RCC is the third cancer most robustly associated with increased BMI after endometrial and oesophageal tumours [8–10]. There is a growing knowledge on the impact of obesity and the role of adipose tissue in renal carcinogenesis. Obesity in both men and women increases the risk. The relative risk ranged from 1.04 to 1.08 per unit of increase in BMI (corresponding to 3 kg body weight increase for a subject of average height) [11]. Several mechanisms were hypothesized, but direct evidence is limited. Abdominal fat is an endocrine organ producing adipose tissue-derived hormones (adipokines) which play a role in conflicting between growing tumours and the immune system. Other mechanisms include chronic tissue hypoxia, insulin resistance, compensatory hyperinsulinaemia, altered endocrine milieu, obesity-induced inflammatory response, lipid peroxidation and oxidative stress [6, 12, 13]. There is inverse association of physical activity with obesity but little evidence to support the relation with RCC [14]. A recent population-based case control study suggested that physical activity may be inversely associated with RCC risk in whites, but there was no evidence of such an association in blacks [15]. Further investigations are needed to clarify the relationship in this population.

There is sufficient evidence to support that long-term hypertension predisposes to RCC [16, 17]. Users of diuretics and antihypertensive medications were associated with an elevated risk of RCC, but an independent effect of hypertension per se has not been established. Risk is higher among individual who are both hypertensive and obese than those affected by one of these. The mechanisms attributed are chronic hypoxia and lipid peroxidation with formation of reactive oxygen species [6].