Short-term therapy with R568 ameliorated secondary hyperparathyroidism but does not prevent aortic valve calcification in uremic rats
Renal failure associated aortic valve calcification (AVC) is the result of hyperphosphatemia and hyperparathyroidism. Calcimimetics is an effective tool for management of secondary hyperparathyroidism. Our goal was to evaluate the effect of the medical intervention with calcimimetic R568 on the AVC...
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| Published in | Frontiers in Nephrology (Online) Vol. 4; p. 1385705 |
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| Main Authors | , , , , , |
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| Language | English |
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06.08.2024
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| Abstract | Renal failure associated aortic valve calcification (AVC) is the result of hyperphosphatemia and hyperparathyroidism. Calcimimetics is an effective tool for management of secondary hyperparathyroidism. Our goal was to evaluate the effect of the medical intervention with calcimimetic R568 on the AVC process.
The experimental design consisted of administering a uremia-inducing phosphate-enriched diet to rats for six weeks. Rats received a daily R568 injection at different times. Biochemical analysis demonstrated increased urea (34.72 ± 3.57
. 5.18 ± 0.15 mmol/L,
<0.05) and creatinine (293.93 ± 79.6
. 12.82 ± 1.56 µmol/L,
<0.05). R568 treatment markedly reduced parathyroid hormone (PTH) levels in both treated groups (192.63 ± 26.85, 301.23 ± 101.79
. 3570 ± 986.63 pg/mL,
<0.05), with no impact on serum calcium and phosphate. von Kossa staining showed increase in AVC in uremic rats compared to control (1409 ± 159.5
. 27.33 ± 25.83,
<0.05). AVC was not affected by R568 in both groups (3343 ± 2462, 1593 ± 792
. 1409 ± 159.5, NS). Similarly, the inflammatory marker CD68 was elevated in uremic rats (15592 ± 3792
. 181.8 ± 15.29,
<0.01), and was not influenced by R568 treatment (8453 ± 818.5, 9318 ± 2232
. 15592 ± 3792, NS). Runt-related transcription factor 2 (Runx2), the regulator of osteoblast differentiation, was upregulated in uremic rats (23186 ± 9226
. 3184 ± 2495), that accompanied by elevated levels of Osteopontin (158395 ± 45911
. 237.7 ± 81.5,
<0.05) and Osteocalcin (22203 ± 8525
. 489.7 ± 200.6,
<0.05). R568 had no impact on osteoblastic markers (Runx2: 21743 ± 3193, 23004 ± 10871
. 23186 ± 9226, NS; osteopontin: 57680 ± 19522, 137116 ± 60103
. 158395 ± 45911, NS; osteocalcin: 10496 ± 5429, 8522 ± 5031
. 22203 ± 8525, NS).
In an adenine-induced uremic rat model, we showed that short-term R568 therapy had no effect on AVC. Treatment with R568 decreased PTH levels but had no effect on high phosphate levels. Regression of AVC necessitates not only a decrease in PTH levels, but also a decline in phosphate levels. To achieve improved outcomes, it is advisable to consider administering a combination of R568 with other medications, such as calcium supplements or phosphate binders. Additional studies are required for further evaluation of the potential treatment of chronic kidney disease (CKD)-associated AVC. |
|---|---|
| AbstractList | Renal failure associated aortic valve calcification (AVC) is the result of hyperphosphatemia and hyperparathyroidism. Calcimimetics is an effective tool for management of secondary hyperparathyroidism. Our goal was to evaluate the effect of the medical intervention with calcimimetic R568 on the AVC process.IntroductionRenal failure associated aortic valve calcification (AVC) is the result of hyperphosphatemia and hyperparathyroidism. Calcimimetics is an effective tool for management of secondary hyperparathyroidism. Our goal was to evaluate the effect of the medical intervention with calcimimetic R568 on the AVC process.The experimental design consisted of administering a uremia-inducing