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Adriana Dusso - One of the best experts on this subject based on the ideXlab platform.
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sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long term experimental uremia
Kidney International, 2003Co-Authors: Mario Cozzolino, Steven K Burke, Mark E Staniforth, Helen Liapis, Jane Finch, Adriana DussoAbstract:Sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long-term experimental uremia. Background In chronic renal failure (CRF), hyperphosphatemia and an elevated calcium-phosphate product are associated with vascular Calcification and increased cardiovascular morbidity and mortality. Previous data have demonstrated that 3-month treatment of uremic rats with sevelamer was associated with less nephrocalcinosis compared to calcium carbonate (CaCO 3 ), despite similar control of serum phosphorus, calcium-phosphorus product (Ca x P product), and secondary hyperparathyroidism. There was no evidence of aortic Calcification after 3 months of uremia ( J Am Soc Nephrol 13:2299–2308, 2002). The present studies explore the influence of sevelamer and CaCO 3 on cardiovascular and Kidney Calcifications in long-term experimental uremia over 6 months. Methods Normal and 5/6 nephrectomized rats (U) were fed a high phosphorus (HP) diet for 6 months. Two phosphate binders, CaCO 3 and sevelamer, were administered and their influence on hyperphosphatemia, secondary hyperparathyroidism, Kidney/myocardial/aortic Calcification, and renal function was compared. Results All uremic rats began the study with the same degree of renal failure. Sevelamer was as effective as CaCO 3 in reducing serum phosphorus, Ca x P product, and attenuating secondary hyperparathyroidism. Despite similar serum cholesterol levels, rats in the U-HP + sevelamer group had markedly lower calcium deposition in the myocardium and aorta (myocardium, 72 ± 4 μg/g wet tissue; aorta, 736 ± 156 μg/g wet tissue) compared to rats in either the U-HP + CaCO 3 group (myocardium, 179 ± 48, P P P 3 (1196 ± 180 μg/g wet tissue). Sevelamer-treated rats had less deterioration in renal function with an associated lower serum creatinine, higher creatinine clearance, and less proteinuria. There was no difference in overall mortality between the three experimental groups. Conclusion In long-term experimental CRF, in addition to controlling serum phosphorus and secondary hyperparathyroidism as efficiently as CaCO 3 , treatment with the phosphate-binder sevelamer attenuates vascular and Kidney Calcification.
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Sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long-term experimental uremia
'Wiley', 2003Co-Authors: Mario Cozzolino, Steven K Burke, Mark E Staniforth, Helen Liapis, Jane Finch, Adriana Dusso, E. SlatopolskyAbstract:BACKGROUND: In chronic renal failure (CRF), hyperphosphatemia and an elevated calcium-phosphate product are associated with vascular Calcification and increased cardiovascular morbidity and mortality. Previous data have demonstrated that 3-month treatment of uremic rats with sevelamer was associated with less nephrocalcinosis compared to calcium carbonate (CaCO3), despite similar control of serum phosphorus, calcium-phosphorus product (Ca x P product), and secondary hyperparathyroidism. There was no evidence of aortic Calcification after 3 months of uremia (J Am Soc Nephrol 13:2299-2308, 2002). The present studies explore the influence of sevelamer and CaCO3 on cardiovascular and Kidney Calcifications in long-term experimental uremia over 6 months. METHODS: Normal and 5/6 nephrectomized rats (U) were fed a high phosphorus (HP) diet for 6 months. Two phosphate binders, CaCO3 and sevelamer, were administered and their influence on hyperphosphatemia, secondary hyperparathyroidism, Kidney/myocardial/aortic Calcification, and renal function was compared. RESULTS: All uremic rats began the study with the same degree of renal failure. Sevelamer was as effective as CaCO3 in reducing serum phosphorus, Ca x P product, and