Oral Adsorbent AST-120 Decreases Serum Levels of AGEs in Patients with Chronic Renal Failure

Ueda, Seinosuke; Yamagishi, Sho‐ichi; Takeuchi, Masayoshi; Kohno, Keisuke; Shibata, Ryoko; Matsumoto, Yukie; Kaneyuki, Utako; Fujimura, Toshiko; Hayashida, Ayako; Okuda, Seiya

doi:10.2119/2005-00034.ueda

Cited by 56 publications

(57 citation statements)

References 25 publications

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“…Since AGEs represent an important class of uremic toxins and that, as described above, diet-derived AGEs could play an important role in atherogenesis, we investigated whether Kremezin R treatment could decrease serum levels of AGEs in non-diabetic CRF patients. Administration of Kremezin R (6 g/day) for 3 months significantly decreased serum levels of AGEs in non-diabetic CRF patients, whereas AGE levels remained unchanged in age-and renal function-matched CRF patients without Kremezin R [44]. In addition, patient serum after Kremezin R treatment significantly reduced mRNA levels of RAGE, MCP-1, and VCAM-1 in HUVEC compared with serum before treatment.…”

Section: (2) Renal Injurymentioning

confidence: 91%

Food-Derived Advanced Glycation end Products (AGEs): A Novel Therapeutic Target for Various Disorders

Yamagishi

Ueda²,

Okuda

2007

CPD

Self Cite

112

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Non-enzymatic modification of proteins by reducing sugars, a process that is also known as Maillard reaction, leads to the formation of advanced glycation end products (AGEs) in vivo. It is now well established that formation and accumulation of AGEs progress during normal aging, and at an extremely accelerated rate under diabetes, thus being implicated in various types of AGE-related disorders such as diabetic vascular complications, neurodegenerative diseases and cancers. Further, there is accumulating evidence that AGEs and their receptor RAGE interaction elicits oxidative stress generation and subsequently alters gene expression in various types of cells. In addition, digested food-derived AGEs are found to play an important role in the pathogenesis of the AGE-related disorders as well. Indeed, restriction of diet-derived AGEs not only blocks the progression of atherosclerosis and renal injury, but also improves insulin resistance in animal models. AGE-poor diets reduce serum levels of inflammatory biomarkers in patients with diabetes or chronic renal failure. These observations suggest that the restriction of food-derived AGEs or the inhibition of absorption of dietary AGEs may be a novel target for therapeutic intervention in the AGE-related disorders. In this paper, we review the pathological role of food-derived AGEs in various types of disorders and discuss the potential utility of oral adsorbent that inhibits the absorption of AGEs in these devastating diseases.

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Section: (2) Renal Injurymentioning

confidence: 91%

Food-Derived Advanced Glycation end Products (AGEs): A Novel Therapeutic Target for Various Disorders

Yamagishi

Ueda²,

Okuda

2007

CPD

Self Cite

112

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“…The oral adsorbent AST-120 could be an interesting alternative means of lowering uremic toxin levels. It reduces intestinal absorption of IS (127) and decreases AGEs levels in non diabetic CKD patients (128). In uremic rats, it lowers the serum concentration of IS and reduces kidney fibrosis and progression of CKD (129).…”

Section: Drugsmentioning

confidence: 99%

Vascular Incompetence in Dialysis Patients—Protein‐Bound Uremic Toxins and Endothelial Dysfunction

Jourde-Chiche

Dou

Cérini

et al. 2011

Seminars in Dialysis

162

145

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Patients with chronic kidney disease (CKD) have a much higher risk of cardiovascular diseases than the general population. Endothelial dysfunction, which participates in accelerated atherosclerosis, is a hallmark of CKD. Patients with CKD display impaired endothelium-dependent vasodilatation, elevated soluble biomarkers of endothelial dysfunction, and increased oxidative stress. They also present an imbalance between circulating endothelial populations reflecting endothelial injury (endothelial microparticles and circulating endothelial cells) and repair (endothelial progenitor cells). Endothelial damage induced by a uremic environment suggests an involvement of uremia-specific factors. Several uremic toxins, mostly protein-bound, have been shown to have specific endothelial toxicity: ADMA, homocysteine, AGEs, and more recently, p-cresyl sulfate and indoxyl sulfate. These toxins, all poorly removed by hemodialysis therapies, share mechanisms of endothelial toxicity: they promote pro-oxidant and pro-inflammatory response and inhibit endothelial repair. This article (i) reviews the evidence for endothelial dysfunction in CKD, (ii) specifies the involvement of protein-bound uremic toxins in this dysfunction, and (iii) discusses therapeutic strategies for lowering uremic toxin concentrations or for countering the effects of uremic toxins on the endothelium.

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“…We have recently found that administration of AST‐120 (Kremezin) (6 g/day) for three months significantly decreases the serum level of AGEs in non‐diabetic CRF patients, whereas AGE levels remain unchanged in age‐ and renal function‐matched CRF patients without AST‐120 (26). In addition, patient serum after AST‐120 treatment significantly reduced mRNA levels of RAGE, MCP‐1, and VCAM‐1 in endothelial cells compared with serum before treatment.…”

Section: Food‐derived Ages and Vascular Complications In Diabetes: Ormentioning

confidence: 99%

Advanced Glycation End Products and Receptor–Oxidative Stress System in Diabetic Vascular Complications

Yamagishi

2009

Ther Apher Dial

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Reducing sugars can react non-enzymatically with amino groups of protein to form Amadori products. These early glycation products undergo further complex reactions, such as rearrangement, dehydration, and condensation, to become irreversibly cross-linked, heterogeneous fluorescent derivatives, termed advanced glycation end products (AGEs). The formation and accumulation of AGEs have been known to progress at an accelerated rate in patients with diabetes mellitus, thus being involved in the development and progression of diabetic micro- and macroangiopathy. Indeed, there is accumulating evidence that an interaction between an AGE and its receptor (RAGE) generates oxidative stress and subsequently evokes vascular inflammation and thrombosis, thereby playing a central role in diabetic vascular complications. In this paper, we review the pathophysiological role of AGE-RAGE-oxidative stress system and its therapeutic interventions in diabetic micro- and macroangiopathy.

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Oral Adsorbent AST-120 Decreases Serum Levels of AGEs in Patients with Chronic Renal Failure

Cited by 56 publications

References 25 publications

Food-Derived Advanced Glycation end Products (AGEs): A Novel Therapeutic Target for Various Disorders

Food-Derived Advanced Glycation end Products (AGEs): A Novel Therapeutic Target for Various Disorders

Vascular Incompetence in Dialysis Patients—Protein‐Bound Uremic Toxins and Endothelial Dysfunction

Advanced Glycation End Products and Receptor–Oxidative Stress System in Diabetic Vascular Complications

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