Aluminium-related osteodystrophy and desferrioxamine treatment: role of phosphorus
We investigated (1) the prevalence of aluminium overload among 96 patients with symptomatic bone disease haemodialysed from 1987 to 1989 in the Sao Paulo area, Brazil; (2) the effect of 6 months desferrioxamine (DFO) treatment (1–2 g/week). All patients underwent a first bone biopsy. Aluminium overl...
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| Veröffentlicht in: | Nephrology, dialysis, transplantation dialysis, transplantation, 1994, Vol.9 (6), p.668-674 |
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| creator | Jorgetti, V. Ricco Soeiro, N. M. Mendes, V. Pereira, R. C. Crivellari, M. E. Coutris, G. Borelli, A. Ribeiro Leite, M. O. Nussenzweig, I. Marcondes, M. Drüeke, T. Cournot, G. |
| description | We investigated (1) the prevalence of aluminium overload among 96 patients with symptomatic bone disease haemodialysed from 1987 to 1989 in the Sao Paulo area, Brazil; (2) the effect of 6 months desferrioxamine (DFO) treatment (1–2 g/week). All patients underwent a first bone biopsy. Aluminium overload (extent of stainable bone aluminium more than 20% trabecular surface) was observed in 74 of 96 patients. Forty overloaded patients were divided into patients with high bone formation rate (BFR) (group 1; n=17) and patients with low BFR (group 2; n=23), and had a second biopsy after DFO therapy. In both groups aluminium surface was reduced after treatment (P |
| doi_str_mv | 10.1093/oxfordjournals.ndt.a092948 |
| format | Article |
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E. ; Coutris, G. ; Borelli, A. ; Ribeiro Leite, M. O. ; Nussenzweig, I. ; Marcondes, M. ; Drüeke, T. ; Cournot, G.</creator><creatorcontrib>Jorgetti, V. ; Ricco Soeiro, N. M. ; Mendes, V. ; Pereira, R. C. ; Crivellari, M. E. ; Coutris, G. ; Borelli, A. ; Ribeiro Leite, M. O. ; Nussenzweig, I. ; Marcondes, M. ; Drüeke, T. ; Cournot, G.</creatorcontrib><description><![CDATA[We investigated (1) the prevalence of aluminium overload among 96 patients with symptomatic bone disease haemodialysed from 1987 to 1989 in the Sao Paulo area, Brazil; (2) the effect of 6 months desferrioxamine (DFO) treatment (1–2 g/week). All patients underwent a first bone biopsy. Aluminium overload (extent of stainable bone aluminium more than 20% trabecular surface) was observed in 74 of 96 patients. Forty overloaded patients were divided into patients with high bone formation rate (BFR) (group 1; n=17) and patients with low BFR (group 2; n=23), and had a second biopsy after DFO therapy. In both groups aluminium surface was reduced after treatment (P<0.001), osteoblast surface (P<0.02-P<0.01) and plasma parathyroid hormone (iPTH) (P<0.01) increased. In group 1 BFR remained high. In group 2 BFR remained low in 16 patients (2a) and increased in seven (P<0.02) (2b). In group 2a plasma phosphorus was below that in group 2b patients, before (P<0.03) and after (P<0.01) DFO. The histological features of group 2a patients resembled hypophos-phataemic osteomalacia, those of group 2b patients aluminium osteodystrophy. These data show a high prevalence of aluminium overload in Brazilian patients. Low-dose DFO therapy was safe, decreased bone pain, prevented fractures, and reduced stainable bone aluminium. Bone lesions only partially improved, suggesting that low phosphorus intake and/or plasma calcitriol concentrations may have prevented improvement of bone formation and mineralization.]]></description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/oxfordjournals.ndt.a092948</identifier><language>eng</language><publisher>Oxford University Press</publisher><subject>aluminium ; bone formation ; bone mineralization ; desferrioxamine ; phosphorus ; renal osteodystrophy</subject><ispartof>Nephrology, dialysis, transplantation, 1994, Vol.9 (6), p.668-674</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4009,27902,27903,27904</link.rule.ids></links><search><creatorcontrib>Jorgetti, V.