Blood acidity is also known as high blood acid, because blood acid is blood uric acid, so it can also be expressed as high blood uric acid. High uric acid is a metabolic disease caused by the increase of uric acid in the blood due to the metabolic disorder of a substance called purine in the human body. The daily production and excretion of uric acid in the body are approximately equal, and the production is one-third from food and two-thirds from internal synthesis. The following diseases can also cause blood acidity: 1, hyperuricemia nephropathy With the improvement of people’s standard of living, longer life expectancy and aging population, the incidence of hyperuricemia and gout is rapidly increasing. Clinically, hyperuricemia is often accompanied by hyperuricuria, whether hyperuricemia or hyperuricuria, can cause uric acid (salt) deposition in kidney tissue causing kidney damage called uric acid nephropathy. Uric acid and uric acid salts can cause gout, acute uric acid nephropathy, uric acid kidney stones, chronic gouty nephropathy and asymptomatic hyperuricemia. Hereditary hyperuricemia is an X-chromosome recessive disorder, first reported by Lesch and Nyban (1964), which presents with choreiform involuntary movements and a marked increase in uric acid. Uric acid is the end product of purine (purine) metabolism. Purines and pyrimidines (pyrimidine) are important raw materials for the synthesis of DNA (deoxyribonucleic acid) and RNA (ribonucleic acid), the genetic material of life. The uric acid produced by the oxidative metabolism of purines is mainly excreted by the kidneys and intestines. The daily production and excretion of uric acid are maintained in a certain balance in the body; if there is excess production or poor excretion, uric acid will accumulate in the body, resulting in excessive uric acid in the blood (i.e. hyperuricemia). Hereditary hyperuricemia is caused by a genetic mutation that leads to a partial or complete deficiency of the enzyme responsible for purine metabolism, namely hypoxanthine-guanine phosphate ribosyltransferase activity in the affected child, which subsequently leads to accelerated purine renewal metabolism and hyperuricemia.