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Background: Recently published guidelines on the medical management of renal stone disease did not address relevant topics in the field of idiopathic calcium nephrolithiasis, which are important also for clinical research. Design: A steering committee identified 27 questions, which were proposed to a faculty of 44 experts in nephrolithiasis and allied fields. A systematic review of the literature was conducted and 5216 potentially relevant articles were selected; from these, 407 articles were deemed to provide useful scientific information. The Faculty, divided into working groups, analysed the relevant literature. Preliminary statements developed by each group were exhaustively discussed in plenary sessions and approved. Results: Statements were developed to inform clinicians on the identification of secondary forms of calcium nephrolithiasis and systemic complications; on the definition of idiopathic calcium nephrolithiasis; on the use of urinary tests of crystallization and of surgical observations during stone treatment in the management of these patients; on the identification of patients warranting preventive measures; on the role of fluid and nutritional measures and of drugs to prevent recurrent episodes of stones; and finally, on the cooperation between the urologist and nephrologist in the renal stone patients. Conclusions: This document has addressed idiopathic calcium nephrolithiasis from the perspective of a disease that can associate with systemic disorders, emphasizing the interplay needed between urologists and nephrologists. It is complementary to the American Urological Association and European Association of Urology guidelines. Future areas for research are identified.

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Item does not contain fulltext, CONTEXT: Advances in basic research will enhance prognosis, diagnosis, and treatment of renal cancer patients. OBJECTIVE: To discuss advances in our understanding of the molecular basis of renal cancer, targeted therapies, renal cancer and immunity, and genetic factors and renal cell carcinoma (RCC). EVIDENCE ACQUISITION: Data on recently published (2005-2011) basic science papers were reviewed. EVIDENCE SYNTHESIS: Advances in basic research have shown that renal cancers can be subdivided based on specific genetic profiles. Now that this molecular basis has been established, it is becoming clear that additional events play a major role in the development of renal cancer. For example, aberrant chromatin remodelling appears to be a main driving force behind tumour progression in clear cell RCC. A large number of potential biomarkers have emerged using various high-throughput platforms, but adequate biomarkers for RCC are still lacking. To bring the potential biomarkers and biomarker profiles to the clinical arena is a major challenge for the field. The introduction of tyrosine kinase inhibitors (TKIs) for therapy has shifted the interest away from immunologic approaches. Nevertheless, a wealth of evidence supports immunotherapy for RCC. Interestingly, studies are now appearing that suggest a combination of TKI and immunotherapy may be beneficial. Thus far, little attention has been paid to patient-specific differences. With high-throughput methods becoming cheaper and with the advances in sequencing possibilities, this situation is expected to change rapidly. CONCLUSIONS: Great strides have been made in the understanding of molecular mechanisms of RCC. This has led this field to the enviable position of having a range of molecularly targeted therapies. Large sequencing efforts are now revealing more and more genes responsible for tumour development and progression, offering new targets for therapy. It is foreseen that through integration of high-throughput platforms

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Item does not contain fulltext, CONTEXT: Although an ever-increasing number of patients are being incidentally diagnosed with small renal masses, there is still a sizable portion of patients with renal cell carcinoma (RCC) who present with locally advanced or metastatic disease. Those with locally advanced disease present a challenge because they may be difficult to distinguish from those with organ-confined disease at the time of diagnosis. However, this distinction is important because they may require a different management strategy. These advanced RCC patients include those with venous tumour thrombi, extracapsular tumour extension, adjacent organ involvement, as well as nodal disease. EVIDENCE ACQUISITION: A thorough literature search of the following terms was undertaken: advanced renal cell carcinoma, renal cell carcinoma venous tumour thrombi, renal cell carcinoma extra-capsular extension, renal cell carcinoma nodal metastasis, and locally recurrent renal cell carcinoma. An international expert panel convened by the International Consultation on Urologic Diseases and the European Association of Urology reviewed these articles. EVIDENCE SYNTHESIS: Review of the available literature allowed for assessment of the level of evidence for the diagnosis, management, and therapy of locally advanced RCC with the ultimate goal of providing a synthesis of this information with a consensus statement from leaders in the field. CONCLUSIONS: Despite the advances in prognostic markers and targeted molecular therapies for RCC, currently the only curative treatment for locally advanced RCC is aggressive surgical resection.

