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• W2078587593 abstract "Bisphosphonates are inhibitors of bone resorption that are widely used to treat osteoporosis. Price and colleagues demonstrate that ibandronate suppressed the development of uremia-related vascular calcification in rats. These findings extend the link between bone remodeling and vascular calcification to the context of chronic renal failure, opening perspectives toward novel therapeutic strategies. Bisphosphonates are inhibitors of bone resorption that are widely used to treat osteoporosis. Price and colleagues demonstrate that ibandronate suppressed the development of uremia-related vascular calcification in rats. These findings extend the link between bone remodeling and vascular calcification to the context of chronic renal failure, opening perspectives toward novel therapeutic strategies. Chronic kidney disease is associated with a strong increase in cardiovascular risk, which is responsible for approximately 50% of the mortality in the hemodialysis population. Increased vascular calcification is a prominent feature of vascular disease in uremic patients. Coronary calcification is already present in young hemodialysis patients and shows rapid progression. In addition to increased calcification of atherosclerotic plaques, patients on dialysis also show characteristic calcifications of the vascular tunica media, which also contribute significantly to the excess cardiovascular mortality observed in uremic patients.1.London G.M. Guerin A.P. Marchais S.J. et al.Arterial media calcification in end-stage renal disease: impact on all-cause and cardiovascular mortality.Nephrol Dial Transplant. 2003; 18: 1731-1740Crossref PubMed Scopus (1432) Google Scholar Price et al.2.Price P.A. Roublick A.M. Williamson M.K. Artery calcification in uremic rats is increased by a low protein diet and prevented by treatment with ibandronate.Kidney Int. 2006; 70: 1577-1583Abstract Full Text Full Text PDF PubMed Scopus (115) Google Scholar (this issue) report that the bisphosphonate ibandronate prevents the development of vascular calcification in rats with adenine-induced chronic renal failure maintained on a low-protein diet. Combination of adenine-induced chronic renal failure with a synthetic diet with low protein content proved to reliably induce media calcification in the large arteries of these animals, whereas the standard model induces vascular calcification only in a subset of animals3.Katsumata K. Kusano K. Hirata M. et al.Sevelamer hydrochloride prevents ectopic calcification and renal osteodystrophy in chronic renal failure rats.Kidney Int. 2003; 64: 441-450Abstract Full Text Full Text PDF PubMed Scopus (128) Google Scholar (V Persy et al., unpublished observations). The availability of a reliable model of uremia-induced vascular calcification is an important asset for future experimental research into the pathomechanisms of pharmacological agents and their impact on artery calcification in chronic renal failure. Moreover, this finding is not without its implications for human disease: dietary protein restriction is still occasionally used in chronic kidney disease patients in order to slow progression of kidney-function deterioration and is one of the standard measures imposed on dialysis patients to keep phosphate levels under control; malnutrition always looms around the corner for these patients. So maintaining a good nutritional status in end-stage renal failure patients is important not only to fight off chronic inflammation, but possibly also to limit the development of vascular calcification. Bisphosphonates are pyrophosphate analogues resistant to enzymatic hydrolysis that are widely used to treat bone diseases characterized by increased bone resorption, such as osteoporosis, Paget's disease, osteolytic lesions, and hypercalcemia associated with multiple myeloma. In high doses these compounds physicochemically inhibit mineralization by inhibiting the formation and aggregation of calcium phosphate crystals and blocking the transformation of amorphous calcium phosphate to hydroxyapatite. However, their therapeutic use depends on their inhibition of bone resorption, which occurs at low doses that do not affect mineralization.4.Fleisch H. Bisphosphonates: mechanisms of action.Endocr Rev. 1998; 19: 80-100Crossref PubMed Scopus (0) Google Scholar Bisphosphonates increase the bone mineral density of osteoporotic patients by inhibiting osteoclastic bone resorption through several mechanisms: they inhibit terminal differentiation of osteoclasts, induce apoptosis of osteoclasts, and decrease osteoclastic activity by inhibiting protein prenylation.4.Fleisch H. Bisphosphonates: mechanisms of action.Endocr Rev. 1998; 19: 80-100Crossref PubMed Scopus (0) Google Scholar However, bisphosphonates are also reported to act on cells of the osteoblastic lineage,5.Giuliani