Clinicopathological characteristics of 163 patients with pT3aN0M0 RCC and subgroup comparison of variables according to the tumor size (cutoff of 7cm).

<p>Clinicopathological characteristics of 163 patients with pT3aN0M0 RCC and subgroup comparison of variables according to the tumor size (cutoff of 7cm).</p

Influence of tumor size on oncological outcomes of pathological T3aN0M0 renal cell carcinoma treated by radical nephrectomy

<div><p>Objective</p><p>To evaluate the prognostic significance of tumor size in pathological T3aN0M0 renal cell carcinoma (RCC) treated by radical nephrectomy.</p><p>Materials and methods</p><p>Patients who underwent radical nephrectomy for sporadic RCC with pathological T3aN0M0 RCC at our institution between January 2006 and June 2015 were identified. The entire cohort was divided into two groups according to the cutoff of tumor size obtained from receiver operating characteristic (ROC) curve. Clinicopathological variables were retrospectively collected and compared. Kaplan-Meier analysis and multivariate Cox regression were conducted to evaluate the effect of tumor size on survival outcomes.</p><p>Results</p><p>163 pT3aN0M0 RCC patients were included with a median follow-up period of 31 months. The optimal cutoff for tumor size was 7 cm according to the ROC curve. 90 cases (55.2%) presented tumors which measured 7 cm or less, and 73 cases (44.8%) showed tumor size greater than 7 cm. Patients with larger tumors tended to exhibit higher rates of symptoms and higher Fuhrman grades; they also indicated more necrosis features, and were more likely to invade the collecting system and renal vein. Compared with patients who exhibited tumor size of≤7 cm, those with tumor size>7 cm were associated with shorter estimated five-year cancer-specific survival (CSS, 46.6% versus 75.0%, <i>P</i> = 0.003) and five-year recurrence-free survival (RFS, 35.6% versus 62.7%, <i>P</i> = 0.011). Multivariate Cox analysis revealed that tumor size was retained as an independent factor for CSS (HR = 2.506, 95% CI 1.169–5.373, <i>P</i> = 0.018).</p><p>Conclusions</p><p>The tumor size significantly affected the survival outcomes of pT3aN0M0 RCC treated by radical nephrectomy, and a cutoff size of 7 cm can help enhance the prognostic discrimination. Thus, the tumor size may be considered in the future TNM classification of stage pT3a.</p></div

Receiver operating characteristic curves were used to identify the optimal cutoff value of tumor size predicting survival.

<p>(A) cancer-specific survival and (B) recurrence-free survival.</p

Kaplan–Meier analysis of survival stratified by tumor size with a cutoff of 7 cm.

<p>(A) cancer-specific survival and (B) recurrence-free survival.</p

Univariate and multivariate Cox regression analysis of clinicaopathological variables for cancer-specific survival.

<p>Univariate and multivariate Cox regression analysis of clinicaopathological variables for cancer-specific survival.</p

Image_7_A two-sample mendelian randomization analysis excludes causal relationships between non-alcoholic fatty liver disease and kidney stones.tif

ObjectivesNon-alcoholic fatty liver disease (NAFLD) has been linked to an increased risk of kidney stones in prior observational studies, However, the results are inconsistent, and the causality remains to be established. We aimed to investigate the potential causal relationship between NAFLD and kidney stones using two-sample Mendelian randomization (MR).MethodsGenetic instruments were used as proxies for NAFLD. Summary-level data for the associations of exposure-associated SNPs with kidney stones were obtained from the UK Biobank study (6536 cases and 388,508 controls) and the FinnGen consortium (9713 cases and 366,693 non-cases). MR methods were conducted, including inverse variance weighted method (IVW), MR-Egger, weighted median, and MR-PRESSO. MR-Egger Regression Intercept and Cochran’s Q test were used to assess the directional pleiotropy and heterogeneity.ResultscALT-associated NAFLD did not exhibit an association with kidney stones in the Inverse variance weighted (IVW) methods, in both the FinnGen consortium (OR: 1.02, 95%CI: 0.94-1.11, p = 0.632) and the UKBB study (OR: 1.000, 95%CI: 0.998-1.002, p = 0.852). The results were consistent in European ancestry (FinnGen OR: 1.05, 95%CI: 0.98-1.14, p = 0.144, UKBB OR: 1.000, 95%CI: 0.998-1.002, p = 0.859). IVW MR analysis also did not reveal a significant causal relationship between NAFLD and the risk of kidney stone for the other three NAFLD-related traits, including imaging-based, biopsy-confirmed NAFLD, and more stringent biopsy-confirmed NAFLD. The results remained consistent and robust in the sensitivity analysis.ConclusionsThe MR study did not provide sufficient evidence to support the causal associations of NAFLD with kidney stones.</p

