Some lifestyle-related factors and risk of chronic renal failure : a population-based approach

Abstract

Some renal diseases, i.e. rapidly progressive glomerulonephritis, are sufficient causes of a rapid, permanent total loss of renal function. However, the majority of renal diseases progress slowly over decades, initially often without symptoms, sometimes making it difficult to define the aetiologies. There is growing evidence that a multitude of lifestyle-related and environmental factors influence the risk and the progression rate of chronic renal failure (CRF), although genetic factors also appear to be of importance. Prevention is important since the prognosis of end-stage renal disease treated with dialysis is poor, but mortality is substantially increased also in patients with mild CRF.

To identify risk factors for CRF, we performed a population-based nation-wide case-control study. The study base was the entire Swedish population born in Sweden and aged 1874 years. Eligible as cases were subjects who had a serum creatinine that for the first time and permanently exceeded 300 µmol/l (men) or 250 µmol/l (women) during the two-year study period, 1996-1998. The final study population included 926 cases and 998 randomly selected controls from the study base. A face-to-face interview and a self-administered questionnaire provided information about various exposures.

Despite an overall non-significant association, high daily smoking dose, long duration of the smoking habit, and a high cumulative dose were associated with a significant excess risk of CRF. In smokers with a cumulative dose of >30 pack-years, the risk was increased by 52 % compared to non-smokers. A more than two-fold increased risk among heavy smokers was observed for CRF classified as nephrosclerosis, but significant positive associations were also noted with glomerulonephritis, and among women - also with diabetic nephropathy. Other tobacco use than smoking was unrelated to risk of CRF.

A high protein intake was strongly and positively related to an increased risk of diabetic nephropathy. We cannot rule out that this association might be the result of reverse causality and recall bias, however, in an analysis confined to diabetic cases and controls, an almost 3fold risk gradient with protein intake remained, albeit imprecise due to small numbers. Protein intake was not associated with other types of renal disease. We could not confirm our hypothesis that a high intake of antioxidants reduces risk of CRF, with the possible exception that a high intake of vitamin E was linked to a low risk in individuals with hypertension.

Being overweight in early adulthood and obese at anytime in life was associated with an increased risk of CRF. A body mass index exceeding 30 kg/m2 in men and 35 kg/m2 in women anytime during lifetime was linked to 3-to 4-fold increases in risk. Although much of the excess risk was driven by the higher prevalence of hypertension and diabetes among obese, an additional pathway may exist. Birth weight was unrelated to risk of CRF, while a short stature was associated with CRF, at least in men. Isolated regular use of either paracetamol or aspirin was associated with a 2.5-fold increased risk of CRF overall, with a positive dose-response. The elevations in risk were observed for most types of underlying renal diseases, albeit not always statistically significant. To avoid bias due to analgesic use triggered by CRF symptoms, we disregarded more recent use, but the risks became only slightly attenuated. Our results are consistent with an exacerbating effect of paracetamol and aspirin, but, we cannot exclude that predisposing conditions of CRF may have prompted analgesic use.