attenuating secondary hyperparathyroidism. Despite similar serum cholesterol levels, rats in the U-HP + sevelamer group had markedly lower calcium deposition in the myocardium and aorta (myocardium, 72 +/- 4 microg/g wet tissue; aorta, 736 +/- 156 microg/g wet tissue) compared to rats in either the U-HP + CaCO3 group (myocardium, 179 +/- 48, P < 0.05; aorta, 1308 +/- 343, P < 0.05) or the U-HP group (myocardium, 98 +/- 10, NS; aorta, 2150 +/- 447, P < 0.05). Dual immunohistochemical analysis for calcium and endothelial cell markers demonstrated that myocardial calcium deposition was intravascular within capillaries. Furthermore, calcium deposition in the Kidney of uremic rats treated with sevelamer (582 +/- 111 microg/g wet tissue) was lower than that found in uremic rats treated with CaCO3 (1196 +/- 180 microg/g wet tissue). Sevelamer-treated rats had less deterioration in renal function with an associated lower serum creatinine, higher creatinine clearance, and less proteinuria. There was no difference in overall mortality between the three experimental groups. CONCLUSION: In long-term experimental CRF, in addition to controlling serum phosphorus and secondary hyperparathyroidism as efficiently as CaCO3, treatment with the phosphate-binder sevelamer attenuates vascular and Kidney Calcification
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The effects of sevelamer hydrochloride and calcium carbonate on Kidney Calcification in uremic rats
'Ovid Technologies (Wolters Kluwer Health)', 2002Co-Authors: M. Cozzolino, Helen Liapis, Adriana Dusso, J. Finch, S.k. Burke, E. SlatopolskyAbstract:The control of serum phosphorus (P) and calcium-phosphate (Ca x P) product is critical to the prevention of ectopic Calcification in chronic renal failure (CRF). Whereas calcium (Ca) salts, the most commonly used phosphate binders, markedly increase serum Ca and positive Ca balance, the new calcium- and aluminum-free phosphate binder, sevelamer hydrochloride (RenaGel), reduces serum P without altering serum Ca in hemodialysis patients. Using an experimental model of CRF, these studies compare sevelamer and calcium carbonate (CaCO(3)) in the control of serum P, secondary hyperparathyroidism (SH), and ectopic Calcifications. 5/6 nephrectomized rats underwent one of the following treatments for 3 mo: uremic + high-P diet (U-HP); UHP + 3% CaCO(3) (U-HP+C); UHP + 3% sevelamer (U-HP+S). Sevelamer treatment controlled serum P independent of increases in serum Ca, thus reducing serum Ca x P product and further deterioration of renal function, as indicated by the highest creatinine clearances. Sevelamer was as effective as CaCO(3) in the control of high-P-induced SH, as shown by similar serum PTH levels, parathyroid (PT) gland weight, and markers of PT hyperplasia. Also, both P binders elicited similar efficacy in reducing the myocardial and hepatic Calcifications induced by uremia. However, sevelamer caused a dramatic reduction of renal Ca deposition (29.8 +/- 8.6 micro g/g wet tissue) compared with both U-HP (175.5 +/- 45.7 micro g/g wet tissue, P < 0.01) and the U-HP+C (58.9 +/- 13.7 micro g/g wet tissue, P < 0.04). Histochemical analyses using Von Kossa and Alizarin red S staining of Kidney sections confirmed these findings. The high number of foci of Calcification in the Kidney of uremic controls (108 +/- 25) was reduced to 33.0 +/- 11.3 by CaCO(3) and decreased even further with sevelamer (16.4 +/- 8.9, P < 0.02 versus CaCO(3)). Importantly, the degree of tubulointerstitial fibrosis was also markedly lower in U-HP+S (5%) compared with either U-HP+C (30%) or U-HP (50%). It is concluded that in experimental CRF in rats, despite a similar control of serum P and SH, sevelamer is more effective than CaCO(3) in preventing renal Ca deposition and tubulointerstitial fibrosis, including better preservation of renal function. These findings cannot be extrapolated to human disease, and further studies in patients are necessary to determine the benefits of either P binder
Helen Liapis - One of the best experts on this subject based on the ideXlab platform.