N. Pedrazzoni M. Negri G. et al.Bisphosphonates stimulate formation of osteoblast precursors and mineralized nodules in murine and human bone marrow cultures in vitro and promote early osteoblastogenesis in young and aged mice in vivo.Bone. 1998; 22: 455-461Abstract Full Text Full Text PDF PubMed Scopus (228) Google Scholar and the effect of different bisphosphonate compounds on osteoblastic cells correlates well with their different potency in vivo.4.Fleisch H. Bisphosphonates: mechanisms of action.Endocr Rev. 1998; 19: 80-100Crossref PubMed Scopus (0) Google Scholar The findings reported in this issue2.Price P.A. Roublick A.M. Williamson M.K. Artery calcification in uremic rats is increased by a low protein diet and prevented by treatment with ibandronate.Kidney Int. 2006; 70: 1577-1583Abstract Full Text Full Text PDF PubMed Scopus (115) Google Scholar extend results previously reported by Price's group showing that bisphosphonates can inhibit the development of arterial calcification in rats with normal renal function treated with warfarin or toxic doses of vitamin D,6.Price P.A. June H.H. Buckley J.R. Williamson M.K. Osteoprotegerin inhibits artery calcification induced by warfarin and by vitamin D.Arterioscler Thromb Vasc Biol. 2001; 21: 1610-1616Crossref PubMed Scopus (324) Google Scholar and they add to the growing body of experimental evidence that links vascular calcification to metabolic bone disease. This study2.Price P.A. Roublick A.M. Williamson M.K. Artery calcification in uremic rats is increased by a low protein diet and prevented by treatment with ibandronate.Kidney Int. 2006; 70: 1577-1583Abstract Full Text Full Text PDF PubMed Scopus (115) Google Scholar represents the first experimental evidence implicating bone resorption in the pathogenesis of uremia-related vascular calcification. Recently, the less potent bisphosphonate etidronate was also reported to prevent aortic calcification in five-sixths nephrectomized rats treated with calcitriol to induce vascular calcification.7.Tamura K. Suzuki Y. Hashiba H. et al.Effect of etidronate on aortic calcification and bone metabolism in calcitriol-treated rats with subtotal nephrectomy.J Pharmacol Sci. 2005; 99: 89-94Crossref PubMed Scopus (21) Google Scholar However, Tamura et al.7.Tamura K. Suzuki Y. Hashiba H. et al.Effect of etidronate on aortic calcification and bone metabolism in calcitriol-treated rats with subtotal nephrectomy.J Pharmacol Sci. 2005; 99: 89-94Crossref PubMed Scopus (21) Google Scholar used a high dose of etidronate (10 mg/kg), which also inhibits mineralization. A few clinical studies in which bisphosphonates were administered to small numbers of hemodialysis patients generated hopeful results for the potential use of these compounds to fight uremia-related arterial calcification: Nitta et al.8.Nitta K. Akiba T. Suzuki K. et al.Effects of cyclic intermittent etidronate therapy on coronary artery calcification in patients receiving long-term hemodialysis.Am J Kidney Dis. 2004; 44: 680-688Abstract Full Text Full Text PDF PubMed Scopus (118) Google Scholar demonstrated that etidronate treatment arrested progression of coronary calcification, whereas Hashiba and colleagues9.Hashiba H. Aizawa S. Tamura K. Kogo H. Inhibition of the progression of aortic calcification by etidronate treatment in hemodialysis patients: long-term effects.Ther Apher Dial. 2006; 10: 59-64Crossref PubMed Scopus (53) Google Scholar found no increase in aorta calcification over a 23-month follow-up period in patients treated with the same compound, contrasting with significant progression of calcification in the control group. In addition, two recent case reports documented the potential usefulness of etidronate and pamidronate, respectively, as treatment options in calciphylaxis.10.Shiraishi N. Kitamura K. Miyoshi T. et al.Successful treatment of a patient with severe calcific uremic arteriolopathy (calciphylaxis) by etidronate disodium.Am J Kidney Dis. 2006; 48: 151-154Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar,11.Monney P. Nguyen Q.V. Perroud H. Descombes E. Rapid improvement of calciphylaxis after intravenous pamidronate therapy in a patient with chronic renal failure.Nephrol Dial Transplant. 