The etiology of renal tumors is still unclear, and almost all the information on the risk factors for renal cell carcinoma comes from case-control studies conducted in a number of countries such as North America, Europe, Australia and Asia. Lifestyle risk factors such as smoking, diet, obesity, alcohol and other beverages, use of different drugs, etc. may be an important part of the etiology of renal tumors, and similarly, environmental risk factors such as exposure to different chemicals, radiation, and hemodialysis may be involved in constituting an important aspect of renal tumors’ etiology. Smoking Although the results of case-control studies are not entirely consistent, a convincing relationship has been established between smoking and renal cancer. Cohort studies also support this view. Cigarette smoking has long been recognized as a moderate risk factor for renal tumors, with an increased risk of 1.2 to 2.3 compared with that of nonsmokers, and there is also a significant relationship with the amount of smoking, with heavy smokers having an increased risk ranging from 2.0 to 3.0. Risks decreased with increasing duration of smoking cessation. Population-attributable risk estimates indicate that 27% to 37% of men with renal tumors and 10% to 24% of women with renal tumors have a strong association with smoking (past or present). Approximately half of the attributable risk was due to current smoking. Another study suggests that there is also a link between passive smoking and kidney cancer. 2. Obesity Virtually every study has concluded that weight and renal cell carcinoma are positively associated. This result is particularly evident in women, but appears to be slightly less pronounced in men. It is not clear from the current research what mechanism causes obesity to be a risk factor for kidney cancer. Hormonal changes, such as changes in endogenous estrogen in obese individuals, may play a role. Estrogen-induced renal tumor models have been made in some experimental animals, but there is still a lack of epidemiological evidence to show the specific relationship between hormonal changes and renal cancer. In addition, obesity may be more likely to induce atherosclerotic glomerulonephritis, which makes renal tubules more susceptible to cancer. Diuretics, which are commonly used in the treatment of obesity, are also considered to be potentially risky. The population-attributable risk ratio shows that the relationship between renal tumors and obesity is more than 40% in women and more than 5% in men. Drugs 3.1 Analgesics It is now well established that the heavy use of finasteride can cause renal pelvic tumors, and studies have also suggested that it may cause renal cancer. However, due to the effects of smoking or the use of other types of analgesic drugs, it is not possible to clearly demonstrate a specific relationship between finasteride and renal tumors. Conflicting conclusions have even emerged from studies of aspirin in the etiology of kidney tumors. A large study in Minnesota showed that the use of aspirin, paracetamol and even finasteride had no effect on renal tumors, while a Danish study showed that women who used large amounts of finasteride had a five-fold increased risk of renal cancer, but the use of paracetamol or aspirin did not significantly increase their risk of renal cancer. 3.2 Diuretics Women taking diuretics have a 5-fold increased risk of kidney cancer. Results may vary by blood pressure status, but both hypertensive and non-hypertensive individuals have a significantly increased risk. Some cohort studies have also shown a clear association between kidney cancer and diuretic use. The most recent case-control studies [data adjusted for known confounders, including hypertension] suggest an approximately 3- to 4-fold increased risk in women. Notably, animal studies have indicated that hydrochlorothiazide and furosemide, the most commonly used diuretics, can induce renal tubular adenomas and adenocarcinomas and liver tumors in experimental rats. The use of diuretics, especially in the elderly, has become quite widespread in many countries of the world in the last few decades and may pose a serious public health problem. 3.3 Estrogens Estrogen-induced renal cancer has been induced in animal models, but epidemiologic evidence is lacking in human studies. Weakly positive results have been reported in menopausal estrogen users and oral contraceptive users. However, the specific association between the two is not clear. Hypertension The effect of hypertension on renal tumors is greatly reduced after excluding the effects of diuretics and some other anti-hypertensive drugs. Some results suggest that hypertension medication may be the primary risk factor rather than hypertension itself. However, in animal models, it can be seen that both the use of diuretic antihypertensive drugs and the lack of them have a certain effect on the development of renal tumors. To date, however, it is inconclusive to identify whether the risk of renal cancer is attributable to hypertension or to hypertensive drugs. However, either one is a definite risk factor, and the key is the proportion. The attributable risk of hypertension or the use of hypertensive drugs for kidney cancer is 21% overall and 39% in women. Diet High-protein diet: Chronic alterations in renal function caused by the consumption of meat and dairy products (which are rich in protein) may predispose to kidney tumors. Although the evidence is somewhat contradictory, it is still considered to be a relevant factor in causing renal tumors. Because there are animal models show that the intake of large amounts of animal protein can induce excessive proliferation of renal tubules, and there are also studies showing that the consumption of vegetables has a protective effect on the kidney. 