Item does not contain fulltext, CONTEXT: Advances in basic research will enhance prognosis, diagnosis, and treatment of renal cancer patients. OBJECTIVE: To discuss advances in our understanding of the molecular basis of renal cancer, targeted therapies, renal cancer and immunity, and genetic factors and renal cell carcinoma (RCC). EVIDENCE ACQUISITION: Data on recently published (2005-2011) basic science papers were reviewed. EVIDENCE SYNTHESIS: Advances in basic research have shown that renal cancers can be subdivided based on specific genetic profiles. Now that this molecular basis has been established, it is becoming clear that additional events play a major role in the development of renal cancer. For example, aberrant chromatin remodelling appears to be a main driving force behind tumour progression in clear cell RCC. A large number of potential biomarkers have emerged using various high-throughput platforms, but adequate biomarkers for RCC are still lacking. To bring the potential biomarkers and biomarker profiles to the clinical arena is a major challenge for the field. The introduction of tyrosine kinase inhibitors (TKIs) for therapy has shifted the interest away from immunologic approaches. Nevertheless, a wealth of evidence supports immunotherapy for RCC. Interestingly, studies are now appearing that suggest a combination of TKI and immunotherapy may be beneficial. Thus far, little attention has been paid to patient-specific differences. With high-throughput methods becoming cheaper and with the advances in sequencing possibilities, this situation is expected to change rapidly. CONCLUSIONS: Great strides have been made in the understanding of molecular mechanisms of RCC. This has led this field to the enviable position of having a range of molecularly targeted therapies. Large sequencing efforts are now revealing more and more genes responsible for tumour development and progression, offering new targets for therapy. It is foreseen that through integration of high-throughput platforms

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Item does not contain fulltext, CONTEXT: Although an ever-increasing number of patients are being incidentally diagnosed with small renal masses, there is still a sizable portion of patients with renal cell carcinoma (RCC) who present with locally advanced or metastatic disease. Those with locally advanced disease present a challenge because they may be difficult to distinguish from those with organ-confined disease at the time of diagnosis. However, this distinction is important because they may require a different management strategy. These advanced RCC patients include those with venous tumour thrombi, extracapsular tumour extension, adjacent organ involvement, as well as nodal disease. EVIDENCE ACQUISITION: A thorough literature search of the following terms was undertaken: advanced renal cell carcinoma, renal cell carcinoma venous tumour thrombi, renal cell carcinoma extra-capsular extension, renal cell carcinoma nodal metastasis, and locally recurrent renal cell carcinoma. An international expert panel convened by the International Consultation on Urologic Diseases and the European Association of Urology reviewed these articles. EVIDENCE SYNTHESIS: Review of the available literature allowed for assessment of the level of evidence for the diagnosis, management, and therapy of locally advanced RCC with the ultimate goal of providing a synthesis of this information with a consensus statement from leaders in the field. CONCLUSIONS: Despite the advances in prognostic markers and targeted molecular therapies for RCC, currently the only curative treatment for locally advanced RCC is aggressive surgical resection.

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Item does not contain fulltext, CONTEXT: Advances in basic research will enhance prognosis, diagnosis, and treatment of renal cancer patients. OBJECTIVE: To discuss advances in our understanding of the molecular basis of renal cancer, targeted therapies, renal cancer and immunity, and genetic factors and renal cell carcinoma (RCC). EVIDENCE ACQUISITION: Data on recently published (2005-2011) basic science papers were reviewed. EVIDENCE SYNTHESIS: Advances in basic research have shown that renal cancers can be subdivided based on specific genetic profiles. Now that this molecular basis has been established, it is becoming clear that additional events play a major role in the development of renal cancer. For example, aberrant chromatin remodelling appears to be a main driving force behind tumour progression in clear cell RCC. A large number of potential biomarkers have emerged using various high-throughput platforms, but adequate biomarkers for RCC are still lacking. To bring the potential biomarkers and biomarker profiles to the clinical arena is a major challenge for the field. The introduction of tyrosine kinase inhibitors (TKIs) for therapy has shifted the interest away from immunologic approaches. Nevertheless, a wealth of evidence supports immunotherapy for RCC. Interestingly, studies are now appearing that suggest a combination of TKI and immunotherapy may be beneficial. Thus far, little attention has been paid to patient-specific differences. With high-throughput methods becoming cheaper and with the advances in sequencing possibilities, this situation is expected to change rapidly. CONCLUSIONS: Great strides have been made in the understanding of molecular mechanisms of RCC. This has led this field to the enviable position of having a range of molecularly targeted therapies. Large sequencing efforts are now revealing more and more genes responsible for tumour development and progression, offering new targets for therapy. It is foreseen that through integration of high-throughput platforms