Image_8_A two-sample mendelian randomization analysis excludes causal relationships between non-alcoholic fatty liver disease and kidney stones.tif

ObjectivesNon-alcoholic fatty liver disease (NAFLD) has been linked to an increased risk of kidney stones in prior observational studies, However, the results are inconsistent, and the causality remains to be established. We aimed to investigate the potential causal relationship between NAFLD and kidney stones using two-sample Mendelian randomization (MR).MethodsGenetic instruments were used as proxies for NAFLD. Summary-level data for the associations of exposure-associated SNPs with kidney stones were obtained from the UK Biobank study (6536 cases and 388,508 controls) and the FinnGen consortium (9713 cases and 366,693 non-cases). MR methods were conducted, including inverse variance weighted method (IVW), MR-Egger, weighted median, and MR-PRESSO. MR-Egger Regression Intercept and Cochran’s Q test were used to assess the directional pleiotropy and heterogeneity.ResultscALT-associated NAFLD did not exhibit an association with kidney stones in the Inverse variance weighted (IVW) methods, in both the FinnGen consortium (OR: 1.02, 95%CI: 0.94-1.11, p = 0.632) and the UKBB study (OR: 1.000, 95%CI: 0.998-1.002, p = 0.852). The results were consistent in European ancestry (FinnGen OR: 1.05, 95%CI: 0.98-1.14, p = 0.144, UKBB OR: 1.000, 95%CI: 0.998-1.002, p = 0.859). IVW MR analysis also did not reveal a significant causal relationship between NAFLD and the risk of kidney stone for the other three NAFLD-related traits, including imaging-based, biopsy-confirmed NAFLD, and more stringent biopsy-confirmed NAFLD. The results remained consistent and robust in the sensitivity analysis.ConclusionsThe MR study did not provide sufficient evidence to support the causal associations of NAFLD with kidney stones.</p

Image_4_A two-sample mendelian randomization analysis excludes causal relationships between non-alcoholic fatty liver disease and kidney stones.tif

ObjectivesNon-alcoholic fatty liver disease (NAFLD) has been linked to an increased risk of kidney stones in prior observational studies, However, the results are inconsistent, and the causality remains to be established. We aimed to investigate the potential causal relationship between NAFLD and kidney stones using two-sample Mendelian randomization (MR).MethodsGenetic instruments were used as proxies for NAFLD. Summary-level data for the associations of exposure-associated SNPs with kidney stones were obtained from the UK Biobank study (6536 cases and 388,508 controls) and the FinnGen consortium (9713 cases and 366,693 non-cases). MR methods were conducted, including inverse variance weighted method (IVW), MR-Egger, weighted median, and MR-PRESSO. MR-Egger Regression Intercept and Cochran’s Q test were used to assess the directional pleiotropy and heterogeneity.ResultscALT-associated NAFLD did not exhibit an association with kidney stones in the Inverse variance weighted (IVW) methods, in both the FinnGen consortium (OR: 1.02, 95%CI: 0.94-1.11, p = 0.632) and the UKBB study (OR: 1.000, 95%CI: 0.998-1.002, p = 0.852). The results were consistent in European ancestry (FinnGen OR: 1.05, 95%CI: 0.98-1.14, p = 0.144, UKBB OR: 1.000, 95%CI: 0.998-1.002, p = 0.859). IVW MR analysis also did not reveal a significant causal relationship between NAFLD and the risk of kidney stone for the other three NAFLD-related traits, including imaging-based, biopsy-confirmed NAFLD, and more stringent biopsy-confirmed NAFLD. The results remained consistent and robust in the sensitivity analysis.ConclusionsThe MR study did not provide sufficient evidence to support the causal associations of NAFLD with kidney stones.</p

