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Effects of Sucroferric Oxyhydroxide Compared to Lanthanum Carbonate and Sevelamer Carbonate on Phosphate Homeostasis and Vascular Calcifications in a Rat Model of Chronic Kidney Failure.

Phan O, Maillard M, Malluche HH, Stehle JC, Funk F, Burnier M - Biomed Res Int (2015)

Bottom Line: Only sucroferric oxyhydroxide was associated with significantly decreased FGF23.Vascular calcifications of the thoracic aorta were decreased by all three phosphate binders.The role of FGF23 in calcification remains to be confirmed.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Service of Nephrology and Hypertension, Centre Hospitalier Universitaire Vaudois (CHUV) and University of Lausanne, Lausanne, Switzerland.

ABSTRACT
Elevated serum phosphorus, calcium, and fibroblast growth factor 23 (FGF23) levels are associated with cardiovascular disease in chronic renal disease. This study evaluated the effects of sucroferric oxyhydroxide (PA21), a new iron-based phosphate binder, versus lanthanum carbonate (La) and sevelamer carbonate (Se), on serum FGF23, phosphorus, calcium, and intact parathyroid hormone (iPTH) concentrations, and the development of vascular calcification in adenine-induced chronic renal failure (CRF) rats. After induction of CRF, renal function was significantly impaired in all groups: uremic rats developed severe hyperphosphatemia, and serum iPTH increased significantly. All uremic rats (except controls) then received phosphate binders for 4 weeks. Hyperphosphatemia and increased serum iPTH were controlled to a similar extent in all phosphate binder-treatment groups. Only sucroferric oxyhydroxide was associated with significantly decreased FGF23. Vascular calcifications of the thoracic aorta were decreased by all three phosphate binders. Calcifications were better prevented at the superior part of the thoracic and abdominal aorta in the PA21 treated rats. In adenine-induced CRF rats, sucroferric oxyhydroxide was as effective as La and Se in controlling hyperphosphatemia, secondary hyperparathyroidism, and vascular calcifications. The role of FGF23 in calcification remains to be confirmed.

No MeSH data available.


Related in: MedlinePlus

von Kossa stains of the vascular calcifications of adenine fed rats after 4 weeks of treatment. Vascular calcifications were evaluated by von Kossa staining and histomorphometrically with a magnification of 40. (a) Superior thoracic aorta, (b) carotid, and (c) abdominal aorta from CRF control rats. (d) Superior thoracic aorta, (e) carotid, and (f) abdominal aorta from CRF rats treated by sucroferric oxyhydroxide (PA21).
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fig4: von Kossa stains of the vascular calcifications of adenine fed rats after 4 weeks of treatment. Vascular calcifications were evaluated by von Kossa staining and histomorphometrically with a magnification of 40. (a) Superior thoracic aorta, (b) carotid, and (c) abdominal aorta from CRF control rats. (d) Superior thoracic aorta, (e) carotid, and (f) abdominal aorta from CRF rats treated by sucroferric oxyhydroxide (PA21).

Mentions: Vascular calcifications were observed in more than 70% of the uremic control rats. Vascular calcifications were evaluated at different sites: (a) carotids, (b) inferior and superior part of the thoracic aorta, and (c) abdominal aorta. Vascular calcifications of the thoracic aorta (inferior and superior part) were significantly decreased in all three phosphate binder groups (Figures 3 and 4 and Table 4). Vascular calcifications of the abdominal aorta were only decreased in the sucroferric oxyhydroxide (PA21) group and PA21 was more effective than lanthanum carbonate in preventing calcifications in the superior part of the thoracic aorta (Figures 3 and 4 and Table 4).


Effects of Sucroferric Oxyhydroxide Compared to Lanthanum Carbonate and Sevelamer Carbonate on Phosphate Homeostasis and Vascular Calcifications in a Rat Model of Chronic Kidney Failure.

Phan O, Maillard M, Malluche HH, Stehle JC, Funk F, Burnier M - Biomed Res Int (2015)

von Kossa stains of the vascular calcifications of adenine fed rats after 4 weeks of treatment. Vascular calcifications were evaluated by von Kossa staining and histomorphometrically with a magnification of 40. (a) Superior thoracic aorta, (b) carotid, and (c) abdominal aorta from CRF control rats. (d) Superior thoracic aorta, (e) carotid, and (f) abdominal aorta from CRF rats treated by sucroferric oxyhydroxide (PA21).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4499607&req=5

fig4: von Kossa stains of the vascular calcifications of adenine fed rats after 4 weeks of treatment. Vascular calcifications were evaluated by von Kossa staining and histomorphometrically with a magnification of 40. (a) Superior thoracic aorta, (b) carotid, and (c) abdominal aorta from CRF control rats. (d) Superior thoracic aorta, (e) carotid, and (f) abdominal aorta from CRF rats treated by sucroferric oxyhydroxide (PA21).
Mentions: Vascular calcifications were observed in more than 70% of the uremic control rats. Vascular calcifications were evaluated at different sites: (a) carotids, (b) inferior and superior part of the thoracic aorta, and (c) abdominal aorta. Vascular calcifications of the thoracic aorta (inferior and superior part) were significantly decreased in all three phosphate binder groups (Figures 3 and 4 and Table 4). Vascular calcifications of the abdominal aorta were only decreased in the sucroferric oxyhydroxide (PA21) group and PA21 was more effective than lanthanum carbonate in preventing calcifications in the superior part of the thoracic aorta (Figures 3 and 4 and Table 4).

Bottom Line: Only sucroferric oxyhydroxide was associated with significantly decreased FGF23.Vascular calcifications of the thoracic aorta were decreased by all three phosphate binders.The role of FGF23 in calcification remains to be confirmed.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Service of Nephrology and Hypertension, Centre Hospitalier Universitaire Vaudois (CHUV) and University of Lausanne, Lausanne, Switzerland.

ABSTRACT
Elevated serum phosphorus, calcium, and fibroblast growth factor 23 (FGF23) levels are associated with cardiovascular disease in chronic renal disease. This study evaluated the effects of sucroferric oxyhydroxide (PA21), a new iron-based phosphate binder, versus lanthanum carbonate (La) and sevelamer carbonate (Se), on serum FGF23, phosphorus, calcium, and intact parathyroid hormone (iPTH) concentrations, and the development of vascular calcification in adenine-induced chronic renal failure (CRF) rats. After induction of CRF, renal function was significantly impaired in all groups: uremic rats developed severe hyperphosphatemia, and serum iPTH increased significantly. All uremic rats (except controls) then received phosphate binders for 4 weeks. Hyperphosphatemia and increased serum iPTH were controlled to a similar extent in all phosphate binder-treatment groups. Only sucroferric oxyhydroxide was associated with significantly decreased FGF23. Vascular calcifications of the thoracic aorta were decreased by all three phosphate binders. Calcifications were better prevented at the superior part of the thoracic and abdominal aorta in the PA21 treated rats. In adenine-induced CRF rats, sucroferric oxyhydroxide was as effective as La and Se in controlling hyperphosphatemia, secondary hyperparathyroidism, and vascular calcifications. The role of FGF23 in calcification remains to be confirmed.

No MeSH data available.


Related in: MedlinePlus