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sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long term experimental uremia
Kidney International, 2003Co-Authors: Mario Cozzolino, Steven K Burke, Mark E Staniforth, Helen Liapis, Jane Finch, Adriana DussoAbstract:Sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long-term experimental uremia. Background In chronic renal failure (CRF), hyperphosphatemia and an elevated calcium-phosphate product are associated with vascular Calcification and increased cardiovascular morbidity and mortality. Previous data have demonstrated that 3-month treatment of uremic rats with sevelamer was associated with less nephrocalcinosis compared to calcium carbonate (CaCO 3 ), despite similar control of serum phosphorus, calcium-phosphorus product (Ca x P product), and secondary hyperparathyroidism. There was no evidence of aortic Calcification after 3 months of uremia ( J Am Soc Nephrol 13:2299–2308, 2002). The present studies explore the influence of sevelamer and CaCO 3 on cardiovascular and Kidney Calcifications in long-term experimental uremia over 6 months. Methods Normal and 5/6 nephrectomized rats (U) were fed a high phosphorus (HP) diet for 6 months. Two phosphate binders, CaCO 3 and sevelamer, were administered and their influence on hyperphosphatemia, secondary hyperparathyroidism, Kidney/myocardial/aortic Calcification, and renal function was compared. Results All uremic rats began the study with the same degree of renal failure. Sevelamer was as effective as CaCO 3 in reducing serum phosphorus, Ca x P product, and attenuating secondary hyperparathyroidism. Despite similar serum cholesterol levels, rats in the U-HP + sevelamer group had markedly lower calcium deposition in the myocardium and aorta (myocardium, 72 ± 4 μg/g wet tissue; aorta, 736 ± 156 μg/g wet tissue) compared to rats in either the U-HP + CaCO 3 group (myocardium, 179 ± 48, P P P 3 (1196 ± 180 μg/g wet tissue). Sevelamer-treated rats had less deterioration in renal function with an associated lower serum creatinine, higher creatinine clearance, and less proteinuria. There was no difference in overall mortality between the three experimental groups. Conclusion In long-term experimental CRF, in addition to controlling serum phosphorus and secondary hyperparathyroidism as efficiently as CaCO 3 , treatment with the phosphate-binder sevelamer attenuates vascular and Kidney Calcification.
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Sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long-term experimental uremia
'Wiley', 2003Co-Authors: Mario Cozzolino, Steven K Burke, Mark E Staniforth, Helen Liapis, Jane Finch, Adriana Dusso, E. SlatopolskyAbstract:BACKGROUND: In chronic renal failure (CRF), hyperphosphatemia and an elevated calcium-phosphate product are associated with vascular Calcification and increased cardiovascular morbidity and mortality. Previous data have demonstrated that 3-month treatment of uremic rats with sevelamer was associated with less nephrocalcinosis compared to calcium carbonate (CaCO3), despite similar control of serum phosphorus, calcium-phosphorus product (Ca x P product), and secondary hyperparathyroidism. There was no evidence of aortic Calcification after 3 months of uremia (J Am Soc Nephrol 13:2299-2308, 2002). The present studies explore the influence of sevelamer and CaCO3 on cardiovascular and Kidney Calcifications in long-term experimental uremia over 6 months. METHODS: Normal and 5/6 nephrectomized rats (U) were fed a high phosphorus (HP) diet for 6 months. Two phosphate binders, CaCO3 and sevelamer, were administered and their influence on hyperphosphatemia, secondary hyperparathyroidism, Kidney/myocardial/aortic Calcification, and renal function was compared. RESULTS: All uremic rats began the study with the same degree of renal failure. Sevelamer was as effective as CaCO3 in reducing serum phosphorus, Ca x P product, and attenuating secondary hyperparathyroidism. Despite similar serum cholesterol