Renal cell carcinoma is mostly caused by deficiency of kidney qi, hydrops, endogenous damp toxin or exogenous damp-heat toxin, and pathogenic accumulation in Hefei waterway. Kidney deficiency can not absorb blood, only hematuria, waist is the house of kidney. Kidney deficiency leads to low back pain, toxic dampness and heat, and qi stagnation and blood stasis for a long time.
The etiology of renal cancer and renal pelvis cancer in modern medicine is also unclear, which may be related to the long-term stimulation of carcinogens. For example, smokers have a higher incidence of renal cancer, and those who take finasteride drugs for a long time to relieve pain and fever often have cryptoglenoid nephritis, renal pelvis cancer and the incidence rate have also increased. Long-term diseases and infections in kidney calculi can induce epithelial metaplasia and atypical hyperplasia, and then develop into cancer.
The cause of renal tumor is still unknown. In recent years, aromatic amines, aromatic hydrocarbons, aflatoxins, nitroso compounds, alkyl compounds, diamines, lead, cadmium and some drugs such as anticancer drugs, phenacetin, amphetamines, diuretics, potassium bromate and other coffee and food additives have carcinogenic effects. Most scholars believe that renal cell carcinoma originated from the proximal convoluted tubule, and the incidence of renal cell carcinoma increases obviously in people who directly inhale tobacco or cigars with pipes. A study shows that the incidence of renal cancer in smokers is 1.7 times that of non-smokers, and there is a direct and significant relationship between smoking and risk. The relative risk of light smoking is 1. 1, moderate smoking is 1.9 and heavy smoking is 2.3. Smoking degree and smoking age are positively correlated with the incidence of renal cancer. Even if smokers quit smoking, the risk of kidney cancer is twice as high as that of never-smokers. Animal experiments have confirmed that dimethylnitrosamine in tobacco can induce renal cancer. Vecchia believes that smoking combined with alcoholism, occupational exposure and other risk factors will further increase the risk of kidney cancer. There are β -naphthylamine and ethylamino -7 naphthol in the urine of smokers, which have been proved to cause bladder cancer and kidney cancer. Luck'e herpesvirus and mouse mammary tumor virus can cause renal tumors in animals, but their carcinogenic effects on human kidneys have not been confirmed. Renal cell carcinoma mostly occurs in men, especially in elderly men with decreased male hormones, suggesting that sex hormones are related to the occurrence of renal cell carcinoma, and the exact mechanism is still unclear. The incidence of renal cell carcinoma is high in overweight women, but not in overweight men. What nutrients promote the occurrence of renal cancer is still unknown. Some hereditary diseases, such as tuberous sclerosis and neurofibroma, can be combined with renal cell carcinoma. Kidney calculi may be complicated with renal pelvis cancer due to long-term local inflammatory stimulation. Long-term hemodialysis patients induce acquired renal cystic disease and canceration due to the accumulation of carcinogens such as cysts and polyamines that cannot be removed by hemodialysis.
In short, the occurrence of renal cell carcinoma may be related to many chemical and biological factors. Smoking and/or obesity, other factors including aluminum phosphate, dimethylnitrosamine, long-term estrogen intake, aflatoxin B 1 and streptozotocin, and some special diseases such as Von~Hippel-Lindau disease can cause renal cell carcinoma. Some patients with chronic renal failure or renal cyst acquired by dialysis treatment can also develop renal cell carcinoma. About 30% to 50% of long-term dialysis patients can develop acquired renal cysts, and 6% of them can develop renal cancer with acquired cystic diseases.