Image_3_A two-sample mendelian randomization analysis excludes causal relationships between non-alcoholic fatty liver disease and kidney stones.tif

ObjectivesNon-alcoholic fatty liver disease (NAFLD) has been linked to an increased risk of kidney stones in prior observational studies, However, the results are inconsistent, and the causality remains to be established. We aimed to investigate the potential causal relationship between NAFLD and kidney stones using two-sample Mendelian randomization (MR).MethodsGenetic instruments were used as proxies for NAFLD. Summary-level data for the associations of exposure-associated SNPs with kidney stones were obtained from the UK Biobank study (6536 cases and 388,508 controls) and the FinnGen consortium (9713 cases and 366,693 non-cases). MR methods were conducted, including inverse variance weighted method (IVW), MR-Egger, weighted median, and MR-PRESSO. MR-Egger Regression Intercept and Cochran’s Q test were used to assess the directional pleiotropy and heterogeneity.ResultscALT-associated NAFLD did not exhibit an association with kidney stones in the Inverse variance weighted (IVW) methods, in both the FinnGen consortium (OR: 1.02, 95%CI: 0.94-1.11, p = 0.632) and the UKBB study (OR: 1.000, 95%CI: 0.998-1.002, p = 0.852). The results were consistent in European ancestry (FinnGen OR: 1.05, 95%CI: 0.98-1.14, p = 0.144, UKBB OR: 1.000, 95%CI: 0.998-1.002, p = 0.859). IVW MR analysis also did not reveal a significant causal relationship between NAFLD and the risk of kidney stone for the other three NAFLD-related traits, including imaging-based, biopsy-confirmed NAFLD, and more stringent biopsy-confirmed NAFLD. The results remained consistent and robust in the sensitivity analysis.ConclusionsThe MR study did not provide sufficient evidence to support the causal associations of NAFLD with kidney stones.</p

Image_10_A two-sample mendelian randomization analysis excludes causal relationships between non-alcoholic fatty liver disease and kidney stones.tif

ObjectivesNon-alcoholic fatty liver disease (NAFLD) has been linked to an increased risk of kidney stones in prior observational studies, However, the results are inconsistent, and the causality remains to be established. We aimed to investigate the potential causal relationship between NAFLD and kidney stones using two-sample Mendelian randomization (MR).MethodsGenetic instruments were used as proxies for NAFLD. Summary-level data for the associations of exposure-associated SNPs with kidney stones were obtained from the UK Biobank study (6536 cases and 388,508 controls) and the FinnGen consortium (9713 cases and 366,693 non-cases). MR methods were conducted, including inverse variance weighted method (IVW), MR-Egger, weighted median, and MR-PRESSO. MR-Egger Regression Intercept and Cochran’s Q test were used to assess the directional pleiotropy and heterogeneity.ResultscALT-associated NAFLD did not exhibit an association with kidney stones in the Inverse variance weighted (IVW) methods, in both the FinnGen consortium (OR: 1.02, 95%CI: 0.94-1.11, p = 0.632) and the UKBB study (OR: 1.000, 95%CI: 0.998-1.002, p = 0.852). The results were consistent in European ancestry (FinnGen OR: 1.05, 95%CI: 0.98-1.14, p = 0.144, UKBB OR: 1.000, 95%CI: 0.998-1.002, p = 0.859). IVW MR analysis also did not reveal a significant causal relationship between NAFLD and the risk of kidney stone for the other three NAFLD-related traits, including imaging-based, biopsy-confirmed NAFLD, and more stringent biopsy-confirmed NAFLD. The results remained consistent and robust in the sensitivity analysis.ConclusionsThe MR study did not provide sufficient evidence to support the causal associations of NAFLD with kidney stones.</p