Renal cell carcinoma (RCC) is a malignant tumor originating from the urinary tubular epithelial system of the renal parenchyma, also known as renal adenocarcinoma, which accounts for 80% to 90% of renal malignancies. It includes various subtypes of renal cell carcinoma originating from different parts of the urinary tubules, but does not include various tumors originating from the renal interstitium and the epithelial system of the renal pelvis.
I. Epidemiology and etiology
Kidney cancer accounts for about 2%~3% of adult malignant tumors, and the incidence rate varies among countries or regions, with the incidence rate in developed countries being higher than that in developing countries. The incidence rate and mortality rate of kidney cancer vary greatly among regions in China, according to the National Cancer Prevention and Treatment Research Office and the Health Statistics Information Center of the Ministry of Health, the incidence and mortality data of tumors in pilot cities and counties in China from 1988 to 2002 show that
①The incidence rates of malignant tumors of kidney and other malignant tumors of urinary tract (renal pelvis, ureter, urethra) in the three time periods of 1998-1992, 1993-1997 and 1998-2002 were 4.26/100,000, 5.40/100,000 and 6.63/100,000 respectively, and the incidence rates of other malignant tumors of kidney and urinary tract showed an increasing trend year by year;
②The ratio of male to female patients is about 2:1;
③The incidence rate in urban areas is higher than that in rural areas, with a maximum difference of 43 times between the two. The age of onset can be seen in all age groups, with a high incidence at 50-70 years old.
The etiology of kidney cancer is not known. Its development is associated with genetics, smoking obesity, hypertension and anti-hypertensive treatment [9] (level of evidence IIa), and hereditary or familial renal cancer accounts for 2-4% of all renal cancers. Non-smoking and avoidance of obesity are important ways to prevent the development of kidney cancer (recommendation level B). Kidney cancer not caused by genetic factors is called sporadic kidney cancer.
II. Pathology
(i) Gross
The vast majority of renal cancers occur in one side of the kidney, often as a single tumor, and 10%-20% are multifocal. Multifocal cases are common in patients with hereditary renal cancer and papillary adenocarcinoma of the kidney [10]. The tumors are mostly located in the upper and lower poles of the kidney and vary greatly in size, with an average diameter of 7 cm, often with a pseudo-envelope separating them from the surrounding renal tissue. Bilateral onset (sequential or simultaneous) accounts for only 2%-4% of sporadic renal carcinomas.
(ii) Classification
In the past 20 years, WHO has introduced 3 versions of renal tumor classification standards, the most widely used one is the 1981 WHO classification standards (1st edition), which classifies renal cell carcinoma into 5 pathological types: clear cell carcinoma, granular cell carcinoma, papillary carcinoma, sarcomatoid carcinoma and undifferentiated carcinoma.
In 1997, WHO established the classification criteria for renal parenchymal epithelial tumors (2nd edition) based on the origin of tumor cells and genetic alterations, which classified renal cancer into clear cell carcinoma (60%-85%), renal papillary carcinoma or chromophobe carcinoma (7%-14%), suspicious cell carcinoma (4%-10%), collecting duct carcinoma (1%-2%) and unclassified renal cell carcinoma (level of evidence IIa). The 2 types of granular cell carcinoma and sarcomatoid carcinoma in the traditional classification were eliminated. Based on morphological changes, renal papillary carcinoma was classified into type I and type II.
In 2004, WHO revised the 1997 histological classification of renal cell carcinoma (3rd edition), retaining the original 4 types of renal clear cell carcinoma, renal papillary carcinoma (type I and II), renal suspicious cell carcinoma and unclassified renal cell carcinoma, further dividing the collecting duct carcinoma into Bellini collecting duct carcinoma and medullary carcinoma, in addition to adding multifocal cystic renal cell carcinoma, Xp11 translocation renal carcinoma, neuroblastoma-associated carcinoma, mucinous tubular and spindle cell carcinoma subtypes were added.