Background: Intravesical chemotherapy and bacillus Calmette-Guérin (BCG) reduce the recurrence rate in patients with stage Ta T1 urothelial bladder cancer; however, the benefit of BCG relative to chemotherapy for long-term end points is controversial, especially in intermediate-risk patients. Objective: The aim of the study was to compare the long-term efficacy of BCG and epirubicin. Design, setting, and participants: From January 1992 to February 1997, 957 patients with intermediate- or high-risk stage Ta T1 urothelial bladder cancer were randomized after transurethral resection to one of three treatment groups in the European Organization for Research and Treatment of Cancer Genito-Urinary Group phase 3 trial 30911. Intervention: Patients received six weekly instillations of epirubicin, BCG, or BCG plus isoniazid (INH) followed by three weekly maintenance instillations at months 3, 6, 12, 18, 24, 30, and 36. Measurements: End points were time to recurrence, progression, distant metastases, overall survival, and disease-specific survival. Results and limitations: With 837 eligible patients and a median follow-up of 9.2 yr, time to first recurrence (p < 0.001), distant metastases (p = 0.046), overall survival (p = 0.023), and disease-specific survival (p = 0.026) were significantly longer in the two BCG arms combined as compared with epirubicin; however, there was no difference for progression. Three hundred twenty-three patients with stage T1 or grade 3 tumors were high risk, and the remaining 497 patients were intermediate risk. The observed treatment benefit was at least as large, if not larger, in the intermediate-risk patients compared with the high-risk patients. Conclusions: In patients with intermediate- and high-risk stage Ta and T1 urothelial bladder cancer, intravesical BCG with or without INH is superior to intravesical epirubicin not only for time to first recurrence but also for time to distant metastases, overall survival, and disease-specific surviva

Contains fulltext : 47838.pdf (publisher's version ) (Closed access), Bladder cancer is a heterogeneous disease with a variable natural history. At one end of the spectrum, low-grade Ta tumors have a low progression rate and require initial endoscopic treatment and surveillance but rarely present a threat to the patient. At the other extreme, high-grade tumors have a high malignant potential associated with significant progression and cancer death rates. In the Western world, bladder cancer is the fourth most common malignancy in men and the eighth most common in women. In Europe and the United States, bladder cancer accounts for 5% to 10% of all malignancies in men. The risk of developing bladder cancer at <75 years of age is 2% to 4% for men and 0.5% to 1% in women compared with the risk of lung cancer, for example, which is 8% in men and 2% in women. For the geographic and temporal comparison of bladder cancer incidence, it is crucial to separate the low-grade from the high-grade tumors. In epidemiologic studies on risk factors for bladder cancer, it is important to distinguish the low-grade Ta tumors from high-grade carcinoma in situ (CIS) and tumors >T1. Current studies do not support the routine screening for bladder cancer. However, prospective long-term studies are required to evaluate the benefits of bladder cancer screening, particularly in those at high risk. After assessing all available evidence, the Epidemiology and Diagnosis Committee has made recommendations on various diagnostic issues, including pathologic evaluation, urinary cytology, and imaging studies. Optimal resection techniques, role of repeat transurethral resection in high-grade T1 tumors, random bladder biopsy, and prostatic urethral biopsy are discussed, and appropriate recommendations are made according to the strength of available evidence.

