- 1School of Dietetics and Human Nutrition, McGill University, Montreal, QC, Canada
- 2Department of Nephrology, Hospital Universitario de la Princesa, Madrid, Spain
- 3School of Medicine, Federal University of Uberlandia, Uberlandia, Brazil
Editorial on the Research Topic
Improving body composition and functional capacity in chronic kidney disease patients
Chronic kidney disease (CKD) is a major global public health problem, with an annual economic burden of more than $114 billion (1). CKD moved from the 21st (1990) to the 11th (2016) position in the world ranking of causes of death and years of life lost (2).
Metabolic disorders present in chronic kidney disease (CKD) lead to increased protein catabolism (3) resulting in loss of muscle mass and function (4). Protein catabolism is worsened by other typical conditions, such as uremia-related gastrointestinal symptoms, physical inactivity, nutrient malabsorption, and nutrient loss into the dialysate (5). Therefore, muscle impairment leading to sarcopenia (6) and protein energy wasting (PEW) is common among patients with CKD (7) and is associated with higher mortality rates (8), decreased physical function and physical activity (9), and worse outcomes (10). Obesity is also common among CKD patients (7) and is associated with higher risk of mortality (11) and disease progression (12).
This recent Research Topic on “Improving body composition and functional capacity in chronic kidney disease patients” represents a collection of five original research articles in the field of CKD, ranging from development of more feasible methods to diagnose PEW and central obesity to dietary and exercise interventions aimed to prevent muscle depletion and increase responsiveness to pharmacological treatment, as well as evaluation of the association between obesity and cardiovascular disease (CVD) risk. A common theme across all articles is the importance of body composition and/or nutritional status and its association with clinical outcomes in patients with kidney disease. This is an important Research Topic for investigation since PEW, sarcopenia, and obesity have high prevalence rates among patients with CKD and are associated with adverse clinical outcomes.
Among patients under hemodialysis, 60% are alive 3 years after starting treatment (13). Cardiovascular disease (CVD) is the main cause of death in this population (14), but the nutritional status deterioration (15) as a result of PEW syndrome is also associated with increased death risk from CVD (16, 17). PEW, a modifiable risk factor, is present in 28–54% of patients under dialysis (18). PEW diagnosis is recommended to be done by the International Society of Renal Nutrition and Metabolism (ISRNM) according to assessment of biochemical criteria: low body weight, reduced total body fat, or weight loss; a decrease in muscle mass; and low protein or energy intake (19). However, given the need of meeting multiple criteria, in particular the difficult and usually unreliable estimating of dietary intake (20), the ISRNM diagnosis is rarely implemented in clinical practice. In order to make the diagnosis more objective, Chen et al. analyzed the independent influencing factors of PEW among 380 hemodialysis patients. The three model for prediction of PEW proposed by Chen et al. had an area under the curve from 0.85 to 0.91, and no significant difference was found compared to ISRNM diagnostic criteria (p > 0.05) was observed. The novel PEW prediction model is more convenient than the traditional diagnostic criteria and can be applied to identify PEW in HD patients.
Patients under HD treatment suffer from worse muscle function (21), anabolic resistance (22), and poorer protein and calorie balance (23) than patients under other CKD treatments. As a result, sarcopenia is more prevalent among patients undergoing dialysis (30%) (24) as compared to the general population (10%) (25). As HD patients are more vulnerable to sarcopenia development, Ju et al. evaluated the preventive effects of leucine-enriched amino acid supplementation and resistance exercise in non-sarcopenic HD patients. After 12 weeks, the intervention induced significant improvement in muscle mass (increased in 64% of patients), strength (increased in 32% of patients), and physical function (improved in 60% of patients). This proposed intervention was a safe and effective way to prevent muscle deterioration in HD patients.
Patients under HD also suffer from a high prevalence of anemia (90–100%) (26), a common complication of CKD that can lead to adverse clinical outcomes (27). Erythropoiesis-stimulating agent (ESA) is the treatment of choice. However, as high doses of ESA increase the risk of all-cause mortality and cardiovascular (CV) events (27), strategies aimed to improve responsiveness need to be investigated. Lee et al. found an association between the ESA responsiveness and body composition in patients undergoing HD. Therefore, dietary and exercise interventions (such as the one from Ju et al. study) can have additional clinical benefits.
Obesity is an epidemic problem around the world, with increasing prevalence among CKD patients (28). Central obesity reflects visceral adipose tissue and is a well-known risk factor for CVD (29), the main cause of death in the CKD population (14). Diagnosis of central obesity is important not only to prevent CVD but also CKD progression as it can cause kidney damage (12). Among 35,018 participants from the National Health and Nutrition Examination Survey 2005–2018, Qin et al. found an association among visceral adiposity index and increased likelihood of decline in renal function (ORadjusted = 1.04; 95% CI: 1.02–1.06) and albuminuria (ORadjusted = 1.03; 95% CI:1.00–1.06). Visceral adiposity index was determined using waist circumference, BMI, TG, and high-density lipoprotein-cholesterol, parameters commonly available in clinical practice.