(2) Pathogenesis
Renal cell carcinoma is usually a single lesion on one side, about 2% are bilateral or multiple lesions, and the incidence rate on the left and right sides is similar. Typical renal cell carcinoma is round and varies greatly in size. According to a group of 100 cases of renal cell carcinoma, the lesion sites were: upper 44 cases, lower 4/kloc-0 cases, and multiple lesions 15 cases. The tumor has no histological capsule, but there is a pseudocapsule formed by compressed renal parenchyma and fibrous tissue. A few of them are yellow or brown, and most of them are accompanied by bleeding, necrosis and fibrotic plaques. Hemorrhage and necrosis can form cysts. The tumor may have punctate or patchy calcified lesions. There are more calcified lesions of renal cell carcinoma in adolescents than in the elderly. Tumors can destroy the whole kidney and invade adjacent adipose tissue, muscle tissue, blood vessels and lymphatic vessels. Renal cell carcinoma is easy to spread to veins to form tumor thrombus, which can enter renal veins, inferior vena cava and even right atrium. Perirenal fascia is a barrier to prevent the local spread of tumor. The ipsilateral adrenal gland is involved in about 10%, and distant metastasis is common in lung, brain, bone, liver, skin and thyroid.
Renal cell carcinoma has a variety of tissues and cells, and the gross specimens can be solid sheet, trabecular, papillary, honeycomb and glandular tubular. Typical renal cell carcinoma cells are transparent cells, polygonal, cubic or columnar, with a cell diameter of10 ~ 40μ m. Because the cytoplasm contains glycogen and lipids, the cytoplasm stained by HE is transparent or vacuolar. The lipids in cytoplasm are mainly phosphonates and neutral lipids. Hale colloidal iron staining electron microscope showed focal microvilli formation and vesicle formation in cytoplasm. The nucleus is small and regular with a small amount of mitosis. If renal cell carcinoma is a granular cell, its cytoplasm is glassy and uniform, and the size of cells and nuclei is different, and mitotic images are common. Most renal cell carcinomas are clear cells, but there are also granular cells. Some renal cell carcinomas are spindle cells, which are difficult to distinguish from fibrosarcoma. In renal cell carcinoma, clear cells, granular cells or spindle cells can exist alone or in combination.
Pathological grading of renal cell carcinoma: The morphological grading system of renal cell carcinoma proposed by Fuhrman et al. (1982) has been accepted and adopted by most scholars in the world.
Grading according to the shape and size of the nucleus has the advantages of clear standards and easy mastery. When there are different levels of cells in the same tumor or the same area, the highest level of cancer cells is the final level of pathological diagnosis. If most cells are G2 and a few cells are G3, the tumor should be named G3.
Staging: The staging of renal cell carcinoma is not uniform. At present, Robson staging and TNM staging are the most widely used in clinic.
Robson staging:
Stage 1: The tumor was confined in the renal capsule.
Stage ⅱ: The tumor penetrated the renal capsule and invaded the perirenal fat, but it was confined in the renal fascia, and there was no infiltration in renal veins and local lymph nodes.
Stage ⅲ: The tumor invaded renal vein or local lymph nodes, with or without inferior vena cava and perirenal fat involvement.
Stage Ⅳ: Distant metastasis or invasion of adjacent organs.
The above is a simplified Robson stage, which is convenient for application. Its disadvantage is that the prognosis of stage II and III is the same. The TNM staging proposed by the International Anti-Cancer Association in 1987 is as follows.
TNM staging:
T0: No primary tumor.
T 1: The maximum diameter of the tumor is ≤2.5cm, which is confined in the renal capsule.
T2: the largest diameter of tumor >; 2.5cm, confined to the renal capsule.
T3: The tumor invaded the great vessels, adrenal glands and tissues around the kidney, and was confined to the renal fascia.
T3a: Invasion of adipose tissue around kidney or adrenal gland.
T3b: Invasion of renal vein or inferior vena cava.
T4: Invasion beyond renal fascia.
N0: No lymph node metastasis.
Nl: Single unilateral lymph node metastasis with the largest diameter ≤2.5cm.
N2: local multiple lymph node metastasis, or the maximum diameter of a single lymph node is 2 ~ 5cm.
N3: The maximum diameter of local metastatic lymph nodes is more than 5 cm.
M 1: remote transmission.