levels, rats in the U-HP + sevelamer group had markedly lower calcium deposition in the myocardium and aorta (myocardium, 72 +/- 4 microg/g wet tissue; aorta, 736 +/- 156 microg/g wet tissue) compared to rats in either the U-HP + CaCO3 group (myocardium, 179 +/- 48, P < 0.05; aorta, 1308 +/- 343, P < 0.05) or the U-HP group (myocardium, 98 +/- 10, NS; aorta, 2150 +/- 447, P < 0.05). Dual immunohistochemical analysis for calcium and endothelial cell markers demonstrated that myocardial calcium deposition was intravascular within capillaries. Furthermore, calcium deposition in the Kidney of uremic rats treated with sevelamer (582 +/- 111 microg/g wet tissue) was lower than that found in uremic rats treated with CaCO3 (1196 +/- 180 microg/g wet tissue). Sevelamer-treated rats had less deterioration in renal function with an associated lower serum creatinine, higher creatinine clearance, and less proteinuria. There was no difference in overall mortality between the three experimental groups. CONCLUSION: In long-term experimental CRF, in addition to controlling serum phosphorus and secondary hyperparathyroidism as efficiently as CaCO3, treatment with the phosphate-binder sevelamer attenuates vascular and Kidney Calcification
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The effects of sevelamer hydrochloride and calcium carbonate on Kidney Calcification in uremic rats
'Ovid Technologies (Wolters Kluwer Health)', 2002Co-Authors: M. Cozzolino, Helen Liapis, Adriana Dusso, J. Finch, S.k. Burke, E. SlatopolskyAbstract:The control of serum phosphorus (P) and calcium-phosphate (Ca x P) product is critical to the prevention of ectopic Calcification in chronic renal failure (CRF). Whereas calcium (Ca) salts, the most commonly used phosphate binders, markedly increase serum Ca and positive Ca balance, the new calcium- and aluminum-free phosphate binder, sevelamer hydrochloride (RenaGel), reduces serum P without altering serum Ca in hemodialysis patients. Using an experimental model of CRF, these studies compare sevelamer and calcium carbonate (CaCO(3)) in the control of serum P, secondary hyperparathyroidism (SH), and ectopic Calcifications. 5/6 nephrectomized rats underwent one of the following treatments for 3 mo: uremic + high-P diet (U-HP); UHP + 3% CaCO(3) (U-HP+C); UHP + 3% sevelamer (U-HP+S). Sevelamer treatment controlled serum P independent of increases in serum Ca, thus reducing serum Ca x P product and further deterioration of renal function, as indicated by the highest creatinine clearances. Sevelamer was as effective as CaCO(3) in the control of high-P-induced SH, as shown by similar serum PTH levels, parathyroid (PT) gland weight, and markers of PT hyperplasia. Also, both P binders elicited similar efficacy in reducing the myocardial and hepatic Calcifications induced by uremia. However, sevelamer caused a dramatic reduction of renal Ca deposition (29.8 +/- 8.6 micro g/g wet tissue) compared with both U-HP (175.5 +/- 45.7 micro g/g wet tissue, P < 0.01) and the U-HP+C (58.9 +/- 13.7 micro g/g wet tissue, P < 0.04). Histochemical analyses using Von Kossa and Alizarin red S staining of Kidney sections confirmed these findings. The high number of foci of Calcification in the Kidney of uremic controls (108 +/- 25) was reduced to 33.0 +/- 11.3 by CaCO(3) and decreased even further with sevelamer (16.4 +/- 8.9, P < 0.02 versus CaCO(3)). Importantly, the degree of tubulointerstitial fibrosis was also markedly lower in U-HP+S (5%) compared with either U-HP+C (30%) or U-HP (50%). It is concluded that in experimental CRF in rats, despite a similar control of serum P and SH, sevelamer is more effective than CaCO(3) in preventing renal Ca deposition and tubulointerstitial fibrosis, including better preservation of renal function. These findings cannot be extrapolated to human disease, and further studies in patients are necessary to determine the benefits of either P binder
Mark E Staniforth - One of the best experts on this subject based on the ideXlab platform.