Among patients at stage 5 of CKD, Ryu et al. found that abdominal fat indices such as the conicity index and a-body shape index predicted CV outcomes and all-cause mortality and were associated with inflammatory status. Therefore, high central obesity is an important predictor of CV outcomes and may represent a mortality risk factor. Conicity index and a-body shape index are easily available in clinical settings, facilitating central obesity diagnosis.
In the last quarter of a century, there was an increased mortality and disability among patients with CKD. To prevent this undesirable scenario, there is a need for better understanding of the role of body composition in clinical and patient outcomes as well as the best intervention to prevent development of PEW, sarcopenia, and obesity. This volume brings a conjunction of articles aimed to fill this gap. We are certain that this reading will add new information to advance the research, promote knowledge transfer, and improve clinical practice in the field of CKD.
Author contributions
NTB was involved in the Research Topic conception and drafted the editorial article. NTB, GB, and EPO critically revised articles submitted under the Research Topic. All authors critically revised the editorial manuscript.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
References
1. Johansen KL, Chertow GM, Gilbertson DT, Herzog CA, Ishani A, Israni AK, et al. US renal data system 2021 annual data report: epidemiology of kidney disease in the United States. Am J Kidney Dis. (2022) 79(4Suppl.1):A8–12. doi: 10.1053/j.ajkd.2022.02.001
2. GBD. Global, regional, and national age-sex specific mortality for 264 causes of death, 1980-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet. (2017) 390:1151–210. doi: 10.1016/S0140-6736(17)32152-9
3. Bataille S, Chauveau P, Fouque D, Aparicio M, Koppe L. Myostatin and muscle atrophy during chronic kidney disease. Nephrol Dial Transplant. (2021) 36:1986–93. doi: 10.1093/ndt/gfaa129
4. Fahal I. Uraemic sarcopenia: aetiology and implications. Nephrol Dial Transplant. (2014) 29:1655–65. doi: 10.1093/ndt/gft070
5. Mafra D, Borges NA, Lindholm B, Shiels PG, Evenepoel P, Stenvinkel P. Food as medicine: targeting the uraemic phenotype in chronic kidney disease. Nat Rev Nephrol. (2021) 17:153–71. doi: 10.1038/s41581-020-00345-8
6. Dierkes J, Dahl H, Welland NL, Sandnes K, Sæle K, Sekse I, et al. High rates of central obesity and sarcopenia in CKD irrespective of renal replacement therapy - an observational cross-sectional study. BMC Nephrol. (2018) 19:259. doi: 10.1186/s12882-018-1055-6
7. Androga L, Sharma D, Amodu A, Abramowitz M. Sarcopenia, obesity, and mortality in US adults with and without chronic kidney disease. Kidney Int Rep. (2017) 2:201–11. doi: 10.1016/j.ekir.2016.10.008
8. Moorthi RN, Avin KG. Clinical relevance of sarcopenia in chronic kidney disease. Curr Opin Nephrol Hypertens. (2017) 26:219–28. doi: 10.1097/MNH.0000000000000318
9. Zhang F, Yin X, Huang L, Zhang H. The “adult inactivity triad” in patients with chronic kidney disease: a review. Front Med. (2023) 10:1160450. doi: 10.3389/fmed.2023.1160450
10. Sabatino A, Cuppari L, Stenvinkel P, Lindholm B, Avesani CM. Sarcopenia in chronic kidney disease: what have we learned so far? J Nephrol. (2021) 34:1347–72. doi: 10.1007/s40620-020-00840-y
11. Chan W, Chin SH, Whittaker AC, Jones D, Kaur O, Bosch JA, et al. The associations of muscle strength, muscle mass, and adiposity with clinical outcomes and quality of life in prevalent kidney transplant recipients. J Ren Nutr. (2019) 29:536–47. doi: 10.1053/j.jrn.2019.06.009
12. Hruby A, Hu FB. The epidemiology of obesity: a big picture. Pharmacoeconomics. (2015) 33:673–89. doi: 10.1007/s40273-014-0243-x
13. Bailey A, Brody R, Sackey J, Parrott JS, Peters E, Byham-Gray L. Current methods for developing predictive energy equations in maintenance dialysis are imprecise. Ann Med. (2022) 54:909–20. doi: 10.1080/07853890.2022.2057581
