Background
Oxidative stress contributes to the pathogenesis of protein-energy wasting
(PEW) in maintenance hemodialysis (MHD) patients. It remains uncertain, however, whether
and how food intake is involved in the causal relationship between oxidative stress and
PEW.
Methods
71 adult MHD Patients and 24 healthy subjects (Control) were studied
cross-sectionally with analyses of diet record and of oxidative stress, as measured by a
battery of plasma thiols including the protein sulfhydryl (-SH) group levels (PSH, a
marker of total protein –SH reducing capacity), the protein thiolation index
(PTI, the ratio between disulfide, i.e. oxidized, and reduced –SH groups in
proteins), low molecular mass (LMM) thiols, LMM disulfides and mixed LMM-protein
disulfides. In addition, interleukin-6 (IL-6), albumin, C-reactive protein (CRP) and
neutrophil gelatinase-associated lipocalin (NGAL) were measured as markers of
inflammation.
Results
The Patients showed low energy (22.0±8.4 Kcal/kg/d) and adequate protein
(1.0±0.4 g/kg/d) intakes, high levels of cystine [CySS; Patients vs. Control:
113.5 (90.9-132.8) vs. 68.2 (56.2-75.7) μM], cysteinylated proteins [CySSP; 216.0
(182.8-254.0) vs. 163.5 (150.0-195.5) μM] and high PTI [0.76 (0.61 – 0.88)
vs. 0.43 (0.40 – 0.54); p<0.001 in all comparisons]. In Patients,
variation of CySSP was explained by a standard regression model (R=0.775; p=0.00001)
that included significant contributions of protein intake (β=−0.361), NGAL
(β=0.387), age (β=0.295) and albumin (β=0.457). In the same model,
variation of PTI (R=0.624; p=0.01) was explained by protein intake
(β=−0.384) and age (β=0.326) and NGAL (β=0.311). However,
when PSH was entered as dependent variable (R=0.730; p=0.0001) only serum albumin
(β=0.495) and age (β=−0.280), but not dietary intake or NGAL,
contributed to the model.
Conclusions
In MHD, markers of thiol oxidation including CySSP and PTI show independent
association with dietary intake and NGAL, while PSH, a marker of thiol reducing
capacity, did not associate with these same variables. The mechanism(s) responsible for
inverse association between oxidative stress and food intake in MHD remain
undefined.