» Articles » PMID: 20111974

Inflammation and Cachexia in Chronic Kidney Disease

Overview
Journal Pediatr Nephrol
Specialties Nephrology
Pediatrics
Date 2010 Jan 30
PMID 20111974
Citations 71
Authors
Affiliations
Soon will be listed here.
Abstract

Chronic inflammation is associated with cachexia and increased mortality risk in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). Inflammation suppresses appetite and causes the loss of protein stores. In CKD patients, increased serum levels of pro-inflammatory cytokines may be caused by reduced renal function, volume overload, oxidative or carbonyl stress, decreased levels of antioxidants, increased susceptibility to infection in uremia, and the presence of comorbid conditions. Cachexia is brought about by the synergistic combination of a dramatic decrease in appetite and an increase in the catabolism of fat and lean body mass. Pro-inflammatory cytokines act on the central nervous system to alter appetite and energy metabolism and to provide a signal-through the nuclear factor-kappaB and ATP-ubiquitin-dependent proteolytic pathways-that causes muscle wasting. Further research into the molecular pathways leading to inflammation and cachexia may lead to novel therapeutic therapies for this devastating and potentially fatal complication of chronic disease.

Citing Articles

Combating chronic kidney disease-associated cachexia: A literature review of recent therapeutic approaches.

Rahbar Saadat Y, Abbasi A, Hejazian S, Hekmatshoar Y, Ardalan M, Farnood F BMC Nephrol. 2025; 26(1):133.

PMID: 40069669 PMC: 11895341. DOI: 10.1186/s12882-025-04057-8.


Characteristics of soybean () protein hydrolysate by bromelain and its effect on inflammation and kidney disorders in gentamicin-induced male Wistar rats.

Hidayat M, Barnas A, Nussy V, Wantania T, Prahastuti S, Sriwidodo S Iran J Basic Med Sci. 2025; 28(1):56-62.

PMID: 39877638 PMC: 11771338. DOI: 10.22038/ijbms.2024.78131.16885.


The lived experience of renal cachexia: An interpretive phenomenological analysis.

Blair C, Shields J, Mullan R, Johnston W, Davenport A, Fouque D Int J Nurs Stud Adv. 2024; 7:100235.

PMID: 39328835 PMC: 11426076. DOI: 10.1016/j.ijnsa.2024.100235.


Regulation of Satellite Cells Functions during Skeletal Muscle Regeneration: A Critical Step in Physiological and Pathological Conditions.

Careccia G, Mangiavini L, Cirillo F Int J Mol Sci. 2024; 25(1).

PMID: 38203683 PMC: 10778731. DOI: 10.3390/ijms25010512.


Editorial: Immunology of cachexia.

Kumar V, Stewart 4th J Front Immunol. 2023; 14:1339263.

PMID: 38116001 PMC: 10728869. DOI: 10.3389/fimmu.2023.1339263.


References
1.
Sietsema K, Hiatt W, Esler A, Adler S, Amato A, Brass E . Clinical and demographic predictors of exercise capacity in end-stage renal disease. Am J Kidney Dis. 2002; 39(1):76-85. DOI: 10.1053/ajkd.2002.29884. View

2.
Merino A, Nogueras S, Buendia P, Ojeda R, Carracedo J, Ramirez-Chamond R . Microinflammation and endothelial damage in hemodialysis. Contrib Nephrol. 2008; 161:83-88. DOI: 10.1159/000130412. View

3.
Wanner C, Zimmermann J . Causes of coronary heart disease in patients on renal replacement therapy. Kidney Blood Press Res. 1998; 21(2-4):287-9. DOI: 10.1159/000025881. View

4.
Stenvinkel P . New insights on inflammation in chronic kidney disease-genetic and non-genetic factors. Nephrol Ther. 2006; 2(3):111-9. DOI: 10.1016/j.nephro.2006.04.004. View

5.
Verma S, Kuliszewski M, Li S, Szmitko P, Zucco L, Wang C . C-reactive protein attenuates endothelial progenitor cell survival, differentiation, and function: further evidence of a mechanistic link between C-reactive protein and cardiovascular disease. Circulation. 2004; 109(17):2058-67. DOI: 10.1161/01.CIR.0000127577.63323.24. View