Effect of uremic toxin-indoxyl sulfate on the skeletal system

Wen Chih Liu, Chia Chao Wu, Paik Seong Lim, Shiaw Wen Chien, Yi Chou Hou, Cai Mei Zheng, Jia Fwu Shyu, Yuh Feng Lin, Kuo Cheng Lu

研究成果: 雜誌貢獻回顧型文獻

1 引文 (Scopus)

摘要

Chronic kidney disease-mineral bone disorders (CKD-MBD) exhibit abnormalities in the circulating mineral levels, vitamin D metabolism, and parathyroid function that contribute to the formation of a bone lesion. The uremic toxin, indoxyl sulfate (IS), accumulates in the blood in cases of renal failure and leads to bone loss. The bone and renal responses to the action of the parathyroid hormone (PTH) are progressively decreased in CKD in spite of increasing PTH levels, a condition commonly called PTH resistance. There is a high prevalence of low bone turnover or adynamic bone disease in the early stages of CKD. This could be due to the inhibition of bone turnover, such as in PTH resistance, reduced active vitamin D levels, diabetes, aluminum, and, increased IS. With an increase in IS, there is a decrease in the osteoblast Wnt/b-catenin signaling and increase in the expression of Wnt signaling inhibitors, such as sclerostin and Dickkopf-1 (DKK1). Thus, a majority of early CKD patients exhibit deterioration of bone quality owing to the action of IS, this scenario could be termed uremic osteoporosis. However, this mechanism is complicated and not fully understood. With progressive deterioration in the renal function, IS accumulates along with persistent PTH secretion, potentially leading to high-turnover bone disease because high serum PTH levels have the ability of overriding peripheral PTH resistance and other inhibitory factors of bone formation. Finally, it leads to deterioration in bone quantity with prominent bone resorption in end stage renal disease. Uremic toxins adsorbents may decelerate oxidative stress and improve bone health in CKD patients. This review article focuses on IS and bone loss in CKD patients.
原文英語
頁(從 - 到)197-206
頁數10
期刊Clinica Chimica Acta
484
DOIs
出版狀態已發佈 - 九月 1 2018

指紋

Indican
Parathyroid Hormone
Bone
Bone and Bones
Bone Remodeling
Bone Diseases
Osteogenesis
Vitamin D
Chronic Kidney Disease-Mineral and Bone Disorder
Kidney
Deterioration
Catenins
Bone Resorption
Aluminum
Osteoblasts
Osteoporosis
Chronic Kidney Failure
Renal Insufficiency
Minerals
Oxidative Stress

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Biochemistry, medical

引用此文

Liu, W. C., Wu, C. C., Lim, P. S., Chien, S. W., Hou, Y. C., Zheng, C. M., ... Lu, K. C. (2018). Effect of uremic toxin-indoxyl sulfate on the skeletal system. Clinica Chimica Acta, 484, 197-206. https://doi.org/10.1016/j.cca.2018.05.057

Effect of uremic toxin-indoxyl sulfate on the skeletal system. / Liu, Wen Chih; Wu, Chia Chao; Lim, Paik Seong; Chien, Shiaw Wen; Hou, Yi Chou; Zheng, Cai Mei; Shyu, Jia Fwu; Lin, Yuh Feng; Lu, Kuo Cheng.

於: Clinica Chimica Acta, 卷 484, 01.09.2018, p. 197-206.

研究成果: 雜誌貢獻回顧型文獻

Liu, WC, Wu, CC, Lim, PS, Chien, SW, Hou, YC, Zheng, CM, Shyu, JF, Lin, YF & Lu, KC 2018, 'Effect of uremic toxin-indoxyl sulfate on the skeletal system', Clinica Chimica Acta, 卷 484, 頁 197-206. https://doi.org/10.1016/j.cca.2018.05.057
Liu, Wen Chih ; Wu, Chia Chao ; Lim, Paik Seong ; Chien, Shiaw Wen ; Hou, Yi Chou ; Zheng, Cai Mei ; Shyu, Jia Fwu ; Lin, Yuh Feng ; Lu, Kuo Cheng. / Effect of uremic toxin-indoxyl sulfate on the skeletal system. 於: Clinica Chimica Acta. 2018 ; 卷 484. 頁 197-206.
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abstract = "Chronic kidney disease-mineral bone disorders (CKD-MBD) exhibit abnormalities in the circulating mineral levels, vitamin D metabolism, and parathyroid function that contribute to the formation of a bone lesion. The uremic toxin, indoxyl sulfate (IS), accumulates in the blood in cases of renal failure and leads to bone loss. The bone and renal responses to the action of the parathyroid hormone (PTH) are progressively decreased in CKD in spite of increasing PTH levels, a condition commonly called PTH resistance. There is a high prevalence of low bone turnover or adynamic bone disease in the early stages of CKD. This could be due to the inhibition of bone turnover, such as in PTH resistance, reduced active vitamin D levels, diabetes, aluminum, and, increased IS. With an increase in IS, there is a decrease in the osteoblast Wnt/b-catenin signaling and increase in the expression of Wnt signaling inhibitors, such as sclerostin and Dickkopf-1 (DKK1). Thus, a majority of early CKD patients exhibit deterioration of bone quality owing to the action of IS, this scenario could be termed uremic osteoporosis. However, this mechanism is complicated and not fully understood. With progressive deterioration in the renal function, IS accumulates along with persistent PTH secretion, potentially leading to high-turnover bone disease because high serum PTH levels have the ability of overriding peripheral PTH resistance and other inhibitory factors of bone formation. Finally, it leads to deterioration in bone quantity with prominent bone resorption in end stage renal disease. Uremic toxins adsorbents may decelerate oxidative stress and improve bone health in CKD patients. This review article focuses on IS and bone loss in CKD patients.",
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AU - Liu, Wen Chih