</creatorcontrib><creatorcontrib>Ricco Soeiro, N. M.</creatorcontrib><creatorcontrib>Mendes, V.</creatorcontrib><creatorcontrib>Pereira, R. C.</creatorcontrib><creatorcontrib>Crivellari, M. E.</creatorcontrib><creatorcontrib>Coutris, G.</creatorcontrib><creatorcontrib>Borelli, A.</creatorcontrib><creatorcontrib>Ribeiro Leite, M. O.</creatorcontrib><creatorcontrib>Nussenzweig, I.</creatorcontrib><creatorcontrib>Marcondes, M.</creatorcontrib><creatorcontrib>Drüeke, T.</creatorcontrib><creatorcontrib>Cournot, G.</creatorcontrib><title>Aluminium-related osteodystrophy and desferrioxamine treatment: role of phosphorus</title><title>Nephrology, dialysis, transplantation</title><description><![CDATA[We investigated (1) the prevalence of aluminium overload among 96 patients with symptomatic bone disease haemodialysed from 1987 to 1989 in the Sao Paulo area, Brazil; (2) the effect of 6 months desferrioxamine (DFO) treatment (1–2 g/week). All patients underwent a first bone biopsy. Aluminium overload (extent of stainable bone aluminium more than 20% trabecular surface) was observed in 74 of 96 patients. Forty overloaded patients were divided into patients with high bone formation rate (BFR) (group 1; n=17) and patients with low BFR (group 2; n=23), and had a second biopsy after DFO therapy. In both groups aluminium surface was reduced after treatment (P<0.001), osteoblast surface (P<0.02-P<0.01) and plasma parathyroid hormone (iPTH) (P<0.01) increased. In group 1 BFR remained high. In group 2 BFR remained low in 16 patients (2a) and increased in seven (P<0.02) (2b). In group 2a plasma phosphorus was below that in group 2b patients, before (P<0.03) and after (P<0.01) DFO. The histological features of group 2a patients resembled hypophos-phataemic osteomalacia, those of group 2b patients aluminium osteodystrophy. These data show a high prevalence of aluminium overload in Brazilian patients. Low-dose DFO therapy was safe, decreased bone pain, prevented fractures, and reduced stainable bone aluminium. Bone lesions only partially improved, suggesting that low phosphorus intake and/or plasma calcitriol concentrations may have prevented improvement of bone formation and mineralization.]]></description><subject>aluminium</subject><subject>bone formation</subject><subject>bone mineralization</subject><subject>desferrioxamine</subject><subject>phosphorus</subject><subject>renal osteodystrophy</subject><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><recordid>eNqVzrFqwzAUBVBRGqib5h9EdrlyLMdxt7a0hBQ6hAyhixDomSix9cyTDPbfV0N_oMPlLofLZWxdyLyQTfmMU4tkrziSN13IvY25kc2mUbs7lhVqK8Wm3FX3LEu4ELKSzQN7DOEqZVJ1nbHjazf2zruxFwSdiWA5hgho5xAJh8vMjbfcQmiByOFkEgYeCUzswccXTtgBx5YPFwwpNIYntmjTGVj99ZKJz4_T-164NDzpgVxvaNaGbnpbl3Wl9-cffT5-f70ppfSh_K__BSZgVFk</recordid><startdate>1994</startdate><enddate>1994</enddate><creator>Jorgetti, V.</creator><creator>Ricco Soeiro, N. M.</creator><creator>Mendes, V.</creator><creator>Pereira, R. C.</creator><creator>Crivellari, M. E.</creator><creator>Coutris, G.</creator><creator>Borelli, A.</creator><creator>Ribeiro Leite, M. O.</creator><creator>Nussenzweig, I.</creator><creator>Marcondes, M.</creator><creator>Drüeke, T.</creator><creator>Cournot, G.