The granular cell carcinoma in the traditional classification was also classified as a low-differentiated (high-graded) clear cell carcinoma, and the proportion of the sarcomatoid carcinoma component in the tumor tissue was described for each subtype. The 2004 WHO pathologic classification criteria for renal cell carcinoma [14] (recommended grading B) are recommended.
(iii) Histological grading
The most commonly used classification used in the past was the 1982 Fuhrman four-grade classification [15]. 1997 WHO recommended combining grades I and II of the Fuhrman classification into one grade, i.e., highly differentiated, grade III as moderately differentiated, and grade IV as poorly differentiated or undifferentiated. The grading criteria of classifying renal cancer into highly differentiated, moderately differentiated, and poorly differentiated (undifferentiated) are recommended [11] (recommended grading B).
(iv) Staging
The TNM staging and staging combinations of the 2002 AJCC (Tables-2, -3) are recommended [16] (recommended grading B). 2002 AJCC pathological staging requires that the number of detected lymph nodes should include at least 8 resected lymph nodes when evaluating N staging, and if all lymph node pathological findings are negative or only 1 is positive, and the number of detected lymph nodes is <8, then it cannot be evaluated as N0 or N1. However, if the pathology determines the number of lymph node metastases ≥ 2, the N stage is not affected by the number of detected lymph nodes and is determined as N2.
III. Clinical manifestations
At present, the clinical occurrence rate of the “triad of kidney cancer”, which used to be classical hematuria, lumbar pain and abdominal mass, is less than 15%, and patients with these symptoms are often diagnosed at an advanced stage [1,10]. The detection rate of asymptomatic kidney cancer has been increasing year by year, with the rate reported in domestic literature from 1995 to 2005 ranging from 13.8% to 48.9%, with an average of 33%, and overseas reports as high as 50%.
The symptoms of paraneoplastic syndrome are hypertension, anemia, weight loss, cachexia, fever, erythrocytosis, abnormal liver function, hypercalcemia, hyperglycemia, increased sedimentation, neuromuscular lesions, amyloidosis, overflow, abnormal coagulation mechanism, etc. 30% of the patients have metastatic renal cancer and may be seen for symptoms such as bone pain, fracture, cough and hemoptysis due to tumor metastasis. .
IV. Diagnosis
The clinical diagnosis of kidney cancer mainly relies on imaging examination. Laboratory examination is used as an evaluation index for preoperative general condition, liver and kidney function as well as prognosis, while pathological examination is required for confirmation of diagnosis.
⒈ must include laboratory tests urea nitrogen, creatinine, liver function, complete blood count, hemoglobin, blood calcium, blood glucose, blood sedimentation, alkaline phosphatase and lactate dehydrogenase (recommended grade C).
Imaging tests that must be included in the PAK Abdominal ultrasound or color Doppler ultrasound, chest X-ray (frontal and lateral), abdominal CT plain and enhanced scan (for those with negative iodine allergy test and no relevant contraindications). Abdominal CT plain and enhanced scans and chest X-ray are the main basis for preoperative clinical staging (recommended grading A).
The optional imaging examinations are: abdominal plain film: it can help to select the surgical incision for open surgery; nuclear nephrography or IVU examination indications: those who have not performed CT-enhanced scan and cannot evaluate the contralateral renal function; nuclear bone imaging indications.
① with corresponding bone symptoms;
②High alkaline phosphatase;
③Patients with clinical stage ≥ III (evidence level Ⅰb);
Indications for CT scan of the chest
①Suspicious nodules on chest x-ray;
Patients with clinical stage ≥ III (Evidence Level Ib); MRI and CT scans of the head: patients with headache or corresponding neurological symptoms (Evidence Level Ib); MRI scans of the abdomen: patients with renal insufficiency, ultrasound or CT examinations suggesting inferior vena cava tumor thrombosis (Evidence Level Ib).
Singed imaging options for hospitals with the following facilities and for patients with good financial conditions Positron emission tomography (PET) or PET-CT is expensive and is used to detect distant metastases and to evaluate the efficacy of chemotherapy, cytokine therapy, molecular targeted therapy or radiotherapy.