phosphate-enriched diet to rats for six weeks. Rats received a daily R568 injection at different times. Biochemical analysis demonstrated increased urea (34.72 ± 3.57 vs. 5.18 ± 0.15 mmol/L, p<0.05) and creatinine (293.93 ± 79.6 vs. 12.82 ± 1.56 µmol/L, p<0.05). R568 treatment markedly reduced parathyroid hormone (PTH) levels in both treated groups (192.63 ± 26.85, 301.23 ± 101.79 vs. 3570 ± 986.63 pg/mL, p<0.05), with no impact on serum calcium and phosphate. von Kossa staining showed increase in AVC in uremic rats compared to control (1409 ± 159.5 vs. 27.33 ± 25.83, p<0.05). AVC was not affected by R568 in both groups (3343 ± 2462, 1593 ± 792 vs. 1409 ± 159.5, NS). Similarly, the inflammatory marker CD68 was elevated in uremic rats (15592 ± 3792 vs. 181.8 ± 15.29, p<0.01), and was not influenced by R568 treatment (8453 ± 818.5, 9318 ± 2232 vs. 15592 ± 3792, NS). Runt-related transcription factor 2 (Runx2), the regulator of osteoblast differentiation, was upregulated in uremic rats (23186 ± 9226 vs. 3184 ± 2495), that accompanied by elevated levels of Osteopontin (158395 ± 45911 vs. 237.7 ± 81.5, p<0.05) and Osteocalcin (22203 ± 8525 vs. 489.7 ± 200.6, p<0.05). R568 had no impact on osteoblastic markers (Runx2: 21743 ± 3193, 23004 ± 10871 vs. 23186 ± 9226, NS; osteopontin: 57680 ± 19522, 137116 ± 60103 vs. 158395 ± 45911, NS; osteocalcin: 10496 ± 5429, 8522 ± 5031 vs. 22203 ± 8525, NS).Methods and resultsThe experimental design consisted of administering a uremia-inducing phosphate-enriched diet to rats for six weeks. Rats received a daily R568 injection at different times. Biochemical analysis demonstrated increased urea (34.72 ± 3.57 vs. 5.18 ± 0.15 mmol/L, p<0.05) and creatinine (293.93 ± 79.6 vs. 12.82 ± 1.56 µmol/L, p<0.05). R568 treatment markedly reduced parathyroid hormone (PTH) levels in both treated groups (192.63 ± 26.85, 301.23 ± 101.79 vs. 3570 ± 986.63 pg/mL, p<0.05), with no impact on serum calcium and phosphate. von Kossa staining showed increase in AVC in uremic rats compared to control (1409 ± 159.5 vs. 27.33 ± 25.83, p<0.05). AVC was not affected by R568 in both groups (3343 ± 2462, 1593 ± 792 vs. 1409 ± 159.5, NS). Similarly, the inflammatory marker CD68 was elevated in uremic rats (15592 ± 3792 vs. 181.8 ± 15.29, p<0.01), and was not influenced by R568 treatment (8453 ± 818.5, 9318 ± 2232 vs. 15592 ± 3792, NS). Runt-related transcription factor 2 (Runx2), the regulator of osteoblast differentiation, was upregulated in uremic rats (23186 ± 9226 vs. 3184 ± 2495), that accompanied by elevated levels of Osteopontin (158395 ± 45911 vs. 237.7 ± 81.5, p<0.05) and Osteocalcin (22203 ± 8525 vs. 489.7 ± 200.6, p<0.05). R568 had no impact on osteoblastic markers (Runx2: 21743 ± 3193, 23004 ± 10871 vs. 23186 ± 9226, NS; osteopontin: 57680 ± 19522, 137116 ± 60103 vs. 158395 ± 45911, NS; osteocalcin: 10496 ± 5429, 8522 ± 5031 vs. 22203 ± 8525, NS).In an adenine-induced uremic rat model, we showed that short-term R568 therapy had no effect on AVC. Treatment with R568 decreased PTH levels but had no effect on high phosphate levels. Regression of AVC necessitates not only a decrease in PTH levels, but also a decline in phosphate levels. To achieve improved outcomes, it is advisable to consider administering a combination of R568 with other medications, such as calcium supplements or phosphate binders. Additional studies are required for further evaluation of the potential treatment of chronic kidney disease (CKD)-associated AVC.ConclusionIn an adenine-induced uremic rat model, we showed that short-term R568 therapy had no effect on AVC. Treatment with R568 decreased PTH levels but had no effect on high phosphate levels. Regression of AVC necessitates not only a decrease in PTH levels, but also a decline in phosphate levels. To achieve improved outcomes, it is advisable to consider administering a combination of R568 with other medications, such as