title: Dietary Intake of Proteins and Calories Is Inversely Associated With The Oxidation State of Plasma Thiols in End-Stage Renal Disease Patients.
abstract: OBJECTIVE
  Oxidative stress contributes to the pathogenesis of protein-energy wasting in maintenance hemodialysis (MHD) patients, but knowledge of specific effectors and mechanisms remains fragmented. Aim of the study was to define whether and how food intake is involved in the causal relationship between oxidative stress and protein-energy wasting.
  
  
  METHODS
  Seventy-one 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 (PSH) levels (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, and neutrophil gelatinase-associated lipocalin (NGAL) were measured as markers of inflammation.
  
  
  RESULTS
  The patients showed low energy (22.0 ± 8.4 kcal/kg/day) and adequate protein (1.0 ± 0.4 g/kg/day) intakes, high levels of cystine (CySS; patients vs.
  
  
  METHODS
  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 < .001 in all comparisons). In patients, variation of CySSP was explained by a standard regression model (R = 0.775; P = .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 = .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 = .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, whereas 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.
authors.affiliation: Division of Nephrology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas; Renal Section Medicine Service, South Texas Veteran Health Care System, San Antonio, Texas. Electronic address: fanti@uthscsa.edu.
authors.forename: Paolo
authors.initials: P
authors.lastname: Fanti
authors.affiliation: Department of Life Sciences, Laboratory of Pharmacology and Toxicology, University of Siena, Siena, Italy.
authors.forename: Daniela
authors.initials: D
authors.lastname: Giustarini
authors.affiliation: Department of Life Sciences, Laboratory of Pharmacology and Toxicology, University of Siena, Siena, Italy.
authors.forename: Ranieri
authors.initials: R
authors.lastname: Rossi
authors.affiliation: School of Health Professions, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
authors.forename: Sue E D
authors.initials: SE
authors.lastname: Cunningham
authors.affiliation: Division of Diabetes, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
authors.forename: Franco
authors.initials: F
authors.lastname: Folli
authors.affiliation: Nephrology and Hypertension Unit, Western Galilee Hospital, Nahariya, Israel.
authors.forename: Khaled
authors.initials: K
authors.lastname: Khazim
authors.affiliation: Department of Epidemiology and Biostatistics, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
authors.forename: John
authors.initials: J
authors.lastname: Cornell
authors.affiliation: Department of Medicine, University of Pisa, Pisa, Italy.
authors.forename: Elena
authors.initials: E
authors.lastname: Matteucci
authors.affiliation: Division of Nephrology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
authors.forename: Shweta
authors.initials: S
authors.lastname: Bansal
mesh_terms: D000209:Acute-Phase Proteins; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D015930:Diet Records; D004044:Dietary Proteins / Q000008:administration & dosage*; D002149:Energy Intake; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000628:therapy*; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D011518:Proto-Oncogene Proteins / Q000097:blood; D006435:Renal Dialysis; D012709:Serum Albumin / Q000378:metabolism; D013438:Sulfhydryl Compounds / Q000097:blood* / Q000737:chemistry; D055815:Young Adult
chemical_list: D000209:Acute-Phase Proteins; D015415:Biomarkers; D004044:Dietary Proteins; C508600:IL6 protein, human; D015850:Interleukin-6; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins; D012709:Serum Albumin; D013438:Sulfhydryl Compounds; D002097:C-Reactive Protein