Tests not recommended with caution Renal puncture biopsy and renal angiography have limited diagnostic value for kidney cancer (level of evidence IIIa) and are not recommended as routine tests for patients with kidney cancer. For patients with small tumors whose nature is difficult to be determined by imaging diagnosis, they can choose to undergo kidney unit preservation surgery or regular (1-3 months) follow-up examinations.
For patients with advanced renal tumors that cannot be treated surgically and need chemotherapy or other treatments, kidney aspiration biopsy can be chosen to obtain pathological diagnosis before treatment in order to clarify the diagnosis. For patients who need palliative renal artery embolization or preserved renal unit surgery, renal angiography can be chosen to understand the distribution of renal vessels and tumor vascularity.
V. Treatment
Clinical stage grouping (cTNM) is performed based on the results of comprehensive imaging examination, and treatment principles are initially formulated according to the cTNM stage. If there is any deviation between pTNM and cTNM, the postoperative treatment plan will be revised according to the pTNM staging results.
(i) Treatment of limited renal cancer
Surgery is the treatment of choice for limited renal cancer. When radical nephrectomy is performed, the addition of regional or expanded lymph node dissection is not recommended [20] (level of evidence Ib, recommendation grade A).
The ⒈ radical nephrectomy is a recognized potential cure for renal cancer. Classical radical nephrectomy includes the perinephric fascia, perinephric fat, the affected kidney, the ipsilateral adrenal gland, the lymph nodes adjacent to the abdominal aorta or inferior vena cava from the foot of the diaphragm to the bifurcation of the abdominal aorta, and the ureter above the bifurcation of the iliac vessels.
Over the past 40 years, the concept of using classical radical nephrectomy for kidney cancer has partially changed, especially in terms of the extent of surgical resection (e.g., selection of appropriate cases for performing ipsilateral adrenal gland-preserving radical nephrectomy, kidney unit-preserving surgery) has reached a consensus, and the treatment modality is no longer a single open surgery (e.g., laparoscopic surgery, minimally invasive treatment).
The modern view is that radical nephrectomy with preservation of the ipsilateral adrenal gland is an option for those who meet the following 4 conditions (level of evidence IIIa).
① Clinical stage I or II;
②Tumor located in the middle or lower part of the kidney;
③Tumor <8cm;
④Preoperative CT showed normal adrenal gland. However, in such cases, if the ipsilateral adrenal gland is found to be abnormal during surgery, the ipsilateral adrenal gland should be removed. Radical nephrectomy can be performed through open surgery or laparoscopic surgery. Open surgery can be performed with either a transabdominal or transumbilical approach, and there is no evidence to suggest which approach is more advantageous. Radical nephrectomy has a mortality rate of approximately 2% and a local recurrence rate of 1% to 2%. Routine renal artery embolization prior to radical nephrectomy is not recommended (recommended classification B).
Nephron sparing surgery (NSS) is recommended for all indications, and the efficacy of NSS is the same as that of radical nephrectomy (Evidence level IIIa). The thickness of the margin does not affect the tumor recurrence rate (evidence level IIIa), and tumor enucleation is not recommended for the treatment of sporadic renal cancer.
NSS can be performed by open surgery or laparoscopic surgery. The mortality rate of NSS is 1%-2%.
Indications for NSS: Kidney cancer occurs in patients with anatomical or functional isolated kidney, radical nephrectomy will lead to renal insufficiency or uremia, such as congenital isolated kidney, contralateral renal insufficiency or non-functional person, and bilateral kidney cancer.
Relative indications for NSS: patients with certain benign diseases in the contralateral kidney of kidney cancer, such as kidney stones, chronic pyelonephritis or other diseases that may lead to deterioration of kidney function (such as hypertension, diabetes, renal artery stenosis, etc.).
The indications and relative indications for NSS are not specifically limited to renal tumor size.
Selectable indications for NSS: clinical stage T1a (tumor ≤ 4 cm), tumor located in the periphery of the kidney, solitary renal cancer, and normal contralateral renal function can choose to perform NSS (evidence level IIb).