2004; 19: 2130-2132Crossref PubMed Scopus (103) Google Scholar Outside the uremic setting, the phenotype of the osteoprotegerin knockout mouse also implicates bone resorption in ectopic calcification, as mice that do not express the osteoclast inhibitor osteoprotegerin show a combination of osteoporosis and extensive vascular calcification.12.Bucay N. Sarosi I. Dunstan C.R. et al.Osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification.Genes Dev. 1998; 12: 1260-1268Crossref PubMed Scopus (2025) Google Scholar This paradoxical association has also been reported in postmenopausal women with osteoporosis. The exact mechanism by which ibandronate prevents vascular calcification in rats with adenine-induced chronic renal failure is not clear yet. Possibly, the inhibition of bone resorption is the cause of this effect, as a decrease in bone resorption goes along with a reduced efflux of calcium and phosphate from bone into the circulatory system, thereby limiting their availability for deposition in the vasculature, particularly when a normal bone formation is maintained. However, Price et al.2.Price P.A. Roublick A.M. Williamson M.K. Artery calcification in uremic rats is increased by a low protein diet and prevented by treatment with ibandronate.Kidney Int. 2006; 70: 1577-1583Abstract Full Text Full Text PDF PubMed Scopus (115) Google Scholar did not study (yet) the effect of ibandronate on bone histology in this model, so inhibition of bone resorption by bisphosphonate treatment remains to be proved, and possible effects on bone formation and osteoblastic activity will need to be checked for. Alternatively, a direct effect of ibandronate on the vessel wall cannot be precluded, as vascular smooth muscle cells can acquire an osteoblast-like phenotype in calcifying vessels and when cultured in the presence of increased phosphate or calcium levels or uremic serum, and bisphosphonates are also known to have cell-biological effects on osteoblastic cells. Moreover, preliminary results suggest that osteoclast-like cells, potential targets for bisphosphonate treatment, are sometimes present in calcifying vessels of uremic rats (E Neven et al., unpublished data). Finally, despite that the ibandronate doses used in these experiments are unlikely to cause pyrophosphate-like effects at the arterial wall, uremia may be a state of pyrophosphate deficiency, and thus this potential quality of bisphosphonates should be kept in mind.13.Lomashvili K.A. Khawandi W. O'Neill W.C. Reduced plasma pyrophosphate levels in hemodialysis patients.J Am Soc Nephrol. 2005; 16: 2495-2500Crossref PubMed Scopus (137) Google Scholar Another question to be resolved before bisphosphonates can be widely accepted as drugs to prevent vascular calcification in hemodialysis patients is how the inhibition of vascular calcification by bisphosphonates is influenced by the bone turnover rate. The effect reported by Price et al.2.Price P.A. Roublick A.M. Williamson M.K. Artery calcification in uremic rats is increased by a low protein diet and prevented by treatment with ibandronate.Kidney Int. 2006; 70: 1577-1583Abstract Full Text Full Text PDF PubMed Scopus (115) Google Scholar was seen in an experimental model with high bone turnover: adenine-induced uremia causes hyperparathyroid bone disease with severely elevated parathyroid hormone levels. However, further inhibition of the already dramatically impaired bone resorption and/or bone formation in low-turnover osteodystrophy might not at all be beneficial, as epidemiological studies reported the highest calcification scores in the patients with the lowest parathyroid hormone values, that is, those with adynamic bone disease.1.London G.M. Guerin A.P. Marchais S.J. et al.Arterial media calcification in end-stage renal disease: impact on all-cause and cardiovascular mortality.Nephrol Dial Transplant. 2003; 18: 1731-1740Crossref PubMed Scopus (1432) Google Scholar Experimental evidence pointing this out is the fact that treatment of uremic low-density lipoprotein receptor knockout mice with bone morphogenetic protein-7 prevents the development of vascular calcification by increasing bone turnover in this experimental model of adynamic bone disease.14.Davies M.R. Lund R.J. Mathew S. Hruska K.A. Low turnover osteodystrophy and vascular calcification are amenable to skeletal anabolism in an animal model of chronic kidney disease and the metabolic syndrome.J Am Soc Nephrol. 2005; 16: 917-928Crossref PubMed Scopus (129) Google Scholar In summary, Price et al.2.Price P.A. Roublick A.M. Williamson M.K. Artery calcification in uremic rats is increased by a low protein diet and prevented by treatment with ibandronate.Kidney Int. 2006; 70: 1577-1583Abstract Full Text Full Text PDF PubMed Scopus (115) Google Scholar report interesting new effects of bisphosphonates in experimental uremia-induced chronic renal failure, which emphasize once more that the mechanisms regulating ectopic calcification and bone remodeling are intricately intertwined. Therefore, future studies to elucidate the mechanisms of and evaluate treatment strategies for uremia-related vascular calcification will have to take into account the complex interplay of bone and vessels. V Persy is a Postdoctoral Fellow of the Fund for Scientific Research, Flanders (Belgium)." @default.
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• W2078587593 title "Bisphosphonates prevent experimental vascular calcification: Treat the bone to cure the vessels?" @default.
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