14. Turkmen K, Ozer H, Kusztal M. The relationship of epicardial adipose tissue and cardiovascular disease in chronic kidney disease and hemodialysis patients. J Clin Med. (2022) 11:51308. doi: 10.3390/jcm11051308
15. Barril G, Nogueira A, Alvarez-García G, Núñez A, Sánchez-González C, Ruperto M. Nutritional predictors of mortality after 10 years of follow-up in patients with chronic kidney disease at a multidisciplinary unit of advanced chronic kidney disease. Nutrients. (2022) 14:183848. doi: 10.3390/nu14183848
16. MacLaughlin HL, Friedman AN, Ikizler TA. Nutrition in kidney disease: core curriculum 2022. Am J Kidney Dis. (2022) 79:437–49. doi: 10.1053/j.ajkd.2021.05.024
17. Chan W. Chronic kidney disease and nutrition support. Nutr Clin Pract. (2021) 36:312–30. doi: 10.1002/ncp.10658
18. Obi Y, Qader H, Kovesdy CP, Kalantar-Zadeh K. Latest consensus and update on protein-energy wasting in chronic kidney disease. Curr Opin Clin Nutr Metab Care. (2015) 18:254–62. doi: 10.1097/MCO.0000000000000171
19. Fouque D, Kalantar-Zadeh K, Kopple J, Cano N, Chauveau P, Cuppari L, et al. A proposed nomenclature and diagnostic criteria for protein-energy wasting in acute and chronic kidney disease. Kidney Int. (2008) 73:391–8. doi: 10.1038/sj.ki.5002585
20. Bross R, Noori N, Kovesdy CP, Murali SB, Benner D, Block G, et al. Dietary assessment of individuals with chronic kidney disease. Semin Dial. (2010) 23:359–64. doi: 10.1111/j.1525-139X.2010.00743.x
21. Thome T, Salyers ZR, Kumar RA, Hahn D, Berru FN, Ferreira LF, et al. Uremic metabolites impair skeletal muscle mitochondrial energetics through disruption of the electron transport system and matrix dehydrogenase activity. Am J Physiol Cell Physiol. (2019) 317:C701–13. doi: 10.1152/ajpcell.00098.2019
22. van Vliet S, Skinner SK, Beals JW, Pagni BA, Fang H-Y, Ulanov AV, et al. Dysregulated handling of dietary protein and muscle protein synthesis after mixed-meal ingestion in maintenance hemodialysis patients. Kidney Int Rep. (2018) 3:1403–15. doi: 10.1016/j.ekir.2018.08.001
23. Kaplan AA, Halley SE, Lapkin RA, Graeber CW. Dialysate protein losses with bleach processed polysulphone dialyzers. Kidney Int. (1995) 47:573–8. doi: 10.1038/ki.1995.72
24. Shu X, Lin T, Wang H, Zhao Y, Jiang T, Peng X, et al. Diagnosis, prevalence, and mortality of sarcopenia in dialysis patients: a systematic review and meta-analysis. J Cachexia Sarcopenia Muscle. (2022) 13:145–58. doi: 10.1002/jcsm.12890
25. Shafiee G, Keshtkar A, Soltani A, Ahadi Z, Larijani B, Heshmat R. Prevalence of sarcopenia in the world: a systematic review and meta- analysis of general population studies. J Diabetes Metab Disord. (2017) 16:21. doi: 10.1186/s40200-017-0302-x
26. Ryu SR, Park SK, Jung JY, Kim YH, Oh YK, Yoo TH, et al. The prevalence and management of anemia in chronic kidney disease patients: result from the KoreaN cohort study for outcomes in patients with chronic kidney disease (KNOW-CKD). J Korean Med Sci. (2017) 32:249–56. doi: 10.3346/jkms.2017.32.2.249
27. Babitt JL, Lin HY. Mechanisms of anemia in CKD. J Am Soc Nephrol. (2012) 23:1631–4. doi: 10.1681/ASN.2011111078
28. Abramowitz MK, Sharma D, Folkert VW. Hidden obesity in dialysis patients: clinical implications. Semin Dial. (2016) 29:391–5. doi: 10.1111/sdi.12516
Keywords: body composition, chronic kidney disease, obesity, protein energy wasting, sarcopenia, exercise, nutrition, physical function
Citation: Bellafronte NT, Barril G and de Oliveira EP (2023) Editorial: Improving body composition and functional capacity in chronic kidney disease patients. Front. Nutr. 10:1223975. doi: 10.3389/fnut.2023.1223975
Received: 16 May 2023; Accepted: 11 July 2023;
Published: 28 July 2023.
Edited and reviewed by: Hassane Zouhal, University of Rennes 2—Upper Brittany, France
Copyright © 2023 Bellafronte, Barril and de Oliveira. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Natalia Tomborelli Bellafronte, bmF0YmVsbGEmI3gwMDA0MDt5bWFpbC5jb20=