🙒 Laparoscopic surgery Surgical procedures include laparoscopic radical nephrectomy and laparoscopic partial nephrectomy. The surgical routes are divided into transabdominal, retroperitoneal and hand-assisted laparoscopic. The scope and standard of resection are the same as open surgery. Laparoscopic surgery is suitable for patients with limited renal cancer whose tumors are confined to the renal peritoneum, without surrounding tissue invasion and without lymphatic metastasis and venous tumor thrombosis, and its efficacy is comparable to that of open surgery (level of evidence IIIa). Laparoscopic surgery is also associated with some mortality.
Singing minimally invasive treatments Radio-frequency ablation (RFA), cryoablation, and high-intensity focused ultrasound (HIFU) can be used to treat patients with small tumors that are not suitable for surgery. The results of studies at the level of evidence are not yet available, and the long-term efficacy is uncertain. These three minimally invasive treatment methods are not recommended as the first choice of treatment for limited renal cancer.
Indications for minimally invasive treatment: Patients with renal cancer who are not suitable for open surgery, need to preserve the function of renal units as much as possible, have contraindications to general anesthesia, have renal insufficiency, and have tumors with maximum diameter <4 cm and located in the periphery of the kidney.
Careful renal artery embolization can be used as a palliative treatment for patients who cannot tolerate surgical treatment. Preoperative renal artery embolization may be beneficial in reducing intraoperative bleeding and increasing the chance of radical surgery, but there is no evidence-based medical grade I-III evidence to support this. Renal artery embolization can cause complications such as puncture site hematoma, post-embolization infarction syndrome, and acute pulmonary infarction. Routine application of renal artery embolization before surgery for limited renal cancer is not recommended.
Select postoperative adjuvant therapy There is no recommended adjuvant therapy after surgery for limited renal cancer. pT1a renal cancer has a 5-year survival rate of more than 90%, so adjuvant therapy is not recommended after surgery. pT1b~pT2 renal cancer has metastasis in about 20%~30% of patients within 1-2 years after surgery, so adjuvant radiotherapy and chemotherapy after surgery cannot reduce the recurrence rate and metastasis rate, so adjuvant radiotherapy and chemotherapy are not recommended routinely after surgery. Adjuvant radiotherapy and chemotherapy are not recommended. It is not recommended to apply adjuvant radiotherapy and chemotherapy routinely after surgery. Effective adjuvant treatment options have to be explored.
(ii) Treatment of locally progressive renal cancer
The preferred treatment for locally progressive renal cancer is radical nephrectomy, while the metastatic lymph nodes or hemangioma plugs need to be resected or not according to the extent of the lesion, the patient’s physical condition and other factors. There is no standard postoperative adjuvant treatment option.
Early studies advocated regional or expanded lymph node dissection, but recent findings suggest that regional or expanded lymph node dissection is only useful for determining tumor stage in postoperative lymph node-negative patients (Level of Evidence Ib); since lymph node-positive patients mostly have distant metastases and require combined medical therapy after surgery, regional or expanded lymph node dissection is only beneficial for a small number of patients. The regional or expanded lymph node dissection is beneficial only for a small proportion of patients.
Most scholars believe that the TNM stage, the length of the thrombus, and whether the thrombus infiltrates the vena cava wall are directly related to the prognosis. Removal of renal or/and vena cava tumor emboli is recommended for patients with a clinical stage of T3bN0M0. This procedure is not recommended for patients with CT or MRI scans suggesting invasion of the vena cava wall or with lymph node metastases or distant metastases. The mortality rate for removal of renal or vena cava aneurysms is approximately 9%.