calcium supplements or phosphate binders. Additional studies are required for further evaluation of the potential treatment of chronic kidney disease (CKD)-associated AVC. Introduction Renal failure associated aortic valve calcification (AVC) is the result of hyperphosphatemia and hyperparathyroidism. Calcimimetics is an effective tool for management of secondary hyperparathyroidism. Our goal was to evaluate the effect of the medical intervention with calcimimetic R568 on the AVC process. Methods and results The experimental design consisted of administering a uremia-inducing phosphate-enriched diet to rats for six weeks. Rats received a daily R568 injection at different times. Biochemical analysis demonstrated increased urea (34.72 ± 3.57 vs . 5.18 ± 0.15 mmol/L, p <0.05) and creatinine (293.93 ± 79.6 vs . 12.82 ± 1.56 µmol/L, p <0.05). R568 treatment markedly reduced parathyroid hormone (PTH) levels in both treated groups (192.63 ± 26.85, 301.23 ± 101.79 vs . 3570 ± 986.63 pg/mL, p <0.05), with no impact on serum calcium and phosphate. von Kossa staining showed increase in AVC in uremic rats compared to control (1409 ± 159.5 vs . 27.33 ± 25.83, p <0.05). AVC was not affected by R568 in both groups (3343 ± 2462, 1593 ± 792 vs . 1409 ± 159.5, NS). Similarly, the inflammatory marker CD68 was elevated in uremic rats (15592 ± 3792 vs . 181.8 ± 15.29, p <0.01), and was not influenced by R568 treatment (8453 ± 818.5, 9318 ± 2232 vs . 15592 ± 3792, NS). Runt-related transcription factor 2 (Runx2), the regulator of osteoblast differentiation, was upregulated in uremic rats (23186 ± 9226 vs . 3184 ± 2495), that accompanied by elevated levels of Osteopontin (158395 ± 45911 vs . 237.7 ± 81.5, p <0.05) and Osteocalcin (22203 ± 8525 vs . 489.7 ± 200.6, p <0.05). R568 had no impact on osteoblastic markers (Runx2: 21743 ± 3193, 23004 ± 10871 vs . 23186 ± 9226, NS; osteopontin: 57680 ± 19522, 137116 ± 60103 vs . 158395 ± 45911, NS; osteocalcin: 10496 ± 5429, 8522 ± 5031 vs . 22203 ± 8525, NS). Conclusion In an adenine-induced uremic rat model, we showed that short-term R568 therapy had no effect on AVC. Treatment with R568 decreased PTH levels but had no effect on high phosphate levels. Regression of AVC necessitates not only a decrease in PTH levels, but also a decline in phosphate levels. To achieve improved outcomes, it is advisable to consider administering a combination of R568 with other medications, such as calcium supplements or phosphate binders. Additional studies are required for further evaluation of the potential treatment of chronic kidney disease (CKD)-associated AVC. IntroductionRenal failure associated aortic valve calcification (AVC) is the result of hyperphosphatemia and hyperparathyroidism. Calcimimetics is an effective tool for management of secondary hyperparathyroidism. Our goal was to evaluate the effect of the medical intervention with calcimimetic R568 on the AVC process.Methods and resultsThe experimental design consisted of administering a uremia-inducing phosphate-enriched diet to rats for six weeks. Rats received a daily R568 injection at different times. Biochemical analysis demonstrated increased urea (34.72 ± 3.57 vs. 5.18 ± 0.15 mmol/L, p<0.05) and creatinine (293.93 ± 79.6 vs. 12.82 ± 1.56 µmol/L, p<0.05). R568 treatment markedly reduced parathyroid hormone (PTH) levels in both treated groups (192.63 ± 26.85, 301.23 ± 101.79 vs. 3570 ± 986.63 pg/mL, p<0.05), with no impact on serum calcium and phosphate. von Kossa staining showed increase in AVC in uremic rats compared to control (1409 ± 159.5 vs. 27.33 ± 25.83, p<0.05). AVC was not affected by R568 in both groups (3343 ± 2462, 1593 ± 792 vs. 1409 ± 159.5, NS). Similarly, the inflammatory marker CD68 was elevated in uremic rats (15592 ± 3792 vs. 181.8 ± 15.29, p<0.01), and was not influenced by R568 treatment (8453 ± 818.5, 9318 ± 2232 vs. 15592 ± 3792, NS). Runt-related transcription