There is a relationship between the incidence of urolithiasis and race. Epidemiologic surveys have shown that all races are at risk for urinary stones, but the incidence of urolithiasis varies significantly by race. The prevalence of urinary stones among Caucasians and non-Caucasians is 4.13:1. Generally, blacks are less likely to suffer from kidney stones, which may be due to: (1) the lower socioeconomic status of blacks compared to whites, and their lower rates of consultation and hospitalization after suffering from urinary stones, which may cause bias in information; (2) black skin protects the body from ultraviolet radiation, thus reducing the synthesis of vitamin D; (3) lower urinary calcium and phosphorus levels in blacks; and (4) lower urinary calcium and phosphorus levels in blacks. (3) urinary calcium and urinary phosphorus levels are lower in blacks;) mucin concentration in black urine is low or even lacking; and (5) there is no familial history of urolithiasis in black patients with stones, while there is a family history in whites. However, the low incidence of urinary stones in blacks is not absolute, but may change when their living environment and economic conditions change. Therefore, further research is needed to determine whether the racial differences in the incidence of urinary stones are due to differences in diet and lifestyle habits or to genetic susceptibility to the disease. Genetic findings suggest that urinary tract stones are autosomal dysgenic diseases with polygenic mediation. At present, alleles at at least three loci have been found to be associated with the excretion of calcium, oxalate and citrate in the urine of patients with calcium oxalate stones. Some urinary stone formation is associated with genetic disorders, the most typical of which are cystinuria (cystine precipitation from poorly soluble cystine due to impaired reabsorption of cystine, arginine, ornithine, and lysine by the renal tubules), familial xanthinuria, primary hyperoxaluria, tubular acidosis (dysfunctional tubular acidification), and some hyperuricemia. It should be noted that patients with a family history of urolithiasis have a risky tendency to develop stones, although no clear genetic cause can be identified at this time. In addition, some genetic disorders such as polycystic kidney, horseshoe kidney, obstruction of the ureteral junction, medullary kidney (40% of cases with stones) and lower urinary tract anomalies are also closely related to urolithiasis. Genetic investigations have revealed a significant familial predisposition to the development of urinary stones. According to statistics, 13% to 46% of patients with urolithiasis have a family history, with a higher rate of consanguineous marriages. The recurrence rate of stones is much higher in patients with a family history of urolithiasis than in those without a family history. Some families can have several members with urolithiasis, such as one family with 7 cases of urolithiasis out of 20 people in three generations. In a study of 7 pediatric patients with urolithiasis, 7.6% had a history of urolithiasis, which is 3 times higher than in unrelated individuals. However, these were not necessarily all genetically related. It has been observed that the incidence of urinary tract stones is higher in one spouse when the other spouse has urinary tract stones, suggesting that in addition to the factors that influence the formation of urinary tract stones, environmental factors also play an important role in their development. This is because there are common living standards, similar living and eating habits in a pro-court, and these. You stone’s orthodontic composition can have a great influence. This situation is similar in other diseases, such as the so-called “husband and wife cancer”, which is mainly related to common habits, but must be a genetic factor at work.