Dietary Intake of Proteins and Calories Is Inversely Associated With The Oxidation State of Plasma Thiols in End-Stage Renal Disease Patients

Abstract

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.

Changes in thiol/disulfide homeostasis in juvenile idiopathic arthritis

“…reported that in patients with acute appendicitis dynamic thiol/disulfide homeostasis shifted towards disulfide formation due to thiol oxidation. The importance of thiol/disulfide homeostasis in many diseases, including chronic renal disease, severe coronary disease, migraine, obstructive sleep apnea, and pulmonary thromboembolism, has been reported . In the present study, although the thiol/disulfide ratio was slightly higher in the JIA patients than in the controls, the difference was not significant.…”

“…The importance of thiol/disulfide homeostasis in many diseases, including chronic renal disease, severe coronary disease, migraine, obstructive sleep apnea, and pulmonary thromboembolism, has been reported. 5,6,[11][12][13][14] In the present study, although the thiol/disulfide ratio was slightly higher in the JIA patients than in the controls, the difference was not significant. The present small sample size may be why the present findings differ from those reported earlier by Altıparmak et al 6 In clinical practice CRP and ESR are used to predict the severity of inflammation in inflammatory disease.…”

Plasma protein-bound di-tyrosines as biomarkers of oxidative stress in end stage renal disease patients on maintenance haemodialysis

“…There are significant differences in total plasma protein and albumin concentrations between healthy subjects and patients with ESRD [23], [40], as well as for each ESRD patient before and after a single HD session [23]. The latter is due to ultrafiltration performed during the dialysis session in order to restore the dry body weight of the patient.…”

“…For example, in haemodialyzed patients plasma protein oxidation is revealed by decreased P-SH [23], which might result from S -thiolation, the formation of mixed disulphides between P-SH and low-molecular-mass aminothiols, which is considered to be the mechanism protecting P-SH from losing their biological activity by irreversible oxidation [47], [48]. S -thiolated plasma proteins are indeed increased in haemodialyzed patients [21], [22], [23], [40]. However, a single HD session, by removing solutes responsible for increasing ROS production and the low-molecular-mass aminothiols involved in S -thiolation [21], caused transient return of plasma P-SH to the level equal or close to that occurring in healthy subjects [20], [21], [23].…”

Functional and Morphostructural Evaluation of the Kidneys of Wistar Rats after the Use of a Protein-Based Food Supplement

“…Protein intake above the physiological need leads to the increase in the catabolic pathways of amino acids, increasing the production of by-products such as urea, adenosine triphosphate (ATP), carbon dioxide, glucose, acetyl coenzyme A, and ketone bodies. Some of these by-products can have adverse effects in the body [19].…”