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sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long term experimental uremia
Kidney International, 2003Co-Authors: Mario Cozzolino, Steven K Burke, Mark E Staniforth, Helen Liapis, Jane Finch, Adriana DussoAbstract:Sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long-term experimental uremia. Background In chronic renal failure (CRF), hyperphosphatemia and an elevated calcium-phosphate product are associated with vascular Calcification and increased cardiovascular morbidity and mortality. Previous data have demonstrated that 3-month treatment of uremic rats with sevelamer was associated with less nephrocalcinosis compared to calcium carbonate (CaCO 3 ), despite similar control of serum phosphorus, calcium-phosphorus product (Ca x P product), and secondary hyperparathyroidism. There was no evidence of aortic Calcification after 3 months of uremia ( J Am Soc Nephrol 13:2299–2308, 2002). The present studies explore the influence of sevelamer and CaCO 3 on cardiovascular and Kidney Calcifications in long-term experimental uremia over 6 months. Methods Normal and 5/6 nephrectomized rats (U) were fed a high phosphorus (HP) diet for 6 months. Two phosphate binders, CaCO 3 and sevelamer, were administered and their influence on hyperphosphatemia, secondary hyperparathyroidism, Kidney/myocardial/aortic Calcification, and renal function was compared. Results All uremic rats began the study with the same degree of renal failure. Sevelamer was as effective as CaCO 3 in reducing serum phosphorus, Ca x P product, and attenuating secondary hyperparathyroidism. Despite similar serum cholesterol levels, rats in the U-HP + sevelamer group had markedly lower calcium deposition in the myocardium and aorta (myocardium, 72 ± 4 μg/g wet tissue; aorta, 736 ± 156 μg/g wet tissue) compared to rats in either the U-HP + CaCO 3 group (myocardium, 179 ± 48, P P P 3 (1196 ± 180 μg/g wet tissue). Sevelamer-treated rats had less deterioration in renal function with an associated lower serum creatinine, higher creatinine clearance, and less proteinuria. There was no difference in overall mortality between the three experimental groups. Conclusion In long-term experimental CRF, in addition to controlling serum phosphorus and secondary hyperparathyroidism as efficiently as CaCO 3 , treatment with the phosphate-binder sevelamer attenuates vascular and Kidney Calcification.
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Sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long-term experimental uremia
'Wiley', 2003Co-Authors: Mario Cozzolino, Steven K Burke, Mark E Staniforth, Helen Liapis, Jane Finch, Adriana Dusso, E. SlatopolskyAbstract:BACKGROUND: In chronic renal failure (CRF), hyperphosphatemia and an elevated calcium-phosphate product are associated with vascular Calcification and increased cardiovascular morbidity and mortality. Previous data have demonstrated that 3-month treatment of uremic rats with sevelamer was associated with less nephrocalcinosis compared to calcium carbonate (CaCO3), despite similar control of serum phosphorus, calcium-phosphorus product (Ca x P product), and secondary hyperparathyroidism. There was no evidence of aortic Calcification after 3 months of uremia (J Am Soc Nephrol 13:2299-2308, 2002). The present studies explore the influence of sevelamer and CaCO3 on cardiovascular and Kidney Calcifications in long-term experimental uremia over 6 months. METHODS: Normal and 5/6 nephrectomized rats (U) were fed a high phosphorus (HP) diet for 6 months. Two phosphate binders, CaCO3 and sevelamer, were administered and their influence on hyperphosphatemia, secondary hyperparathyroidism, Kidney/myocardial/aortic Calcification, and renal function was compared. RESULTS: All uremic rats began the study with the same degree of renal failure. Sevelamer was as effective as