Impact of metabolic syndrome on resting energy expenditure in patients with chronic kidney disease. (October 2016)

• Record Type: Journal Article
• Authors: Rodrigues, Carolina Q.D.; Santos, Jacqueline A.P.; Quinto, Beata M.R.; Marrocos, Mauro S.M.; Teixeira, Andrei A.; Rodrigues, Cássio J.O.; Batista, Marcelo C.
• Is Part Of: Clinical nutrition ESPEN. Volume 15(2016)
• Page Start: 107
• Page End: 113
• Publication Date: 2016-10
• Subjects: Chronic kidney disease -- Metabolic syndrome -- Predialysis -- Resting energy expenditure; REE resting energy expenditure -- CKD chronic kidney disease -- MetS metabolic syndrome -- GFR glomerular filtration rate -- eGFR estimated glomerular filtration rate -- DM diabetes mellitus -- PCR C-reative protein -- IC indirect calorimetry -- BMR basal metabolic rate -- BIA bioelectrical impedance analyzer -- TSF triceps skinfold thickness -- MAMC mid-arm muscle circumference -- CMI corporal mass index -- PNA protein equivalent of nitrogen appearance; Nutritionally induced diseases -- Periodicals; Metabolism -- Disorders -- Periodicals; 616.39005
• DOI: 10.1016/j.clnesp.2016.07.001
• Languages: English
• ISSNs: 2405-4577

Abstract

Summary: Background & aims: Resting energy expenditure (REE) changes in patients with chronic kidney disease (CKD) may contribute to mortality increase. The obesity and inflammation is associated with high REE and when not compensated by adequate intake, may determine an unfavorable clinical outcome in this population. We aimed to evaluate the influence of metabolic syndrome (MetS) on REE in CKD patients. Methods: One hundred eighty-three patients were stratified according to glomerular filtration rate (GFR) and divided in groups: without CKD (GFR > 60 ml/min/1.73 m 2 ) and CKD (GFR < 60 ml/min/1.73 m 2 ) and according to the presence or absence of MetS. REE was measured by indirect calorimetry; body composition was assessed by bioelectrical impedance analysis and blood and urine were collected for biochemical tests. Results: REE was lower in the group with CKD compared with those without CKD (1293 ± 364 vs 1430 ± 370 kcal/d, P = 0.01). The group with CKD without MetS showed decrease in REE compared to the groups without CKD, regardless the presence of Mets, and those with CKD and MetS (1173 ± 315 vs 1392 ± 324 vs 1460 ± 410 vs 1424 ± 376 kcal/d, P < 0.05, respectively). Multivariate analysis showed an independent association of CKD in determining REE when adjusted for lean body mass. The inclusion of MetS as an independent variable in the same analysis model neutralized the impact of CKD on the REE (P = 0.19). Patients without MetS, REE correlated with estimated GFR and the protein equivalent (r = 0.33, P < 0.01, r = 0.21, P = 0.04, respectively), whereas in MetS patients, these correlations were not observed. Conclusion: The presence of CKD is independently associated with reduced REE. The observed decrease in REE is reversed in patients with MetS independent of renal function. Highlights: Patients with CKD stratified according to estimated GFR had reduced REE values. The presence of MetS in these patients given an increase in GER. High GER in patients with reduced GFR was independent of the presence of CKD.