Alcohol consumption and kidney function decline in the elderly

Background. Alcohol consumption appears to be protective for cardiovascular disease; however, its relationship with kidney disease is unclear. Methods. This prospective cohort study included 4343 subjects from the Cardiovascular Health Study, a longitudinal, community-based cohort of persons aged ≥ 65 from four US communities. We used previously defined categories based on weekly alcohol consumption: none, former, <1 drink, 1 – 6 drinks, 7 – 13 drinks and ≥ 14 drinks. Cystatin C was measured at baseline, year 3 and year 7; eligible subjects had at least two measures. Estimated GFR cys was calculated from cystatin C. The primary outcome was rapid kidney function as an annual estimated GFR (eGFR cys ) loss >3 mL/min/1.73 m 2 /year. Results. Eight percent of the cohort reported former alcohol use and 52% reported current alcohol consumption. During a mean follow-up of 5.6 years, 1075 (25%) participants had rapid kidney function decline. In adjusted logistic regression models, there was no association between alcohol use and kidney function decline (odds ratio, 95% confidence interval: none = reference; former = 1.18, 0.89 – 1.56; <1 drink = 1.20, 0.99 – 1.47; 1 – 6 = 1.18, 0.95 – 1.45; 7 – 13 = 1.10, 0.80 – 1.53; >14 = 0.89, 0.61 – 1.13). Results were similar with kidney function decline as a continuous outcome. Conclusions. Our results suggest that moderate alcohol consumption has neither adverse nor beneficial effects on kidney function. Although clinicians will need to consider the potential deleterious effects associated with alcohol consumption, there does not appear to be a basis for recommending that older adults discontinue or initiate light to moderate alcohol consumption to protect against kidney disease. confounders a priori based on biologic plausibility and results from prior studies. model for Abstract Background. Tumour necrosis factor alpha (TNF α ) is implicated in the pathogenesis of ANCA-associated systemic vasculitis (AASV). There is a need for more effec-tive and safer induction therapies for AASV. Uncontrolled studies have pointed to the efficacy of TNF α blockade with infliximab in the induction of remission in systemic vasculitides. We have hypothesized that adjunctive treatment with the humanized anti-TNF α monoclonal anti-body, adalimumab, will permit more rapid remission and reduced prednisolone exposure in AASV. Birmingham (mean; 95% CI, 0 – 4.4) at Week 14 ( P < 0.01). Prednisolone dose (in milligrammes per day) decreased from 37.1 (mean; 95% CI, 28.8 – 45.3) at entry to 8.1 (mean; 95% CI, 5.1 – 11.1) at Week 14 ( P < 0.01). Estimated glomerular filtration rate (in millilitres per minute per 1.73 m 2 ) increased from 17.1 (mean; 95% CI, 8.9 – 25.2) at entry to 30.1 (mean; 95% CI, 18 – 42.2) at 12 weeks ( P < 0.01). One patient died and three infections occurred. Conclusions. The addition of adalimumab to prednisolone and cyclophosphamide for the treatment of severe AASV was associated with response rates and adverse events similar to standard therapy alone but with a reduced prednisolone exposure. Further study is required to demonstrate whether the addition of adalimumab improves the speed of remission, the degree of renal recovery and safety.