CaCO3 in reducing serum phosphorus, Ca x P product, and attenuating secondary hyperparathyroidism. Despite similar serum cholesterol levels, rats in the U-HP + sevelamer group had markedly lower calcium deposition in the myocardium and aorta (myocardium, 72 +/- 4 microg/g wet tissue; aorta, 736 +/- 156 microg/g wet tissue) compared to rats in either the U-HP + CaCO3 group (myocardium, 179 +/- 48, P < 0.05; aorta, 1308 +/- 343, P < 0.05) or the U-HP group (myocardium, 98 +/- 10, NS; aorta, 2150 +/- 447, P < 0.05). Dual immunohistochemical analysis for calcium and endothelial cell markers demonstrated that myocardial calcium deposition was intravascular within capillaries. Furthermore, calcium deposition in the Kidney of uremic rats treated with sevelamer (582 +/- 111 microg/g wet tissue) was lower than that found in uremic rats treated with CaCO3 (1196 +/- 180 microg/g wet tissue). Sevelamer-treated rats had less deterioration in renal function with an associated lower serum creatinine, higher creatinine clearance, and less proteinuria. There was no difference in overall mortality between the three experimental groups. CONCLUSION: In long-term experimental CRF, in addition to controlling serum phosphorus and secondary hyperparathyroidism as efficiently as CaCO3, treatment with the phosphate-binder sevelamer attenuates vascular and Kidney Calcification
Jane Finch - One of the best experts on this subject based on the ideXlab platform.
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sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long term experimental uremia
Kidney International, 2003Co-Authors: Mario Cozzolino, Steven K Burke, Mark E Staniforth, Helen Liapis, Jane Finch, Adriana DussoAbstract:Sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long-term experimental uremia. Background In chronic renal failure (CRF), hyperphosphatemia and an elevated calcium-phosphate product are associated with vascular Calcification and increased cardiovascular morbidity and mortality. Previous data have demonstrated that 3-month treatment of uremic rats with sevelamer was associated with less nephrocalcinosis compared to calcium carbonate (CaCO 3 ), despite similar control of serum phosphorus, calcium-phosphorus product (Ca x P product), and secondary hyperparathyroidism. There was no evidence of aortic Calcification after 3 months of uremia ( J Am Soc Nephrol 13:2299–2308, 2002). The present studies explore the influence of sevelamer and CaCO 3 on cardiovascular and Kidney Calcifications in long-term experimental uremia over 6 months. Methods Normal and 5/6 nephrectomized rats (U) were fed a high phosphorus (HP) diet for 6 months. Two phosphate binders, CaCO 3 and sevelamer, were administered and their influence on hyperphosphatemia, secondary hyperparathyroidism, Kidney/myocardial/aortic Calcification, and renal function was compared. Results All uremic rats began the study with the same degree of renal failure. Sevelamer was as effective as CaCO 3 in reducing serum phosphorus, Ca x P product, and attenuating secondary hyperparathyroidism. Despite similar serum cholesterol levels, rats in the U-HP + sevelamer group had markedly lower calcium deposition in the myocardium and aorta (myocardium, 72 ± 4 μg/g wet tissue; aorta, 736 ± 156 μg/g wet tissue) compared to rats in either the U-HP + CaCO 3 group (myocardium, 179 ± 48, P P P 3 (1196 ± 180 μg/g wet tissue). Sevelamer-treated rats had less deterioration in renal function with an associated lower serum creatinine, higher creatinine clearance, and less proteinuria. There was no difference in overall mortality between the three experimental groups. Conclusion In long-term experimental CRF, in addition to controlling serum phosphorus and secondary hyperparathyroidism as efficiently as CaCO 3 , treatment with the phosphate-binder sevelamer attenuates vascular and Kidney Calcification.
