Association between metabolic syndrome and kidney cancer risk: a prospective cohort study

• Published in: Lipids in health and disease 2024-05, Vol.23 (1), p.142-142, Article 142
• Main Authors: Wang, Lin, Du, Han, Sheng, Chao, Dai, Hongji, Chen, Kexin
• Format: Article
• Language: English
• Subjects: Adult; Aged; Central obesity; Complications and side effects; Dyslipidemia; Dyslipidemias - complications; Dyslipidemias - epidemiology; Female; Humans; Hypertension; Hypertension - complications; Hypertension - epidemiology; Kidney cancer; Kidney Neoplasms - epidemiology; Kidney Neoplasms - etiology; Kidney Neoplasms - genetics; Male; Medical research; Medicine, Experimental; Metabolic syndrome; Metabolic Syndrome - complications; Metabolic Syndrome - epidemiology; Metabolic syndrome X; Middle Aged; Obesity, Abdominal - complications; Obesity, Abdominal - epidemiology; Physiological aspects; Polygenic risk score; Proportional Hazards Models; Prospective Studies; Renal cancer; Risk Factors
• ISSN: 1476-511X; 1476-511X
• DOI: 10.1186/s12944-024-02138-5

Kidney cancer has become known as a metabolic disease. However, there is limited evidence linking metabolic syndrome (MetS) with kidney cancer risk. This study aimed to investigate the association between MetS and its components and the risk of kidney cancer. UK Biobank data was used in this study. MetS was defined as having three or more metabolic abnormalities, while pre-MetS was defined as the presence of one or two metabolic abnormalities. Hazard ratios (HRs) and 95% confidence intervals (CIs) for kidney cancer risk by MetS category were calculated using multivariable Cox proportional hazards models. Subgroup analyses were conducted for age, sex, BMI, smoking status and drinking status. The joint effects of MetS and genetic factors on kidney cancer risk were also analyzed. This study included 355,678 participants without cancer at recruitment. During a median follow-up of 11 years, 1203 participants developed kidney cancer. Compared to the metabolically healthy group, participants with pre-MetS (HR= 1.36, 95% CI: 1.06-1.74) or MetS (HR= 1. 70, 95% CI: 1.30-2.23) had a significantly greater risk of kidney cancer. This risk increased with the increasing number of MetS components (P for trend < 0.001). The combination of hypertension, dyslipidemia and central obesity contributed to the highest risk of kidney cancer (HR= 3.03, 95% CI: 1.91-4.80). Compared with participants with non-MetS and low genetic risk, those with MetS and high genetic risk had the highest risk of kidney cancer (HR= 1. 74, 95% CI: 1.41-2.14). Both pre-MetS and MetS status were positively associated with kidney cancer risk. The risk associated with kidney cancer varied by combinations of MetS components. These findings may offer novel perspectives on the aetiology of kidney cancer and assist in designing primary prevention strategies.