Causes of high creatinine and uric acid

Creatinine is the product of our body's muscle metabolism, and uric acid is the end product of purine metabolism. The content of these two substances can easily change. A typical example is that the values are high. Some are caused by physiological factors, while others are caused by pathological factors. When an increase occurs, it is very important to find out the cause. So, what is the cause of high creatinine and uric acid? Let’s take a look below.

Causes of creatinine: 1. Water loss in the body, such as fever, sweating, reduced water intake, polyuria leading to blood concentration, reduced renal blood flow, and increased creatinine. 2. Fatigue, poor rest and inattention to life details can also cause a certain range of increased blood creatinine. 3. People with abnormal urine, long-term hematuria and proteinuria will experience elevated creatinine levels without realizing it. 4. Patients with kidney disease who take drugs that damage the kidneys without knowing it may experience elevated creatinine, which may even be irreversible. 5. People with renal insufficiency will experience an increase in creatinine in a short period of time when they are infected (including colds, pneumonia, intestinal infections, urinary tract infections, etc.). 6. Patients with hypertension have unstable blood pressure and may have high creatinine levels. 7. Patients with kidney disease may experience elevated creatinine levels due to relapse of the disease.

The first cause of high uric acid is the disorder of purine metabolism in the body, which leads to the increase of uric acid synthesis. 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 consumed are excreted in the urine 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. What has been found are: 1) Increased activity of phosphoribosyl-pyrophosphate synthetase. 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, such as allopurinol tablets. Allopurinol tablets are drugs that inhibit 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. Conversely, when the temperature drops, urate will precipitate in the form of crystals, which will also affect the uric acid concentration. Learn more about the causes of high uric acid levels.

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