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Sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long-term experimental uremia
'Wiley', 2003Co-Authors: Mario Cozzolino, Steven K Burke, Mark E Staniforth, Helen Liapis, Jane Finch, Adriana Dusso, E. SlatopolskyAbstract:BACKGROUND: In chronic renal failure (CRF), hyperphosphatemia and an elevated calcium-phosphate product are associated with vascular Calcification and increased cardiovascular morbidity and mortality. Previous data have demonstrated that 3-month treatment of uremic rats with sevelamer was associated with less nephrocalcinosis compared to calcium carbonate (CaCO3), despite similar control of serum phosphorus, calcium-phosphorus product (Ca x P product), and secondary hyperparathyroidism. There was no evidence of aortic Calcification after 3 months of uremia (J Am Soc Nephrol 13:2299-2308, 2002). The present studies explore the influence of sevelamer and CaCO3 on cardiovascular and Kidney Calcifications in long-term experimental uremia over 6 months. METHODS: Normal and 5/6 nephrectomized rats (U) were fed a high phosphorus (HP) diet for 6 months. Two phosphate binders, CaCO3 and sevelamer, were administered and their influence on hyperphosphatemia, secondary hyperparathyroidism, Kidney/myocardial/aortic Calcification, and renal function was compared. RESULTS: All uremic rats began the study with the same degree of renal failure. Sevelamer was as effective as CaCO3 in reducing serum phosphorus, Ca x P product, and attenuating secondary hyperparathyroidism. Despite similar serum cholesterol levels, rats in the U-HP + sevelamer group had markedly lower calcium deposition in the myocardium and aorta (myocardium, 72 +/- 4 microg/g wet tissue; aorta, 736 +/- 156 microg/g wet tissue) compared to rats in either the U-HP + CaCO3 group (myocardium, 179 +/- 48, P < 0.05; aorta, 1308 +/- 343, P < 0.05) or the U-HP group (myocardium, 98 +/- 10, NS; aorta, 2150 +/- 447, P < 0.05). Dual immunohistochemical analysis for calcium and endothelial cell markers demonstrated that myocardial calcium deposition was intravascular within capillaries. Furthermore, calcium deposition in the Kidney of uremic rats treated with sevelamer (582 +/- 111 microg/g wet tissue) was lower than that found in uremic rats treated with CaCO3 (1196 +/- 180 microg/g wet tissue). Sevelamer-treated rats had less deterioration in renal function with an associated lower serum creatinine, higher creatinine clearance, and less proteinuria. There was no difference in overall mortality between the three experimental groups. CONCLUSION: In long-term experimental CRF, in addition to controlling serum phosphorus and secondary hyperparathyroidism as efficiently as CaCO3, treatment with the phosphate-binder sevelamer attenuates vascular and Kidney Calcification
Steven K Burke - One of the best experts on this subject based on the ideXlab platform.
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sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long term experimental uremia
Kidney International, 2003Co-Authors: Mario Cozzolino, Steven K Burke, Mark E Staniforth, Helen Liapis, Jane Finch, Adriana DussoAbstract:Sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long-term experimental uremia. Background In chronic renal failure (CRF), hyperphosphatemia and an elevated calcium-phosphate product are associated with vascular Calcification and increased cardiovascular morbidity and mortality. Previous data have demonstrated that 3-month treatment of uremic rats with sevelamer was associated with less nephrocalcinosis compared to calcium carbonate (CaCO 3 ), despite similar control of serum phosphorus, calcium-phosphorus product (Ca x P product), and secondary hyperparathyroidism. There was no evidence of aortic Calcification after 3 months of uremia ( J Am Soc Nephrol 13:2299–2308, 2002). The present studies explore the influence of sevelamer and CaCO 3 on cardiovascular and Kidney Calcifications in long-term experimental uremia over 6 months. Methods Normal and 5/6 nephrectomized rats (U) were fed a high phosphorus (HP) diet for 6 months. Two phosphate binders, CaCO 3 and sevelamer, were administered and their influence on hyperphosphatemia, secondary hyperparathyroidism, Kidney/myocardial/aortic Calcification, and renal function was compared. Results All uremic rats began the study with the same degree of renal failure. Sevelamer was as effective as CaCO 3 in reducing serum phosphorus, Ca x P product, and attenuating secondary hyperparathyroidism. Despite similar serum cholesterol levels, rats in the U-HP + sevelamer group had markedly lower calcium deposition in the myocardium and aorta (myocardium, 72 ± 4 μg/g wet tissue; aorta, 736 ± 156 μg/g wet tissue) compared to rats in either the U-HP + CaCO 3 group (myocardium, 179 ± 48, P P P 3 (1196 ± 180 μg/g wet tissue). Sevelamer-treated rats had less deterioration in renal function with an associated lower serum creatinine, higher creatinine clearance, and less proteinuria. There was no difference in overall mortality between the three experimental groups. Conclusion In long-term experimental CRF, in addition to controlling serum phosphorus and secondary hyperparathyroidism as efficiently as CaCO 3 , treatment with the phosphate-binder sevelamer attenuates vascular and Kidney Calcification.