</creator><general>Oxford University Press</general><scope>BSCLL</scope></search><sort><creationdate>1994</creationdate><title>Aluminium-related osteodystrophy and desferrioxamine treatment: role of phosphorus</title><author>Jorgetti, V. ; Ricco Soeiro, N. M. ; Mendes, V. ; Pereira, R. C. ; Crivellari, M. E. ; Coutris, G. ; Borelli, A. ; Ribeiro Leite, M. O. ; Nussenzweig, I. ; Marcondes, M. ; Drüeke, T. ; Cournot, G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-istex_primary_ark_67375_HXZ_XRNKB444_J3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>aluminium</topic><topic>bone formation</topic><topic>bone mineralization</topic><topic>desferrioxamine</topic><topic>phosphorus</topic><topic>renal osteodystrophy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jorgetti, V.</creatorcontrib><creatorcontrib>Ricco Soeiro, N. M.</creatorcontrib><creatorcontrib>Mendes, V.</creatorcontrib><creatorcontrib>Pereira, R. C.</creatorcontrib><creatorcontrib>Crivellari, M. E.</creatorcontrib><creatorcontrib>Coutris, G.</creatorcontrib><creatorcontrib>Borelli, A.</creatorcontrib><creatorcontrib>Ribeiro Leite, M. O.</creatorcontrib><creatorcontrib>Nussenzweig, I.</creatorcontrib><creatorcontrib>Marcondes, M.</creatorcontrib><creatorcontrib>Drüeke, T.</creatorcontrib><creatorcontrib>Cournot, G.</creatorcontrib><collection>Istex</collection><jtitle>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jorgetti, V.</au><au>Ricco Soeiro, N. M.</au><au>Mendes, V.</au><au>Pereira, R. C.</au><au>Crivellari, M. E.</au><au>Coutris, G.</au><au>Borelli, A.</au><au>Ribeiro Leite, M. O.</au><au>Nussenzweig, I.</au><au>Marcondes, M.</au><au>Drüeke, T.</au><au>Cournot, G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aluminium-related osteodystrophy and desferrioxamine treatment: role of phosphorus</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><date>1994</date><risdate>1994</risdate><volume>9</volume><issue>6</issue><spage>668</spage><epage>674</epage><pages>668-674</pages><issn>0931-0509</issn><eissn>1460-2385</eissn><abstract><![CDATA[We investigated (1) the prevalence of aluminium overload among 96 patients with symptomatic bone disease haemodialysed from 1987 to 1989 in the Sao Paulo area, Brazil; (2) the effect of 6 months desferrioxamine (DFO) treatment (1–2 g/week). All patients underwent a first bone biopsy. Aluminium overload (extent of stainable bone aluminium more than 20% trabecular surface) was observed in 74 of 96 patients. Forty overloaded patients were divided into patients with high bone formation rate (BFR) (group 1; n=17) and patients with low BFR (group 2; n=23), and had a second biopsy after DFO therapy. In both groups aluminium surface was reduced after treatment (P<0.001), osteoblast surface (P<0.02-P<0.01) and plasma parathyroid hormone (iPTH) (P<0.01) increased. In group 1 BFR remained high. In group 2 BFR remained low in 16 patients (2a) and increased in seven (P<0.02) (2b). In group 2a plasma phosphorus was below that in group 2b patients, before (P<0.03) and after (P<0.01) DFO. The histological features of group 2a patients resembled hypophos-phataemic osteomalacia, those of group 2b patients aluminium osteodystrophy. These data show a high prevalence of aluminium overload in Brazilian patients. Low-dose DFO therapy was safe, decreased bone pain, prevented fractures, and reduced stainable bone aluminium. Bone lesions only partially improved, suggesting that low phosphorus intake and/or plasma calcitriol concentrations may have prevented improvement of bone formation and mineralization.]]></abstract><pub>Oxford University Press</pub><doi>10.1093/oxfordjournals.ndt.a092948</doi></addata></record> |
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| ispartof | Nephrology, dialysis, transplantation, 1994, Vol.9 (6), p.668-674 |
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| source | Oxford Journals A-Z Collection |
| subjects | aluminium bone formation bone mineralization desferrioxamine phosphorus renal osteodystrophy |
| title | Aluminium-related osteodystrophy and desferrioxamine treatment: role of phosphorus |
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