AU - Wu, Chia Chao

AU - Lim, Paik Seong

AU - Chien, Shiaw Wen

AU - Hou, Yi Chou

AU - Zheng, Cai Mei

AU - Shyu, Jia Fwu

AU - Lin, Yuh Feng

AU - Lu, Kuo Cheng

PY - 2018/9/1

Y1 - 2018/9/1

N2 - Chronic kidney disease-mineral bone disorders (CKD-MBD) exhibit abnormalities in the circulating mineral levels, vitamin D metabolism, and parathyroid function that contribute to the formation of a bone lesion. The uremic toxin, indoxyl sulfate (IS), accumulates in the blood in cases of renal failure and leads to bone loss. The bone and renal responses to the action of the parathyroid hormone (PTH) are progressively decreased in CKD in spite of increasing PTH levels, a condition commonly called PTH resistance. There is a high prevalence of low bone turnover or adynamic bone disease in the early stages of CKD. This could be due to the inhibition of bone turnover, such as in PTH resistance, reduced active vitamin D levels, diabetes, aluminum, and, increased IS. With an increase in IS, there is a decrease in the osteoblast Wnt/b-catenin signaling and increase in the expression of Wnt signaling inhibitors, such as sclerostin and Dickkopf-1 (DKK1). Thus, a majority of early CKD patients exhibit deterioration of bone quality owing to the action of IS, this scenario could be termed uremic osteoporosis. However, this mechanism is complicated and not fully understood. With progressive deterioration in the renal function, IS accumulates along with persistent PTH secretion, potentially leading to high-turnover bone disease because high serum PTH levels have the ability of overriding peripheral PTH resistance and other inhibitory factors of bone formation. Finally, it leads to deterioration in bone quantity with prominent bone resorption in end stage renal disease. Uremic toxins adsorbents may decelerate oxidative stress and improve bone health in CKD patients. This review article focuses on IS and bone loss in CKD patients.

AB - Chronic kidney disease-mineral bone disorders (CKD-MBD) exhibit abnormalities in the circulating mineral levels, vitamin D metabolism, and parathyroid function that contribute to the formation of a bone lesion. The uremic toxin, indoxyl sulfate (IS), accumulates in the blood in cases of renal failure and leads to bone loss. The bone and renal responses to the action of the parathyroid hormone (PTH) are progressively decreased in CKD in spite of increasing PTH levels, a condition commonly called PTH resistance. There is a high prevalence of low bone turnover or adynamic bone disease in the early stages of CKD. This could be due to the inhibition of bone turnover, such as in PTH resistance, reduced active vitamin D levels, diabetes, aluminum, and, increased IS. With an increase in IS, there is a decrease in the osteoblast Wnt/b-catenin signaling and increase in the expression of Wnt signaling inhibitors, such as sclerostin and Dickkopf-1 (DKK1). Thus, a majority of early CKD patients exhibit deterioration of bone quality owing to the action of IS, this scenario could be termed uremic osteoporosis. However, this mechanism is complicated and not fully understood. With progressive deterioration in the renal function, IS accumulates along with persistent PTH secretion, potentially leading to high-turnover bone disease because high serum PTH levels have the ability of overriding peripheral PTH resistance and other inhibitory factors of bone formation. Finally, it leads to deterioration in bone quantity with prominent bone resorption in end stage renal disease. Uremic toxins adsorbents may decelerate oxidative stress and improve bone health in CKD patients. This review article focuses on IS and bone loss in CKD patients.

KW - Indoxyl sulfate

KW - Low bone turnover

KW - PTH resistance

KW - Uremic osteoporosis

KW - Uremic toxins adsorbent

KW - Wnt inhibitors

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