Administration of oral charcoal adsorbent (AST-120) suppresses low-turnover bone progression in uraemic rats

Iwasaki, Yoshiko; Yamato, Hideyuki; Nii-Kono, Tomoko; Fujieda, Ayako; Uchida, Motoyuki; Hosokawa, Akiko; Motojima, Masaru; Fukagawa, Masafumi

doi:10.1093/ndt/gfl311

Cited by 70 publications

(50 citation statements)

References 17 publications

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“…59 It is likely that IS also contributed to the low bone turnover observed in uremia. Iwasaki et al 10 showed that an in vivo treatment with AST-120 was effective in protecting against the development of low bone turnover in a rat model of CRF. They also reported that the accumulation of IS via rOat3 lowers bone formation and decreases bone turnover in uremic rats.…”

Section: Redox Properties Of Uremic Toxins Indoxyl Sulfatementioning

confidence: 99%

“…These retained solutes, which are involved in the development and manifestation of the uremic syndrome, are referred to as uremic toxins. The European Uremic Toxin Work Group (EUTox) classified 90 retention solutes into three groups according to molecular weight and serum protein binding characteristics: in chronic kidney disease (CKD) [3][4][5][6] and the onset of complications, such as vascular lesions, 7-9 bone disorders, 10,11 and the central nervous system (CNS) dysfunction [12][13][14][15] of CKD. In those tissues, organic anion transporters (OATs) mediate the cellular transport of uremic toxins, and uremic toxins that accumulate intracellularly stimulate the production of proinflammatory cytokines through the production of reactive oxygen species (ROS), which play a pathogenic role in CKD.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Update on the Pharmacokinetics and Redox Properties of Protein-Bound Uremic Toxins

Watanabe

Miyamoto

Otagiri

et al. 2011

Journal of Pharmaceutical Sciences

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Section: Redox Properties Of Uremic Toxins Indoxyl Sulfatementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Update on the Pharmacokinetics and Redox Properties of Protein-Bound Uremic Toxins

Watanabe

Miyamoto

Otagiri

et al. 2011

Journal of Pharmaceutical Sciences

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“…This condition can also be caused by skeletal resistance to PTH [153]. Several factors are considered to be involved in the pathogenesis of this resistance, including accumulation of 7-84PTH [154], down-regulation of the PTH receptor [155,156], and accumulation of osteoprotegerin [157] and indoxyl sulfate [158,159].…”

Section: Hypoparathyroidism In Ckdmentioning

confidence: 99%

Diseases of the parathyroid gland in chronic kidney disease

2011

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During the past few years, remarkable advances have been made in the understanding and the management of parathyroid diseases in patients with chronic kidney disease (CKD). One of the important insights is the identification of fibroblastic growth factor 23, which has greatly reshaped our understanding of secondary hyperparathyroidism (SHPT). The recent introduction of calcimimetic cinacalcet hydrochloride has led to a major breakthrough in the management of SHPT. Recognition of circulating molecular forms of parathyroid hormone (PTH) is also a major milestone in the accurate assessment of parathyroid function in CKD. Primary hyperparathyroidism should also be considered in patients with CKD, because it can cause various renal manifestations and can also occur as a sporadic disease in these patients. Hypoparathyroidism is occasionally seen in dialysis patients in the setting of diabetes mellitus and malnutrition-inflammation complex syndrome, as well as after parathyroidectomy for advanced SHPT. For patients with adynamic bone disease due to hypoparathyroidism and/or skeletal resistance to PTH, teriparatide, a PTH analog, may have potential for improving bone metabolism and reducing the risk of fracture. In this review, we summarize our current knowledge on diseases of the parathyroid gland in CKD patients, with a particular focus on recent work in the field.

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“…For bone histomorphometry, all mice were administered an injection of calcein (8 mg/kg body wt; Wako). 24,25 Statistical Analysis Data are expressed as means Ϯ SD. Differences among multiple groups were analyzed by ANOVA.…”

Section: Bone Analysismentioning

confidence: 99%

Type IIc Sodium–Dependent Phosphate Transporter Regulates Calcium Metabolism

Segawa¹,

Onitsuka²,

Kuwahata³

et al. 2009

Journal of the American Society of Nephrology

115

110

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Primary renal inorganic phosphate (Pi) wasting leads to hypophosphatemia, which is associated with skeletal mineralization defects. In humans, mutations in the gene encoding the type IIc sodiumdependent phosphate transporter lead to hereditary hypophophatemic rickets with hypercalciuria, but whether Pi wasting directly causes the bone disorder is unknown. Here, we generated Npt2c-null mice to define the contribution of Npt2c to Pi homeostasis and to bone abnormalities. Homozygous mutants (Npt2c Ϫ/Ϫ ) exhibited hypercalcemia, hypercalciuria, and elevated plasma 1,25-dihydroxyvitamin D 3 levels, but they did not develop hypophosphatemia, hyperphosphaturia, renal calcification, rickets, or osteomalacia. The increased levels of 1,25-dihydroxyvitamin D 3 in Npt2c Ϫ/Ϫ mice compared with age-matched Npt2c ϩ/ϩ mice may be the result of reduced catabolism, because we observed significantly reduced expression of renal 25-hydroxyvitamin D-24-hydroxylase mRNA but no change in 1␣-hydroxylase mRNA levels. Enhanced intestinal absorption of calcium (Ca) contributed to the hypercalcemia and increased urinary Ca excretion. Furthermore, plasma levels of the phosphaturic protein fibroblast growth factor 23 were significantly decreased in Npt2c Ϫ/Ϫ mice. Sodium-dependent Pi co-transport at the renal brush border membrane, however, was not different among Npt2c ϩ/ϩ , Npt2c ϩ/Ϫ , and Npt2c Ϫ/Ϫ mice.In summary, these data suggest that Npt2c maintains normal Ca metabolism, in part by modulating the vitamin D/fibroblast growth factor 23 axis. 20: 104 -113, 200920: 104 -113, . doi: 10.1681 Inorganic phosphate (Pi) is an essential nutrient in terms of both cellular metabolism and skeletal mineralization. The kidney is a major regulator of Pi homeostasis and can increase or decrease its Pi reabsorptive capacity to accommodate Pi needs. Up to 70% of filtered Pi is reabsorbed in the proximal tubule in which sodium (Na)-dependent Pi transport systems in the brush border membrane (BBM) mediated the rate-limiting step in the overall Pi reabsorptive process. J Am Soc Nephrol

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Administration of oral charcoal adsorbent (AST-120) suppresses low-turnover bone progression in uraemic rats

Abstract: Administration of the oral charcoal adsorbent AST-120 decreases the osteoblast cytotoxicity of UTx including IS, and suppresses progression of low bone turnover in uraemic rats.

Cited by 70 publications

References 17 publications

Update on the Pharmacokinetics and Redox Properties of Protein-Bound Uremic Toxins

Update on the Pharmacokinetics and Redox Properties of Protein-Bound Uremic Toxins

Diseases of the parathyroid gland in chronic kidney disease

Type IIc Sodium–Dependent Phosphate Transporter Regulates Calcium Metabolism

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