There is no uniform classification of venous aneurysm emboli. The Mayo Clinic’s five-grade classification is recommended: Grade 0: the aneurysm is confined to the renal vein; Grade I: the aneurysm invades the inferior vena cava and the tip of the aneurysm is ≤2 cm from the opening of the renal vein; Grade II: the aneurysm invades the inferior vena cava below the level of the hepatic vein and the tip of the aneurysm is >2 cm from the opening of the renal vein; Grade III: the aneurysm grows to the level of the inferior vena cava in the liver and below the level of the diaphragm; Grade IV: the aneurysm grows to the level of the inferior vena cava in the liver and below the level of the diaphragm. Grade IV: the tumor embolus invades into the inferior vena cava above the diaphragm.
3. Postoperative adjuvant therapy There is no standard adjuvant therapy after radical nephrectomy for locally progressive renal cancer. Kidney cancer is a tumor insensitive to radiation, so radiotherapy alone cannot achieve better results. Preoperative radiotherapy is generally rarely used, and postoperative radiotherapy is not recommended for the tumor bed area routinely, but intraoperative or postoperative radiotherapy can be chosen for stage III kidney cancer that cannot be completely resected or refer to the treatment of metastatic kidney cancer.
(iii) Treatment of metastatic kidney cancer (clinical stage IV)
Metastatic renal cell carcinoma (mRCC) should be treated with a comprehensive treatment based on medical therapy. Surgery is mainly an adjuvant treatment for metastatic renal cell carcinoma, and very few patients can achieve longer-term survival through surgery.
⒈ Surgical treatment
(1) Surgical treatment of primary renal lesions: Surgery should be preferred for patients with good physical status and low risk factors. Removal of primary renal lesions can improve the efficacy of IFN-α or (and) IL-2 in the treatment of metastatic renal cancer (level of evidence Ⅰb). Palliative nephrectomy and renal artery embolization can be chosen for patients with severe hematuria, pain and other symptoms caused by renal tumors to relieve symptoms and improve survival quality. The surgical mortality rate of metastatic renal cancer is 2%~11%.
(2) Surgical treatment of metastases: For patients with isolated metastases after radical nephrectomy and patients with kidney cancer with isolated metastases and good behavioral status, surgical treatment can be chosen. For patients with concomitant metastases, it may be performed simultaneously with renal surgery or in stages depending on the patient’s physical condition [65].
Treatment principles of bone metastases from renal cancer: clinical findings show that bone metastases account for 20%-25% of the metastatic sites caused by RCC. And autopsy found that in patients who died from RCC, bone metastasis rate was 40%. Bone metastases of kidney cancer are mostly accompanied by visceral metastases, and the prognosis is poor. It is appropriate to adopt a comprehensive treatment mainly based on internal medicine, and the most effective treatment for bone metastases is surgical resection of metastases. For patients with resectable primary lesions or resected primary lesions with a single bone metastasis (not combined with other metastatic lesions), aggressive surgical treatment should be performed. Patients with bone metastases with weight-bearing bones with fracture risk should undergo prophylactic internal fixation to avoid fracture. Orthopedic surgery should be the first option for patients who have developed pathologic fractures or compression symptoms of the spinal cord that meet the following 3 conditions
①The patient is expected to survive >3 months;
②Good physical status;
③Postoperative can improve the patient’s quality of life and help to receive radiotherapy, chemotherapy and care.
⒉ Internal therapy Over the past 20 years, randomized controlled studies failed to prove the effectiveness of LAK cells, TIL cells, and IFN-γ in the treatment of metastatic kidney cancer. Since the 1990s, medium- and high-dose IFN-α or (and) IL-2 have been used as the standard first-line treatment regimen for metastatic kidney cancer, with an efficiency of about 15%. Numerous clinical studies have confirmed the effectiveness of medium- and high-dose IFN-α in patients with low- and intermediate-risk metastatic renal clear cell carcinoma (level of evidence Ⅰb). Combined with the specific situation in China, medium- and high-dose IFN-α is recommended as the basic drug for the treatment of metastatic renal clear cell carcinoma (recommendation classification A).
Since 2006, the NCCN and EAU have included molecularly targeted therapeutic agents (sorafenib, sunitinib, Temsirolimus, bevacizumab combined with interferon-α) as first and second-line therapeutic agents for metastatic renal cancer (Level of Evidence Ib).
