Abstract
Changes in circulating adiponectin have been related to the risks of various cancers. However, the association between circulating adiponectin and the risk of renal cell carcinoma has not been fully determined. A meta-analysis was performed to evaluate the relationship between circulating adiponectin and renal cell carcinoma risk. Observational studies that evaluated the association between circulating adiponectin and renal cell carcinoma risk were identified via a systematic search of PubMed and Embase databases. The difference between circulating adiponectin in renal cell carcinoma cases and healthy controls, and the multivariable adjusted association between circulating adiponectin and renal cell carcinoma risk were evaluated. A random effects model was used if significant heterogeneity existed; otherwise a fixed effects model was applied. Eight case-control studies with 2624 renal cell carcinoma cases and 2904 healthy controls were included. Pooled results showed that circulating adiponectin was significantly lower in renal cell carcinoma cases than in healthy controls (mean difference = -1.08 ug/mL; 95% confidence interval (CI) -1.62, -0.54; P < 0.001). Higher circulating adiponectin was independently associated with a significantly lowered risk of renal cell carcinoma (adjusted odds ratio for 1 SD increment of adiponectin = 0.78; 95% CI: 0.63, 0.96; P = 0.02). Subgroup analyses according to characteristics including study design, ethnics of participants, blood samples, numbers of participants, mean ages of participants, and study quality showed consistent results. Lower circulating adiponectin is associated with increased risk of renal cell carcinoma. The potential pathophysiological mechanisms underlying the role of circulating adiponectin in the pathogenesis of renal cell carcinoma deserve further investigation.
Highlights
Renal cell carcinoma (RCC) is one of the most common malignancies in the urological system, and the global incidence of the cancer has risen gradually during the last decade.[1,2] Accumulating evidence suggests that the etiology of RCC is multifactorial,[3] and obesity has been generally considered as a key risk factor of RCC pathogenesis.[4,5] the role of obesity in RCC patients may be complicated.[6]
Whether the difference between adiponectin in RCC cases and healthy controls is independent of study characteristics—such as study design, ethnics of participants, blood samples, numbers of participants, mean ages of participants, and study quality—remain to be determined
The results of the Egger’s regression tests did not indicate significant publication biases (P values for Egger’s regression tests: 0.198 and 0.524). In this meta-analysis of eight case-control studies, we found that the circulating adiponectin was significantly lower in RCC cases than the matched healthy controls
Summary
Renal cell carcinoma (RCC) is one of the most common malignancies in the urological system, and the global incidence of the cancer has risen gradually during the last decade.[1,2] Accumulating evidence suggests that the etiology of RCC is multifactorial,[3] and obesity has been generally considered as a key risk factor of RCC pathogenesis.[4,5] the role of obesity in RCC patients may be complicated.[6]. Methods: Observational studies that evaluated the association between circulating adiponectin and renal cell carcinoma risk were identified via a systematic search of PubMed and Embase databases. Results: Eight case-control studies with 2624 renal cell carcinoma cases and 2904 healthy controls were included. Pooled results showed that circulating adiponectin was significantly lower in renal cell carcinoma cases than in healthy controls (mean difference = −1.08 ug/mL; 95% confidence interval (CI) −1.62, −0.54; P < 0.001). Higher circulating adiponectin was independently associated with a significantly lowered risk of renal cell carcinoma (adjusted odds ratio for 1 SD increment of adiponectin = 0.78; 95% CI: 0.63, 0.96; P = 0.02). The potential pathophysiological mechanisms underlying the role of circulating adiponectin in the pathogenesis of renal cell carcinoma deserve further investigation
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