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Sevelamer hydrochloride attenuates Kidney and cardiovascular Calcifications in long-term experimental uremia
'Wiley', 2003Co-Authors: Mario Cozzolino, Steven K Burke, Mark E Staniforth, Helen Liapis, Jane Finch, Adriana Dusso, E. SlatopolskyAbstract:BACKGROUND: In chronic renal failure (CRF), hyperphosphatemia and an elevated calcium-phosphate product are associated with vascular Calcification and increased cardiovascular morbidity and mortality. Previous data have demonstrated that 3-month treatment of uremic rats with sevelamer was associated with less nephrocalcinosis compared to calcium carbonate (CaCO3), despite similar control of serum phosphorus, calcium-phosphorus product (Ca x P product), and secondary hyperparathyroidism. There was no evidence of aortic Calcification after 3 months of uremia (J Am Soc Nephrol 13:2299-2308, 2002). The present studies explore the influence of sevelamer and CaCO3 on cardiovascular and Kidney Calcifications in long-term experimental uremia over 6 months. METHODS: Normal and 5/6 nephrectomized rats (U) were fed a high phosphorus (HP) diet for 6 months. Two phosphate binders, CaCO3 and sevelamer, were administered and their influence on hyperphosphatemia, secondary hyperparathyroidism, Kidney/myocardial/aortic Calcification, and renal function was compared. RESULTS: All uremic rats began the study with the same degree of renal failure. Sevelamer was as effective as CaCO3 in reducing serum phosphorus, Ca x P product, and attenuating secondary hyperparathyroidism. Despite similar serum cholesterol levels, rats in the U-HP + sevelamer group had markedly lower calcium deposition in the myocardium and aorta (myocardium, 72 +/- 4 microg/g wet tissue; aorta, 736 +/- 156 microg/g wet tissue) compared to rats in either the U-HP + CaCO3 group (myocardium, 179 +/- 48, P < 0.05; aorta, 1308 +/- 343, P < 0.05) or the U-HP group (myocardium, 98 +/- 10, NS; aorta, 2150 +/- 447, P < 0.05). Dual immunohistochemical analysis for calcium and endothelial cell markers demonstrated that myocardial calcium deposition was intravascular within capillaries. Furthermore, calcium deposition in the Kidney of uremic rats treated with sevelamer (582 +/- 111 microg/g wet tissue) was lower than that found in uremic rats treated with CaCO3 (1196 +/- 180 microg/g wet tissue). Sevelamer-treated rats had less deterioration in renal function with an associated lower serum creatinine, higher creatinine clearance, and less proteinuria. There was no difference in overall mortality between the three experimental groups. CONCLUSION: In long-term experimental CRF, in addition to controlling serum phosphorus and secondary hyperparathyroidism as efficiently as CaCO3, treatment with the phosphate-binder sevelamer attenuates vascular and Kidney Calcification