(1) Cytokine therapy
1. IL-2
A phase III clinical study of single-agent recombinant humanized IL-2 (Proleukin) administered subcutaneously for the treatment of metastatic kidney cancer was conducted in China between July 2004 and June 2006 [73] in an open, multicenter, uncontrolled clinical study. Forty-one patients with pathologically confirmed metastatic renal cancer were enrolled. They received IL-2 9MIU Q12h d1-5 in the first week, 9MIU Q12h d1-2 in the second three weeks, 9MIU Qd d3-5, and repeated after a one-week break.
Five cases were discharged due to toxic side effects, 36 cases could be evaluated for objective efficacy, 0 CR, 7 PR (19.4%), 16 SD (44.4%), 13 PD (36.1%), 63.9% disease control rate, median progression-free survival (PFS) not yet reached, but more than 12 months.
Serious adverse reactions (≥ grade 3) were rare and mainly manifested as mild to moderate adverse reactions of multi-system grade 1-2, namely fatigue (100%), fever (82.9%), subcutaneous nodules at the injection site (68.3%), rash/desquamation (43.9%), diarrhea (24.4%), vomiting (17.1%), elevated transaminases (39%), elevated blood creatinine (39%), elevated Urea nitrogen (22%), anemia (12.2%), dyspnea (12.2%), etc. Most of the adverse effects were reversible.
The results of the study showed that the efficacy of low to medium dose IL-2 in the treatment of metastatic kidney cancer in Chinese was the same as that reported abroad, and it could prolong the survival of patients, and the adverse effects were mainly mild to moderate and tolerated by patients.
Recommended dose of IL-2: 18 MIU/d IH. 5d/W × 5~8 weeks (recommended grade B)
2.IFN-α
Recommended therapeutic dose of IFN-α (recommended grade A): IFN-α: 9 MIU per dose, i.m. or IH. 3 times/week for 12 weeks. The dose can be gradually increased from 3MIU per dose, 3MIU per dose in the first week, 6MIU per dose in the second week, and 9MIU per dose in the third week onwards. blood tests should be performed once a week during treatment, and liver function should be checked once a month. white blood cell count <3×109/L or abnormal liver function and other serious adverse reactions should be stopped and treatment should be continued after recovery. If the patient cannot tolerate the dose of 9 MIU per dose, the dose should be reduced to 6 MIU per dose or even 3 MIU per dose.
Although IFN-α combined with IL-2 may improve the efficiency of treatment for mRCC, it does not improve PFS.
(2) Molecular targeted drug therapy
A study on the safety and efficacy analysis of sorafenib for the treatment of Chinese patients with advanced renal cell carcinoma was conducted between April 2006 and August 2007. The study was an open, multicenter, uncontrolled clinical study that enrolled 62 patients with advanced renal cancer (who had received at least one previous systemic treatment regimen). 5 patients withdrew from the trial due to side effects, and 57 patients were evaluable.
The median age of the entire group was 53 years, 43 men received sorafenib 400 mg bid for at least 2 months. Results: 1 CR (1.75%), 11 PR (19.3%), 36 SD (63.16%), disease control rate of 84.21%, median PFS time of 41 weeks, median overall survival (overall survival, OS) not reached. grade 3-4 side effects included skin reactions in hands and feet (16.1%), diarrhea (6.45%). Hypertension (12.9%), leukopenia (3.2%), and hyperuricemia (9.7%). The disease control rate (CR+PR+SD) was consistent with that reported in a foreign phase III randomized double-blind controlled study of sorafenib (TARGET trial).
Recommended Sorafenib dosage 400mg bid/day (recommended classification B)
Clinical experience in China in the last 2 years showed that sorafenib increment (600mg~800mg bid/day) [76] or sorafenib (400mg bid) combined with IFN-α (3MIU i.m. or IH. 5 times a week) [77] regimen could improve the efficiency of treatment of advanced renal cancer (evidence level IIIb), but the associated incidence of toxic side effects was higher than that of sorafenib 400mg bid/day regimen.
