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Effects of sevelamer on HbA1c, inflammation, and advanced glycation end products in diabetic kidney disease.
Clin J Am Soc Nephrol. 2012 Jun; 7(6):934-42.CJ

Abstract

BACKGROUND AND OBJECTIVES

Increased inflammation and oxidative stress may be caused by proteins and lipids modified by cytotoxic advanced glycation end products (AGEs) in food. Restricting food containing elevated AGEs improves these risk factors in diabetic CKD. Because diet adherence can be problematic, this study aimed to remove cytotoxic AGEs from food already ingested and to determine whether sevelamer carbonate sequesters cytotoxic AGEs in the gut, preventing their uptake and thereby reducing AGE-induced abnormalities.

DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS

This single-center, randomized, 2-month, open-label, intention-to-treat, crossover study compared sevelamer carbonate with calcium carbonate treatment in stage 2-4 diabetic CKD. Participants received 2 months of treatment with one drug, had a 1-week washout, and then received the opposite drug for 2 months.

RESULTS

Sevelamer carbonate reduced HbA1c, serum methylglyoxal, serum (ε)N-carboxymethyl-lysine, triglycerides, and 8-isoprostanes. Total cholesterol and fibroblast growth factor 23 were reduced by sevelamer carbonate, relative to calcium carbonate. AGE receptor 1 and sirtuin 1 mRNA were increased and PMNC TNFα levels were decreased by sevelamer carbonate, but not calcium carbonate. Medications and caloric and AGE intake remained unchanged. Sevelamer carbonate reversibly bound AGE-BSA at intestinal, but not stomach, pH.

CONCLUSIONS

Sevelamer carbonate significantly reduces HbA1c, fibroblast growth factor 23, lipids, and markers of inflammation and oxidative stress, and markedly increases antioxidant markers, independently of phosphorus in patients with diabetes and early kidney disease. These novel actions of sevelamer carbonate on metabolic and inflammatory abnormalities in type 2 diabetes mellitus may affect progression of early diabetic CKD.

Authors+Show Affiliations

Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, New York, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22461535

Citation

Vlassara, Helen, et al. "Effects of Sevelamer On HbA1c, Inflammation, and Advanced Glycation End Products in Diabetic Kidney Disease." Clinical Journal of the American Society of Nephrology : CJASN, vol. 7, no. 6, 2012, pp. 934-42.
Vlassara H, Uribarri J, Cai W, et al. Effects of sevelamer on HbA1c, inflammation, and advanced glycation end products in diabetic kidney disease. Clin J Am Soc Nephrol. 2012;7(6):934-42.
Vlassara, H., Uribarri, J., Cai, W., Goodman, S., Pyzik, R., Post, J., Grosjean, F., Woodward, M., & Striker, G. E. (2012). Effects of sevelamer on HbA1c, inflammation, and advanced glycation end products in diabetic kidney disease. Clinical Journal of the American Society of Nephrology : CJASN, 7(6), 934-42. https://doi.org/10.2215/CJN.12891211
Vlassara H, et al. Effects of Sevelamer On HbA1c, Inflammation, and Advanced Glycation End Products in Diabetic Kidney Disease. Clin J Am Soc Nephrol. 2012;7(6):934-42. PubMed PMID: 22461535.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of sevelamer on HbA1c, inflammation, and advanced glycation end products in diabetic kidney disease. AU - Vlassara,Helen, AU - Uribarri,Jaime, AU - Cai,Weijing, AU - Goodman,Susan, AU - Pyzik,Renata, AU - Post,James, AU - Grosjean,Fabrizio, AU - Woodward,Mark, AU - Striker,Gary E, Y1 - 2012/03/29/ PY - 2012/3/31/entrez PY - 2012/3/31/pubmed PY - 2012/10/17/medline SP - 934 EP - 42 JF - Clinical journal of the American Society of Nephrology : CJASN JO - Clin J Am Soc Nephrol VL - 7 IS - 6 N2 - BACKGROUND AND OBJECTIVES: Increased inflammation and oxidative stress may be caused by proteins and lipids modified by cytotoxic advanced glycation end products (AGEs) in food. Restricting food containing elevated AGEs improves these risk factors in diabetic CKD. Because diet adherence can be problematic, this study aimed to remove cytotoxic AGEs from food already ingested and to determine whether sevelamer carbonate sequesters cytotoxic AGEs in the gut, preventing their uptake and thereby reducing AGE-induced abnormalities. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This single-center, randomized, 2-month, open-label, intention-to-treat, crossover study compared sevelamer carbonate with calcium carbonate treatment in stage 2-4 diabetic CKD. Participants received 2 months of treatment with one drug, had a 1-week washout, and then received the opposite drug for 2 months. RESULTS: Sevelamer carbonate reduced HbA1c, serum methylglyoxal, serum (ε)N-carboxymethyl-lysine, triglycerides, and 8-isoprostanes. Total cholesterol and fibroblast growth factor 23 were reduced by sevelamer carbonate, relative to calcium carbonate. AGE receptor 1 and sirtuin 1 mRNA were increased and PMNC TNFα levels were decreased by sevelamer carbonate, but not calcium carbonate. Medications and caloric and AGE intake remained unchanged. Sevelamer carbonate reversibly bound AGE-BSA at intestinal, but not stomach, pH. CONCLUSIONS: Sevelamer carbonate significantly reduces HbA1c, fibroblast growth factor 23, lipids, and markers of inflammation and oxidative stress, and markedly increases antioxidant markers, independently of phosphorus in patients with diabetes and early kidney disease. These novel actions of sevelamer carbonate on metabolic and inflammatory abnormalities in type 2 diabetes mellitus may affect progression of early diabetic CKD. SN - 1555-905X UR - https://www.unboundmedicine.com/medline/citation/22461535/Effects_of_sevelamer_on_HbA1c_inflammation_and_advanced_glycation_end_products_in_diabetic_kidney_disease_ L2 - https://cjasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=22461535 DB - PRIME DP - Unbound Medicine ER -