Contains fulltext : 47838.pdf (publisher's version ) (Closed access), Bladder cancer is a heterogeneous disease with a variable natural history. At one end of the spectrum, low-grade Ta tumors have a low progression rate and require initial endoscopic treatment and surveillance but rarely present a threat to the patient. At the other extreme, high-grade tumors have a high malignant potential associated with significant progression and cancer death rates. In the Western world, bladder cancer is the fourth most common malignancy in men and the eighth most common in women. In Europe and the United States, bladder cancer accounts for 5% to 10% of all malignancies in men. The risk of developing bladder cancer at <75 years of age is 2% to 4% for men and 0.5% to 1% in women compared with the risk of lung cancer, for example, which is 8% in men and 2% in women. For the geographic and temporal comparison of bladder cancer incidence, it is crucial to separate the low-grade from the high-grade tumors. In epidemiologic studies on risk factors for bladder cancer, it is important to distinguish the low-grade Ta tumors from high-grade carcinoma in situ (CIS) and tumors >T1. Current studies do not support the routine screening for bladder cancer. However, prospective long-term studies are required to evaluate the benefits of bladder cancer screening, particularly in those at high risk. After assessing all available evidence, the Epidemiology and Diagnosis Committee has made recommendations on various diagnostic issues, including pathologic evaluation, urinary cytology, and imaging studies. Optimal resection techniques, role of repeat transurethral resection in high-grade T1 tumors, random bladder biopsy, and prostatic urethral biopsy are discussed, and appropriate recommendations are made according to the strength of available evidence.

Contains fulltext : 47838.pdf (publisher's version ) (Closed access), Bladder cancer is a heterogeneous disease with a variable natural history. At one end of the spectrum, low-grade Ta tumors have a low progression rate and require initial endoscopic treatment and surveillance but rarely present a threat to the patient. At the other extreme, high-grade tumors have a high malignant potential associated with significant progression and cancer death rates. In the Western world, bladder cancer is the fourth most common malignancy in men and the eighth most common in women. In Europe and the United States, bladder cancer accounts for 5% to 10% of all malignancies in men. The risk of developing bladder cancer at <75 years of age is 2% to 4% for men and 0.5% to 1% in women compared with the risk of lung cancer, for example, which is 8% in men and 2% in women. For the geographic and temporal comparison of bladder cancer incidence, it is crucial to separate the low-grade from the high-grade tumors. In epidemiologic studies on risk factors for bladder cancer, it is important to distinguish the low-grade Ta tumors from high-grade carcinoma in situ (CIS) and tumors >T1. Current studies do not support the routine screening for bladder cancer. However, prospective long-term studies are required to evaluate the benefits of bladder cancer screening, particularly in those at high risk. After assessing all available evidence, the Epidemiology and Diagnosis Committee has made recommendations on various diagnostic issues, including pathologic evaluation, urinary cytology, and imaging studies. Optimal resection techniques, role of repeat transurethral resection in high-grade T1 tumors, random bladder biopsy, and prostatic urethral biopsy are discussed, and appropriate recommendations are made according to the strength of available evidence.

Renal cell carcinoma (RCC), although occurring less frequently than prostate and bladder cancer, is actually the most malignant urologic disease, killing >35% of affected patients. Therefore, investigation of the nature of premalignant lesions of the kidney is a relevant issue. Following the most recent histological classification RCC can be subdivided into four categories: conventional RCC; papillary RCC; chromophobe RCC; and collecting duct carcinoma. In contrast to many genitourinary malignancies, premalignant alterations in the kidney are scarcely described. Intratubular epithelial dysplasia has been recognized as the most common precursor of RCC. In analogy to prostatic intraepithelial neoplasia (PIN), the premalignant lesions of the kidney are described as high or low-grade renal intratubular neoplasia. In contrast, precancerous lesions have been described as part of the von Hippel-Lindau syndrome (VHL) where the evolution from a simple cyst to an atypical cyst with epithelial hyperplasia to cystic or solid conventional-type RCC is well documented. Finally, in the genesis of papillary RCC an adenoma-carcinoma sequence has been recognized with specific genetic changes. There are no data on the epidemiology of premalignant lesions of the kidney, but research into the etiology of RCC has been extended substantially. Familial and genetic factors are well documented in VHL disease, in hereditary papillary RCC, in the tuberous sclerosis complex and in familial RCC. Cigarette smoking and obesity are established risk factors for RCC. Hypertension or its medication has also been associated with an increased risk. Among dietary factors an inverse relation between risk and consumption of vegetables and fruit has been found. Occupational exposure to substances such as asbestos and solvents has been linked to an increased risk of RCC. Specific RCC variants have distinctive chromosome alterations and several genes have been implicated in the development of RCC. Loss of m