6, coffee, alcohol, beverages, etc. When adjusted for the interfering effects of smoking, the results of the analysis of the relationship between renal tumors and per capita coffee consumption were not in complete agreement with the relevant case-control studies. Two studies have been used to illustrate the possible relationship. On the one hand, it has been shown that decaffeinated coffee consumption (no dose restriction) in the population (no gender distinction) increases the risk by approximately twofold, whereas women who consume regular coffee (no dose restriction) also have an increased risk. On the other hand, a Norwegian cohort study showed the opposite result, with those who consumed 7 or more cups of espresso per day having a risk of only 1/4 compared with those who drank only twice as much or less coffee per day. In conclusion, the analysis showed no significant relationship between coffee consumption per capita and kidney cancer. There is also an association between kidney tumor mortality and per capita alcohol intake, but the analysis does not support these results. The recent DAN ISH case-control study found a statistically significant negative association between alcohol consumption and the risk of kidney cancer. In addition, cohort studies have shown no increased mortality from renal tumors in alcoholics. Some studies have reported that tea consumption also increases the risk of kidney cancer, especially in women. Follow-up studies have shown a dose-dependent relationship between kidney cancer mortality and tea consumption. Although it has been proved that some teas can induce mutations and the tannins they contain can induce tumors in experimental animals, the pathogenic mechanism is still not very clear. 7, Occupation Although kidney cancer has not been evaluated as occupationally related tumor, some occupational factors are still considered as important risk factors for kidney cancer. For example: asbestos: two cohort studies, one of isolated workers and one of asbestos producers, found that the mortality rate of renal tumors in the latter group was significantly higher. Animal studies and autopsies have shown that asbestos fibers can accumulate in the kidneys. PAHs: Exposure of coal and coke workers to PAHs has been epidemiologically reported to increase their chances of developing renal tumors.Redmond (1972, 1973) showed that deaths of steel workers may be associated with renal cancer, and among coke workers, deaths from renal cancer were 5 times higher than among other steel workers.The RR of renal cancer among coke oven workers was 7.5, and the main type of renal cancer was clear cell carcinoma.Thomas ( 1980) showed that in petroleum workers, the mortality rate of kidney tumors in the coke oven workers was 7.5, mainly clear cell carcinoma. Thomas (1980) showed that men who had worked in petroleum refineries and petrochemicals for more than 20 years had a twofold mortality rate from kidney cancer, but those who had worked for less than 19 years did not have such a risk. Perchloroethylene: Studies have shown an increased risk of kidney tumors in laundry and dry-cleaning workers. Gasoline and some other petroleum products: Refinery workers and gas station workers are thought to be at increased risk for kidney tumors, but the latest cohort study showed no evidence of an additional risk. Gasoline is suspected to be a risk factor for renal cell carcinoma, and chronic exposure of male rats to unleaded gasoline increased the incidence of kidney tumors. There are a large number of studies on gasoline exposure with conflicting results. Other occupational factors, such as newspaper journalists association, cardboard printing workers, leather tanning, shoe workers, medical personnel, truck drivers, electric utility workers and architects, the specific results are not known, and many factors on the incidence of renal tumors and the impact of the study is still waiting. 8.Hemodialysis patients, especially men, are prone to develop acquired renal cysts, which can induce renal cancer. However, the mechanism of carcinogenesis is unknown and may be related to uremia caused by long-term renal failure. Some people on dialysis for chronic (long-term) renal failure may develop renal cysts over a long period of time. Renal cell carcinoma may develop from these cysts. Ionizing radiation increases the risk of kidney cancer, and this is particularly evident in radiation therapy for patients with ankylosing spondylitis and cervical cancer, but the effect is not strong. Patients treated with radium-224 for bone tuberculosis and ankylosing spondylitis also had an increased risk. Genetic factors Familial renal cancer can be divided into three types: ① autosomal dominant type of hereditary non-papillary renal cell carcinoma with short-arm translocation of chromosome 3. ① Autosomal dominant type of hereditary non-papillary renal cell carcinoma with short-arm translocation of chromosome 3. (iii) Autosomal dominant papillary renal carcinoma. Familial aggregation of renal cancer has been reported. Some patients with kidney cancer may have one or more genes that make them more likely to develop kidney cancer. The mechanism of how these genes contribute to kidney cancer is still not fully understood. Kidney tumors caused by these genetic factors tend to be bilateral and tend to be complicated by tumors in other systems. Although mutations have resulted in different types of kidney tumors, genetic types of renal cell carcinoma and papillary cell carcinoma have been identified. Studies have shown that some of the oncogenes in renal cancer may originate on the short arm of chromosome 3. Mutations have been found to cause rare conditions such as tuberous sclerosis and VHLD (Von Hippel – Lindau disease). People with these mutations are prone to developing kidney tumors. VHL syndrome is characterized by multiple tumors in the kidneys, brain, spine, eyes, adrenal glands, pancreas, inner ear, or epididymis.VHLD occurs in approximately 1 in 36,000 births with familial clustering. Patients with VHL have a high incidence of clear cell carcinoma of the kidney and develop it at a young age. Bilateral renal cysts or tumors occur in approximately 40% of patients. The causative gene for VHL has been identified and is located on chromosome 3. Tuberous sclerosis is characterized by skin lumps (due to small hemangiomas), epilepsy, mental retardation, renal cysts, hepatic cysts, and pancreatic cysts. This disease also has an increased risk of developing renal cell carcinoma. In toads, herpesviruses have been implicated in kidney tumors. Although almost all toads are infected with the virus, only about 10% develop tumors. This result has led to the study of herpesvirus proteins. Although the study of herpes simplex virus proteins is still premature, research will continue.