BACKGROUND:Adiponectin (ADPN) levels are consistently elevated among patients with advanced chronic kidney disease, but its relationship with cardiovascular outcomes in this population remains controversial. METHODS: We measured baseline and yearly plasma ADPN in 182 prevalent haemodialysis patients recruited to the Haemodialysis (HEMO) Study from two Boston centres. Plasma ADPN at baseline and during follow-up was studied in relation to prevalent cardiovascular disease (CVD) and cardiovascular and all-cause mortality. RESULTS:Baseline plasma ADPN levels were found to be approximately twofold higher than in the general population and correlated inversely with (log-transformed) CRP levels and (log-transformed) body mass index (BMI). Levels measured over time showed a gradual increase (0.95 microg/mL, 95% CI = 0.12-1.78 microg/mL; P = 0.03) by year, although this difference became non-significant after adjustment for covariates. Baseline ADPN levels were lower among patients with pre-existing CVD (adjusted OR of 0.67; P = 0.03). They also predicted all-cause mortality (P < 0.01) and the composite outcome of 'cardiovascular events/cardiovascular mortality' (P < 0.01); levels measured over time predicted the composite outcome of 'cardiovascular events and all-cause mortality' (P < 0.01). These relationships were non-linear (quadratic) with the hazard for each outcome increasing in the lower and upper ranges of the distribution of ADPN, and strengthened after adjustment for baseline covariates including serum albumin, CVD and the flux and dialysis dose categorization of the HEMO study. CONCLUSIONS: In summary, low plasma levels of ADPN were associated with inflammation and pre-existing CVD; ADPN levels predicted cardiovascular and mortality outcomes, the relationship being extensively confounded by multiple patient-related factors.
RCT Entities:
BACKGROUND:Adiponectin (ADPN) levels are consistently elevated among patients with advanced chronic kidney disease, but its relationship with cardiovascular outcomes in this population remains controversial. METHODS: We measured baseline and yearly plasma ADPN in 182 prevalent haemodialysis patients recruited to the Haemodialysis (HEMO) Study from two Boston centres. Plasma ADPN at baseline and during follow-up was studied in relation to prevalent cardiovascular disease (CVD) and cardiovascular and all-cause mortality. RESULTS: Baseline plasma ADPN levels were found to be approximately twofold higher than in the general population and correlated inversely with (log-transformed) CRP levels and (log-transformed) body mass index (BMI). Levels measured over time showed a gradual increase (0.95 microg/mL, 95% CI = 0.12-1.78 microg/mL; P = 0.03) by year, although this difference became non-significant after adjustment for covariates. Baseline ADPN levels were lower among patients with pre-existing CVD (adjusted OR of 0.67; P = 0.03). They also predicted all-cause mortality (P < 0.01) and the composite outcome of 'cardiovascular events/cardiovascular mortality' (P < 0.01); levels measured over time predicted the composite outcome of 'cardiovascular events and all-cause mortality' (P < 0.01). These relationships were non-linear (quadratic) with the hazard for each outcome increasing in the lower and upper ranges of the distribution of ADPN, and strengthened after adjustment for baseline covariates including serum albumin, CVD and the flux and dialysis dose categorization of the HEMO study. CONCLUSIONS: In summary, low plasma levels of ADPN were associated with inflammation and pre-existing CVD; ADPN levels predicted cardiovascular and mortality outcomes, the relationship being extensively confounded by multiple patient-related factors.
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