Causes and treatments of high uric acid levels

When it comes to uric acid, we are all familiar with it. Even if we don’t understand it, we can understand it based on the literal meaning. Uric acid is related to urine, which is related to the kidneys. People with a little professional knowledge will know that uric acid is actually an indicator for checking kidney health. The kidneys are the main excretory organs of the human body. If there is a problem with the kidneys, the excretory system of the entire body will have problems. Then, toxins will be deposited in the body and various diseases will occur.

We all know how important the kidneys are to the human body. If there is a problem with uric acid, it means there is a problem with the kidneys, which is a very serious problem. Therefore, we need to understand the causes of high uric acid and find the best and most suitable treatment for high uric acid through the causes so that our kidneys can restore their normal excretion function.

1. The metabolism of purine substances in the body is disturbed, resulting in increased uric acid synthesis.

1. Excessive intake of purine: High uric acid levels are directly proportional to the purine content in food. 50% of RNA and 25% of DNA in the food consumed are excreted in the form of uric acid in the urine. Strictly limiting purine intake can reduce serum uric acid levels to 60 μmol/L (1.0 mg/dL) and uric acid secretion in urine 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 so far 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.

2. Treatment methods

Based on the mechanism of uric acid production, we can deduce in reverse: to prevent and treat gout, we must reduce the production of uric acid. To reduce the production of uric acid, we must reduce purine in the body. To reduce purine in the body, we must reduce the oxidative decomposition of nucleic acids and the intake of purine, while strengthening the excretion of uric acid. Therefore the measures are:

A normal human body usually accumulates 1200 mg of uric acid, and about 600 mg, or half of the uric acid in the body, is replaced by new one every day. To express it another way, the human body stores approximately 1200 mg of uric acid, of which 600 mg are excreted and 600 mg are newly generated every day. If we break it down further, of the 600 mg of uric acid generated every day, 100 mg is ingested from food, and 500 mg is converted from endogenous purines produced by the decomposition and death of cells in the body. As for the 600 mg of uric acid excreted, 450 mg is excreted in the urine and 150 mg is excreted in sweat and feces. Under normal circumstances, the body carries out its orderly work according to this rhythm and law over and over again, but once this balance is broken, whether the cause is excessive uric acid production or reduced uric acid excretion, uric acid will increase, leading to hyperuricemia and finally gout.

Prescription drugs for uric acid excretion: Uric acid excretion drugs mainly include probenecid, sulfinpyrazone, benzbromarone, etc. This type of drug can prevent the reabsorption of uric acid by the renal tubules and increase the excretion of uric acid, thereby lowering the level of uric acid in the human body. The side effect is that while increasing the excretion of uric acid, other trace elements in the human body are also excreted, which can cause hyponatremia, hypokalemia, and hypocalcemia. Therefore, it cannot be used for a long time. It also has side effects on the liver and kidneys, so it cannot be used for a long time.

Drugs that inhibit uric acid production: Currently, the drug commonly used in clinical practice to inhibit uric acid production is allopurinol. This drug is a powerful purine oxidase inhibitor and is the only drug so far that can effectively reduce uric acid production and lower uric acid levels in the human body. Although allopurinol has fewer adverse reactions, it should be used with caution in patients with impaired liver and kidney function.

Drugs that alkalize urine: Alkaline drugs such as sodium bicarbonate have no effect on lowering uric acid, but they can alkalize urine, increase the solubility of uric acid in the blood, and make it difficult for uric acid to accumulate in the urine and form crystals.

Uric acid excretion tea: can restore the kidney's ability to excrete uric acid and achieve the effect of more uric acid excretion.

The above is a relatively written account of the causes and treatments of high uric acid levels. People without a medical background may not be able to fully understand it, but at least we can understand the treatment methods. We don’t need to know the mechanism of the medication or the causes of the formation. It is enough to just know how to treat it.