Sarcopenic among patients with chronic kidney disease
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Abstract
Sarcopenia is an important problem and a high prevalence among patients with chronic kidney disease has been associated with increased morbidity and mortality. The main causes related to declining renal function comprise hormonal change and chronic inflammation. These contribute to loss of protein synthesis in the muscles and increases muscle fiber degradation. Definitions of sarcopenia involve low muscle strength and muscle quantity or quality leading to low physical performance. Diagnosis is defined by history taking, physical examination, imaging study for muscle cross-sectional area, determining appendicular skeletal muscle mass by DEXA and physical performance testing such as gait speed, grip strength and short physical performance battery. The main prevention and treatment strategies of sarcopenia in chronic kidney disease include increased exercise training, nutritional supplements, correction of metabolic acidosis, hormone replacement therapy, and antisarcopenic agents.
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References
Von Haehling S, Morley JE, Anker SD. An overview of sarcopenia: facts and numbers on prevalence and clinical impact. J Cachexia Sarcopenia Muscle 2010; 1:129–133.
Ong-Ajyooth L, Vareesangthip K, Khonputsa P, Aekplakorn W. Prevalence of chronic kidney disease in Thai adults: a national health survey. BMC Nephrol. 2009; 10:35.
Stenvinkel P, Carrero JJ, von Walden F, Ikizler TA, Nader GA. Muscle wasting in end-stage renal disease promulgates premature death: established, emerging and potential novel treatment strategies. Nephrol Dial Transplant. 2016;31(7):1070-7.
Diesel W, Emms M, Knight BK, Noakes TD, Swanepoel CR, van Zyl Smit R, et al. Morphologic features of the myopathy associated with chronic renal failure. Am J Kidney Dis 1993; 22:677-84.
Mahesh S, Kaskel F. Growth hormone axis in chronic kidney disease. Pediatr Nephrol 2008; 23:41-8.
Phillips SK, Gopinathan J, Meehan K, Bruce SA, Woledge RC. Muscle strength changes during the menstrual cycle in adductor pollicis. J Physiol 1993; 473:125P.
Wang X, Hu Z, Hu J, Du J, Mitch WE. Insulin resistance accelerates muscle protein degradation: Activation of the ubiquitin-proteasome pathway by defects in muscle cell signaling. Endocrinology 2006; 147: 4160-8.
Fahal IH, Bell GM, Bone JM, Edwards RH. Physiological abnormalities of skeletal muscle in dialysis patients. Nephrol Dial Transplant 1997; 12:119-27.
Gilson H, Schakman O, Kalista S, Lause P, TsuchidaK, Thissen JP. Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin. Am J Physiol Endocrinol Metab 2009; 297:E157-64.
Siami G, Clinton ME, Mrak R, et al. Evaluation of the effect of intravenous L-carnitine therapy on function, structure and fatty acid metabolism of skeletal muscle in patients receiving chronic hemodialysis. Nephron 1991; 57:306.
Fahal IH. Uraemic sarcopenia: aetiology and implications. Nephrol Dial Transplant 2014; 29: 1655-65.
Workeneh BT, Mitch WE. Review of muscle wasting associated with chronic kidney disease. Am J Clin Nutr 2010; 91:1128S-1132S.
Roshanravan B, Kestenbaum B, Gamboa J, et al. CKD and Muscle Mitochondrial Energetics. Am J Kidney Dis 2016; 68:658.
Bailey JL, Zheng B, Hu Z, Price SR, Mitch WE. Chronic kidney disease causes defects in signaling through the insulin receptor substrate/phosphatidylinositol3- kinase/Akt pathway: implications for muscle atrophy. J Am Soc Nephrol 2006; 17: 1388- 94.
Cohn RD, van Erp C, Habashi JP, Soleimani AA, Klein EC, Lisi MT, et al. Angiotensin II type 1 receptor blockade attenuates TGF-beta-induced failure of muscle regeneration in multiple myopathic states. Nat Med 2007; 13:204-10.
Kaizu Y, Ohkawa S, Odamaki M, Ikegaya N, Hibi I, Miyaji K, et al. Association between inflammatory mediators and muscle mass in long-term hemodialysis patients. Am J Kidney Dis 2003; 42:295-302.
Campistol JM. Uremic myopathy. Kidney Int 2002; 62:1901.
Diesel W, Emms M, Knight BK, et al. Morphologic features of the myopathy associated with chronic renal failure. Am J Kidney Dis 1993; 22:677.
Cruz-Jentoft AJ, Bahat G, Bauer J, Boirie Y, Bruyere O, Cederholm T, et al. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. 2019; 48(1):16-31.
Johansen KL. Exercise in the end-stage renal disease population. J Am Soc Nephrol 2007; 18:1845.
Fiatarone MA, O’Neill EF, Ryan ND, et al. Exercise training and nutritional supplementation for physical frailty in very elderly people. N Engl J Med 1994; 330:1769.
Hewitt NA, O’Connor AA, O’Shaughnessy DV, Elder GJ. Effects of cholecalciferol on functional, biochemical, vascular, and quality of life outcomes in hemodialysis patients. Clin J Am Soc Nephrol 2013; 8:1143.
Caglar K, Fedje L, Dimmitt R, Hakim RM, Shyr Y, Ikizler TA. Therapeutic effects of oral nutritional supplementation during hemodialysis. Kidney Int 2002; 62:1054-9.
Moorthi RN, Avin KG. Clinical relevance of sarcopenia in chronic kidney disease. Curr Opin Nephrol Hypertens. 2017; 26(3):219-28