Sarcopenia in chronic kidney disease: from bench to bedside

Kim, Da-Woon; Song, Sang Heon

doi:10.3904/kjim.2022.338

Cited by 5 publications

(3 citation statements)

References 235 publications

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“…The results may have also been impacted by methodological considerations such as sample size, PEW measurement techniques, or other confounding variables. It is also conceivable that, despite certain areas of overlap, the mechanisms behind sarcopenia and PEW have significant differences 50 , 51 , and DII might affect only a subset of these pathways. Further research is required to understand the underlying causes of this unequal connection and to consider other potential confounding factors.…”

Section: Discussionmentioning

confidence: 99%

Dietary inflammatory index could increase the risk of sarcopenia in patients with chronic kidney disease

Mansouri,

Jafari,

Ranjbar

et al. 2024

Sci Rep

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Using a system that incorporates a variety of food items rather than focusing on individual components can aid in assessing the inflammatory effects of a diet on disease outcomes such as chronic kidney disease (CKD). Therefore, we decided to investigate the association between dietary inflammatory index (DII) and the risk of protein–energy wasting (PEW) and sarcopenia in patients with CKD. In this cross-sectional study, 109 patients with CKD were selected from two clinics in Shiraz, Iran. The intake of individuals’ diets was recorded using a validated 168-item food frequency questionnaire. Additionally, Asian Working Group for Sarcopenia (AWGS) guidelines were utilized to evaluate muscles’ strength, mass, and function. Also, four International Society of Renal Nutrition and Metabolism (ISRNM) criteria (body mass index, intake of protein, albumin, and urine creatinine) were used to diagnose PEW. Logistic regression was used to assess the association between DII and sarcopenia as well as PEW. The results showed that the intake of saturated fatty acids, trans fatty acids, niacin, beta-carotene, and vitamin C was significantly different between lower and higher DII groups. In the univariate model, higher odds of sarcopenia was observed by each unit increase in DII (odds ratio (OR) = 1.379, 95% confidence interval (CI): 1.042–1.824) and age (OR = 1.073, 95% CI: 1.017–1.132). Additionally, in the multivariate model, the association between DII and age with odds of sarcopenia remained significant (DII: OR = 1.379, 95% CI: 1.030–1.846 and age: OR = 1.063, 95% CI: 1.007–1.121). The current study suggests the possible role of pro-inflammatory foods in worsening muscle health, specifically sarcopenia, in CKD patients. Future longitudinal studies may reveal the causative nature of these correlations.

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Section: Discussionmentioning

confidence: 99%

Dietary inflammatory index could increase the risk of sarcopenia in patients with chronic kidney disease

Mansouri,

Jafari,

Ranjbar

et al. 2024

Sci Rep

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“…Since sarcopenia can be caused by various factors and mechanisms that directly and indirectly damage skeletal muscle tissue, and CKD is associated with various local and systemic changes that can contribute to sarcopenia, a spectrum of pharmacological targets and interventions should be considered (Table 2). Although therapeutic drugs targeting muscle wasting mechanisms have been explored, most trials have focused on aged patients without CKD, and no drugs have yet been approved specifically for sarcopenia treatment [404,477]. Based on the direct pathologic effects of inflammatory cytokines on skeletal muscle cells, antagonizing the actions of specific cytokines might protect skeletal muscle tissue in CKD.…”

Section: Pharmacological Interventions To Protect From Ckd-associated...mentioning

confidence: 99%

Skeletal Muscle Injury in Chronic Kidney Disease—From Histologic Changes to Molecular Mechanisms and to Novel Therapies

Heitman,

Alexander,

Faul

2024

IJMS

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Chronic kidney disease (CKD) is associated with significant reductions in lean body mass and in the mass of various tissues, including skeletal muscle, which causes fatigue and contributes to high mortality rates. In CKD, the cellular protein turnover is imbalanced, with protein degradation outweighing protein synthesis, leading to a loss of protein and cell mass, which impairs tissue function. As CKD itself, skeletal muscle wasting, or sarcopenia, can have various origins and causes, and both CKD and sarcopenia share common risk factors, such as diabetes, obesity, and age. While these pathologies together with reduced physical performance and malnutrition contribute to muscle loss, they cannot explain all features of CKD-associated sarcopenia. Metabolic acidosis, systemic inflammation, insulin resistance and the accumulation of uremic toxins have been identified as additional factors that occur in CKD and that can contribute to sarcopenia. Here, we discuss the elevation of systemic phosphate levels, also called hyperphosphatemia, and the imbalance in the endocrine regulators of phosphate metabolism as another CKD-associated pathology that can directly and indirectly harm skeletal muscle tissue. To identify causes, affected cell types, and the mechanisms of sarcopenia and thereby novel targets for therapeutic interventions, it is important to first characterize the precise pathologic changes on molecular, cellular, and histologic levels, and to do so in CKD patients as well as in animal models of CKD, which we describe here in detail. We also discuss the currently known pathomechanisms and therapeutic approaches of CKD-associated sarcopenia, as well as the effects of hyperphosphatemia and the novel drug targets it could provide to protect skeletal muscle in CKD.

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“…The presence of AGEs in CKD contributes to the development and progression of sarcopenia [136]. Although therapeutic drugs targeting muscle wasting mechanisms have been explored, most trials have focused on aged patients without CKD, and no drugs have been approved specifically for sarcopenia treatment yet [137].…”

Section: Sarcopenia In Ckdmentioning

confidence: 99%

The Potential Influence of Uremic Toxins on the Homeostasis of Bones and Muscles in Chronic Kidney Disease

et al. 2023

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Patients with chronic kidney disease (CKD) often experience a high accumulation of protein-bound uremic toxins (PBUTs), specifically indoxyl sulfate (IS) and p-cresyl sulfate (pCS). In the early stages of CKD, the buildup of PBUTs inhibits bone and muscle function. As CKD progresses, elevated PBUT levels further hinder bone turnover and exacerbate muscle wasting. In the late stage of CKD, hyperparathyroidism worsens PBUT-induced muscle damage but can improve low bone turnover. PBUTs play a significant role in reducing both the quantity and quality of bone by affecting osteoblast and osteoclast lineage. IS, in particular, interferes with osteoblastogenesis by activating aryl hydrocarbon receptor (AhR) signaling, which reduces the expression of Runx2 and impedes osteoblast differentiation. High PBUT levels can also reduce calcitriol production, increase the expression of Wnt antagonists (SOST, DKK1), and decrease klotho expression, all of which contribute to low bone turnover disorders. Furthermore, PBUT accumulation leads to continuous muscle protein breakdown through the excessive production of reactive oxygen species (ROS) and inflammatory cytokines. Interactions between muscles and bones, mediated by various factors released from individual tissues, play a crucial role in the mutual modulation of bone and muscle in CKD. Exercise and nutritional therapy have the potential to yield favorable outcomes. Understanding the underlying mechanisms of bone and muscle loss in CKD can aid in developing new therapies for musculoskeletal diseases, particularly those related to bone loss and muscle wasting.

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Sarcopenia in chronic kidney disease: from bench to bedside

Cited by 5 publications

References 235 publications

Dietary inflammatory index could increase the risk of sarcopenia in patients with chronic kidney disease

Dietary inflammatory index could increase the risk of sarcopenia in patients with chronic kidney disease

Skeletal Muscle Injury in Chronic Kidney Disease—From Histologic Changes to Molecular Mechanisms and to Novel Therapies

The Potential Influence of Uremic Toxins on the Homeostasis of Bones and Muscles in Chronic Kidney Disease

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