levels in malnourished patients (≥3 criteria of PEW) and higher levels in patients with zero PEW criteria (p=0.042). Alterations of ADPN levels during the observation period were dependent on PEW (p=0.021) and the mode of dialysis (p=0.002) (after adjustment for age, dialysis vintage, gender and fat mass index -FMI-). In particular HD patients with ≥3 criteria of PEW increased adiponectin levels over time, whereas PD patients with ≥3 criteria decreased adiponectin levels throughout the study. Leptin alterations over time were not affected by the mode of dialysis or the PEW. In cox regression and multiple cox proportional hazard models, each 1μg/ml increment of ADPN levels was associated with 4% (p=0.013) and 9% increase (p=0.003) in mortality risk respectively. Furthermore, the lowest sex-specific tertile of leptin (<5.1 for men and <14.9ng/ml for women) was associated with higher risk of all-cause mortality compared with middle and highest tertiles [crude hazard ratio: 2.95 (95% CI, 1.17-7.50)]. This low leptin-mortality association persisted even after adjustment for FMI, age, sex, dialysis mode, baseline CVD, serum albumin and CRP.
Conclusions:Our study provides strong evidence that increased ADPN and decreased leptin are independently associated with poor prognosis and PEW. The way that these two adipokines differentially impact on PEW and mortality warrants further investigation.