factor 2 (Runx2), the regulator of osteoblast differentiation, was upregulated in uremic rats (23186 ± 9226 vs. 3184 ± 2495), that accompanied by elevated levels of Osteopontin (158395 ± 45911 vs. 237.7 ± 81.5, p<0.05) and Osteocalcin (22203 ± 8525 vs. 489.7 ± 200.6, p<0.05). R568 had no impact on osteoblastic markers (Runx2: 21743 ± 3193, 23004 ± 10871 vs. 23186 ± 9226, NS; osteopontin: 57680 ± 19522, 137116 ± 60103 vs. 158395 ± 45911, NS; osteocalcin: 10496 ± 5429, 8522 ± 5031 vs. 22203 ± 8525, NS).ConclusionIn an adenine-induced uremic rat model, we showed that short-term R568 therapy had no effect on AVC. Treatment with R568 decreased PTH levels but had no effect on high phosphate levels. Regression of AVC necessitates not only a decrease in PTH levels, but also a decline in phosphate levels. To achieve improved outcomes, it is advisable to consider administering a combination of R568 with other medications, such as calcium supplements or phosphate binders. Additional studies are required for further evaluation of the potential treatment of chronic kidney disease (CKD)-associated AVC. Renal failure associated aortic valve calcification (AVC) is the result of hyperphosphatemia and hyperparathyroidism. Calcimimetics is an effective tool for management of secondary hyperparathyroidism. Our goal was to evaluate the effect of the medical intervention with calcimimetic R568 on the AVC process. The experimental design consisted of administering a uremia-inducing phosphate-enriched diet to rats for six weeks. Rats received a daily R568 injection at different times. Biochemical analysis demonstrated increased urea (34.72 ± 3.57 . 5.18 ± 0.15 mmol/L, <0.05) and creatinine (293.93 ± 79.6 . 12.82 ± 1.56 µmol/L, <0.05). R568 treatment markedly reduced parathyroid hormone (PTH) levels in both treated groups (192.63 ± 26.85, 301.23 ± 101.79 . 3570 ± 986.63 pg/mL, <0.05), with no impact on serum calcium and phosphate. von Kossa staining showed increase in AVC in uremic rats compared to control (1409 ± 159.5 . 27.33 ± 25.83, <0.05). AVC was not affected by R568 in both groups (3343 ± 2462, 1593 ± 792 . 1409 ± 159.5, NS). Similarly, the inflammatory marker CD68 was elevated in uremic rats (15592 ± 3792 . 181.8 ± 15.29, <0.01), and was not influenced by R568 treatment (8453 ± 818.5, 9318 ± 2232 . 15592 ± 3792, NS). Runt-related transcription factor 2 (Runx2), the regulator of osteoblast differentiation, was upregulated in uremic rats (23186 ± 9226 . 3184 ± 2495), that accompanied by elevated levels of Osteopontin (158395 ± 45911 . 237.7 ± 81.5, <0.05) and Osteocalcin (22203 ± 8525 . 489.7 ± 200.6, <0.05). R568 had no impact on osteoblastic markers (Runx2: 21743 ± 3193, 23004 ± 10871 . 23186 ± 9226, NS; osteopontin: 57680 ± 19522, 137116 ± 60103 . 158395 ± 45911, NS; osteocalcin: 10496 ± 5429, 8522 ± 5031 . 22203 ± 8525, NS). In an adenine-induced uremic rat model, we showed that short-term R568 therapy had no effect on AVC. Treatment with R568 decreased PTH levels but had no effect on high phosphate levels. Regression of AVC necessitates not only a decrease in PTH levels, but also a decline in phosphate levels. To achieve improved outcomes, it is advisable to consider administering a combination of R568 with other medications, such as calcium supplements or phosphate binders. Additional studies are required for further evaluation of the potential treatment of chronic kidney disease (CKD)-associated AVC. |
| Author | Gurt, Irina Shuvy, Mony Abu-Snieneh, Asmahan Abedat, Suzan Lotan, Chaim Glikson, Michael |
| AuthorAffiliation | 1 Heart Institute, Cardiovascular Research Center, Hadassah-Hebrew University Medical Center , Jerusalem , Israel 2 Jesselson Integrated Heart Center, Shaare Zedek Medical Center and Faculty of Medicine, Hebrew University , Jerusalem , Israel |
