unchanged, the reabsorption capacity of the renal tubules also decreases, and the ability to clear uric acid outside the kidney increases significantly.

1. Inhibition of renal tubular secretion: one of the most important mechanisms. Inhibition of uric acid excretion and/or increased reabsorption due to drugs, intoxication, or endogenous metabolites. This occurs when anion transport systems are inhibited, two important inhibitors of which are lactate and keto acids.

2. Reduced glomerular filtration: It can also increase uric acid levels. One of the mechanisms is reduced filtration rate, which is the main cause of hyperuricemia in renal insufficiency or failure. Increased net uric acid reabsorption can occur in the setting of volume depletion and is one of the mechanisms by which diuretics may induce hyperuricemia.

3. Increased tubular reabsorption: Hyperuricemia can also be caused by enhanced reabsorption distal to the secretion site. These may occur with dehydration or diuretic therapy in patients with diabetes.

3. Two factors exist at the same time. In many patients, there are two factors: increased uric acid production and decreased excretion.

Such as patients with glucose 6-phosphatase deficiency and hereditary lactose intolerance. Alcohol can also cause uric acid retention in two ways. Excessive alcohol intake accelerates the liver's degradation of ATP and increases the production of uric acid. The uric acid caused by alcohol also prevents the excretion of uric acid. Alcoholic beverages high in purines, such as beer, are also a significant factor.

4. Other external factors can also cause high uric acid levels

For example, allopurinol tablets are a drug that inhibits the synthesis of uric acid. Allopurinol and its metabolite oxypurinol can inhibit xanthine oxidase, preventing hypoxanthine and xanthine from being metabolized into uric acid, thereby reducing the production of uric acid; for example, weather changes, as the temperature rises, the solubility of uric acid will increase accordingly, and conversely, a decrease in temperature will cause urate to precipitate in the form of crystals, which will also affect the uric acid concentration. Learn more about the causes of high uric acid.

The above four factors are the possible causes of hyperuricemia. In real life, I hope everyone can pay attention to the four factors mentioned in this article that may cause the symptoms of hyperuricemia, so that they can do a good job of preventing the onset of hyperuricemia in daily life, and at the same time help the treatment results of high-efficiency acidemia.