Departments of Medical Epidemiology and Biostatistics and.
Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, and.
Clin J Am Soc Nephrol. 2019 Apr 5;14(4):530-539. doi: 10.2215/CJN.10820918. Epub 2019 Mar 14.
Community-based reports regarding eGFR and the risk of cancer are conflicting. We here explore plausible links between kidney function and cancer incidence in a large Scandinavian population-based cohort.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In the Stockholm Creatinine Measurements project, we quantified the associations of baseline eGFR with the incidence of cancer among 719,033 Swedes ages ≥40 years old with no prior history of cancer. Study outcomes were any type and site-specific cancer incidence rates on the basis of International Classification of Diseases-10 codes over a median follow-up of 5 years. To explore the possibility of detection bias and reverse causation, we divided the follow-up time into different time periods (≤12 and >12 months) and estimated risks for each of these intervals.
In total, 64,319 cases of cancer (affecting 9% of participants) were detected throughout 3,338,226 person-years. The relationship between eGFR and cancer incidence was U shaped. Compared with eGFR of 90-104 ml/min, lower eGFR strata associated with higher cancer risk (adjusted hazard ratio, 1.08; 95% confidence interval, 1.05 to 1.11 for eGFR=30-59 ml/min and adjusted hazard ratio, 1.24; 95% confidence interval, 1.15 to 1.35 for eGFR<30 ml/min). Lower eGFR strata were significantly associated with higher risk of skin, urogenital, prostate, and hematologic cancers. Any cancer risk as well as skin (nonmelanoma) and urogenital cancer risks were significantly elevated throughout follow-up time, but they were higher in the first 12 months postregistration. Associations with hematologic and prostate cancers abrogated after the first 12 months of observation, suggesting the presence of detection bias and/or reverse causation.
There is a modestly higher cancer risk in individuals with mild to severe CKD driven primarily by skin and urogenital cancers, and this is only partially explained by bias.
社区报告的 eGFR 和癌症风险存在矛盾。我们在此探索了在一个大型斯堪的纳维亚人群队列中,肾功能与癌症发病率之间的潜在联系。
设计、设置、参与者和测量:在斯德哥尔摩肌酐测量项目中,我们在没有癌症既往史的 719033 名年龄≥40 岁的瑞典人群中,根据基线 eGFR 与癌症发病率之间的关联,根据国际疾病分类第 10 版编码计算了任何类型和特定部位癌症的发病率。为了探索检测偏倚和反向因果关系的可能性,我们将随访时间分为不同的时间段(≤12 个月和>12 个月),并估计了每个时间段的风险。
共发现 64319 例癌症(占参与者的 9%),随访 3338226 人年。eGFR 与癌症发病率之间呈 U 形关系。与 eGFR 为 90-104ml/min 相比,较低的 eGFR 与更高的癌症风险相关(调整后的危险比,1.08;95%置信区间,1.05 至 1.11,eGFR=30-59ml/min;调整后的危险比,1.24;95%置信区间,1.15 至 1.35,eGFR<30ml/min)。较低的 eGFR 与皮肤、泌尿生殖、前列腺和血液癌症的风险增加显著相关。任何癌症风险以及皮肤(非黑色素瘤)和泌尿生殖系统癌症风险在整个随访期间显著升高,但在登记后 12 个月内更高。在观察的前 12 个月后,与血液和前列腺癌的关联消失,表明存在检测偏倚和/或反向因果关系。
轻度至重度 CKD 患者的癌症风险略有增加,主要是由皮肤和泌尿生殖系统癌症引起的,这部分归因于偏倚。