| AuthorAffiliation_xml | – name: 1 Heart Institute, Cardiovascular Research Center, Hadassah-Hebrew University Medical Center , Jerusalem , Israel – name: 2 Jesselson Integrated Heart Center, Shaare Zedek Medical Center and Faculty of Medicine, Hebrew University , Jerusalem , Israel |
| Author_xml | – sequence: 1 givenname: Asmahan surname: Abu-Snieneh fullname: Abu-Snieneh, Asmahan organization: Heart Institute, Cardiovascular Research Center, Hadassah-Hebrew University Medical Center, Jerusalem, Israel – sequence: 2 givenname: Irina surname: Gurt fullname: Gurt, Irina organization: Jesselson Integrated Heart Center, Shaare Zedek Medical Center and Faculty of Medicine, Hebrew University, Jerusalem, Israel – sequence: 3 givenname: Suzan surname: Abedat fullname: Abedat, Suzan organization: Heart Institute, Cardiovascular Research Center, Hadassah-Hebrew University Medical Center, Jerusalem, Israel – sequence: 4 givenname: Chaim surname: Lotan fullname: Lotan, Chaim organization: Heart Institute, Cardiovascular Research Center, Hadassah-Hebrew University Medical Center, Jerusalem, Israel – sequence: 5 givenname: Michael surname: Glikson fullname: Glikson, Michael organization: Jesselson Integrated Heart Center, Shaare Zedek Medical Center and Faculty of Medicine, Hebrew University, Jerusalem, Israel – sequence: 6 givenname: Mony surname: Shuvy fullname: Shuvy, Mony organization: Jesselson Integrated Heart Center, Shaare Zedek Medical Center and Faculty of Medicine, Hebrew University, Jerusalem, Israel |
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| Cites_doi | 10.1093/ndtplus/sfm037 10.1152/ajpheart.00824.2009 10.1016/0735-1097(94)90127-9 10.1097/MED.0000000000000471 10.1038/ki.2008.407 10.1016/j.anclin.2009.07.012 10.1016/j.echo.2006.01.026 10.1210/jc.2011-2107 10.1093/ndt/gfq074 10.1152/ajprenal.90625.2008 10.1038/ki.2010.167 10.1016/j.atherosclerosis.2008.10.043 10.1007/s10157-015-1208-x 10.1073/pnas.95.7.4040 10.1681/ASN.2005070679 10.1093/cvr/cvn088 10.1161/CIRCULATIONAHA.104.473165 10.1097/HJH.0b013e328357c049 10.1007/s00467-008-0900-4 10.1161/CIRCULATIONAHA.108.827972 10.1038/ki.2012.69 10.1038/aps.2016.83 10.1016/j.jacc.2018.12.042 10.1681/ASN.2014070686 10.1093/ndt/gft310 10.1046/j.1523-1755.63.s85.22.x 10.1152/ajpheart.00765.2018 10.1038/ki.2008.546 10.1016/j.atherosclerosis.2013.12.051 10.1161/ATVBAHA.120.313131 10.1681/ASN.2005040342 10.1093/ndt/gfq725 10.1093/ckj/sfv073 10.1038/s41574-018-0115-0 10.1016/j.bone.2009.03.653 10.1038/ki.2008.490 10.3390/jcm9030629 |
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| Copyright | Copyright © 2024 Abu-Snieneh, Gurt, Abedat, Lotan, Glikson and Shuvy. Copyright © 2024 Abu-Snieneh, Gurt, Abedat, Lotan, Glikson and Shuvy 2024 Abu-Snieneh, Gurt, Abedat, Lotan, Glikson and Shuvy |
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| Keywords | phosphate aortic valve calcification chronic kidney disease R568 animal model |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Lisbet Brandi, Nordsjællands Hospital, Denmark These authors have contributed equally to this work Reviewed by: Mariadelina Simeoni, University of Campania Luigi Vanvitelli, Italy Anna Eremkina, Endocrinology Research Center, Russia |
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| Snippet | Renal failure associated aortic valve calcification (AVC) is the result of hyperphosphatemia and hyperparathyroidism. Calcimimetics is an effective tool for... Introduction Renal failure associated aortic valve calcification (AVC) is the result of hyperphosphatemia and hyperparathyroidism. Calcimimetics is an... IntroductionRenal failure associated aortic valve calcification (AVC) is the result of hyperphosphatemia and hyperparathyroidism. Calcimimetics is an effective... |
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| Title | Short-term therapy with R568 ameliorated secondary hyperparathyroidism but does not prevent aortic valve calcification in uremic rats |
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