(3) Chemotherapy
The main chemotherapeutic agents used to treat mRCC are gemcitabine, fluorouracil (5-FU) or capecitabine, cisplatin. Gemcitabine combined with fluorouracil or capecitabine is mainly used for mRCC with clear cell predominant type; gemcitabine combined with cisplatin is mainly used for mRCC with non-clear cell predominant type; gemcitabine combined with cisplatin is mainly used for mRCC with non-clear cell predominant type; cisplatin is mainly used for mRCC with non-clear cell predominant type; cisplatin is mainly used for mRCC with clear cell predominant type. If the tumor tissue contains sarcoma-like components, the chemotherapy regimen can be combined with adriamycin. The efficiency of chemotherapy is about 10-15%. Chemotherapy in combination with IFN-α or (and) IL-2 has also not shown an advantage.
Chemotherapy is recommended as the first-line treatment option for patients with metastatic non-clear cell carcinoma (level of evidence III) [3].
The new Rating of Effectiveness in Solid Tumors (RECIST) [78] is recommended to evaluate the efficacy of immunotherapy or chemotherapy for kidney cancer.
Radiotherapy For patients with local tumor bed recurrence, regional or distant lymph node metastasis, bone or lung metastasis, palliative radiotherapy can achieve pain relief and improve survival quality. Stereotactic radiotherapy (γ-knife, X-knife, 3D conformal radiotherapy, conformal intensity modulated radiotherapy) developed in recent years can play a better control role for recurrent or metastatic lesions, but it should be carried out on the basis of effective systemic treatment.
Treatment principle of brain metastasis of kidney cancer: autopsy results show that 15% of patients who died of kidney cancer had brain metastasis, and 60%~75% of patients with brain metastasis had clinical symptoms or signs, mainly headache (40%~50%), focal neurological symptoms (30%~40%) and epilepsy (15%~20%) and other symptoms and signs.
The treatment of patients with brain metastasis of kidney cancer should be a comprehensive treatment mainly based on internal medicine, but corticosteroids should be added for patients with cerebral edema symptoms; for patients with brain metastasis accompanied by metastasis from other sites, hormone and brain radiotherapy are important means of treatment. For patients with good behavioral status and simple brain metastases, brain surgery (brain metastases ≤3) or stereotactic radiotherapy (maximum diameter of brain metastases ≤3~3.5 cm) or brain surgery combined with radiotherapy are preferred.
Sixth, surgical complications
Whether it is open surgery or laparoscopic surgery for kidney cancer, complications such as bleeding, infection, perirenal organ damage (liver, spleen, pancreas, gastrointestinal tract), pleural injury, pulmonary embolism, renal failure, liver failure and urinary leakage may occur, which should be prevented and handled appropriately. Severe cases can lead to patient death. Patients and their families should be informed of the risks and possible complications of surgery before surgery.
VII. Prognostic influencing factors
The most important factor affecting the prognosis of kidney cancer is the pathological stage. In addition, factors such as histological grading, patients’ behavioral status score, symptoms, whether there is tissue necrosis in the tumor, abnormalities and changes of some biochemical indicators are also related to the prognosis of kidney cancer. It was previously believed that the prognosis of renal cancer was related to the histological type, and the prognosis of renal papillary adenocarcinoma and suspicious cell carcinoma was better than that of clear cell carcinoma; the prognosis of renal papillary adenocarcinoma type I was better than that of type II; the prognosis of collecting duct carcinoma was worse than that of clear cell carcinoma.
However, the results of a multicenter study on cell subtypes and prognosis of RCC patients [83] showed that histologic subtypes were not independent prognostic factors compared with TNM stage, cancer grading and fitness status score, and there was no significant difference in prognosis among subtypes with the same stage and grading of tumors (level of evidence IIa). However, the response rate of mRCC to cytokine therapy varied among histologic types, with approximately 10% to 20% in patients with clear cell carcinoma type and poor cytokine therapy in renal papillary carcinoma and suspicious cell carcinoma. Risk factors for the prognosis of metastatic renal cancer.