Fgf-23 and vascular calcification in a peritoneal dialysis population with residual renal function
Autor(a) principal: | |
---|---|
Data de Publicação: | 2015 |
Outros Autores: | , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10400.16/1904 |
Resumo: | Introduction and Aims: Fibroblast growth factor 23 (FGF-23) induces phosphaturia. Its clinical impact is beyond mineral bone disease in chronic kidney disease (CKD), being coupled with vascular calcification and mortality. Residual renal function (RRF) is associated with significant capacity to excrete phosphate in peri- toneal dialysis (PD). Besides testing whether FGF-23 is still related with glomerular filtration rate (GFR) and phosphate excretion in this late stage of CKD (5d), we aimed to explore its link with vascular calcification.Subjects and Methods: FGF-23 (C terminal) was measured in forty prevalent PD patients with RRF, aged 61.5 (51.0-67.0) years old, in renal replacement therapy (RRT) for 43.5 (23-80.0) months; 36.6% were female, 19.5% had diabetes mellitus and 37.5% were under automated PD regimen; 80% were on PD first, and only 20% had previous RRT. Relevant variables including dietary phosphate (P) intake, CKD-bone laboratory parameters, serum 25-hydroxyvitamin D, magnesium (Mg) levels, GFR, urinary phosphate, fractional excretion of phosphorus (FEP), albumin, proBNP and Adragão vascular calcification score were explored. Results: Median levels (25-75% range) of serum variables were: FGF-23 1997 (1623-2149) RU/mL, Mg 0.94 (0.8-1.0) mmol/L, 25-hydroxyvitamin D 30 (18-47) nmol/L, calcium 2.2 (2.0-2.37) mmol/L, phosphorus 1.69 (1.30-1.90) mmol/L, PTH 429 (309-626) pg/mL. FGF-23 correlated positively with serum phosphate (r = 0.39, p = 0.013) and negatively with urine volume (r = -0.48, p = 0.001), phosphaturia (r = -0.594, p < 0.0001) and GFR (r =-0.61,p < 0.0001). However, FGF-23 was not significantly correlated with age, total time of RRT, dietary P, FEP, Mg, nor 25-hydroxyvitamin D. High FGF-23 group had higher FEP. GFR was the single inde- pendent predictor of increased FGF-23. On the other hand, neither FGF-23 nor low FEP/FGF-23 ratio were significantly associated with the vascular calcification score. Only albumin (lower), magnesium (lower) and proBNP (higher) levels significantly differed in calcified versus non-calcified patients (all with p < 0.05). Conclusions: In our population, FGF-23 was not associated with vascular calcification. GFR was the single independent predictor of increased FGF-23 in patients with diuresis. Increment of FGF-23 in PD patients signalizes an active endocrine phosphaturic process compensating renal function loss, as expressed by higher fractional excretion of phosphorus. It alerts for dietetic and therapy optimization. However, its link with vascular calcification still lacks validation. |
id |
RCAP_6bc98fd043446f13d6578c5324c89c98 |
---|---|
oai_identifier_str |
oai:repositorio.chporto.pt:10400.16/1904 |
network_acronym_str |
RCAP |
network_name_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
repository_id_str |
7160 |
spelling |
Fgf-23 and vascular calcification in a peritoneal dialysis population with residual renal functionFGF-23fractional excretion of phosphorusperitoneal dialysisphosphaturiaresidual renal functionvascular calcificationIntroduction and Aims: Fibroblast growth factor 23 (FGF-23) induces phosphaturia. Its clinical impact is beyond mineral bone disease in chronic kidney disease (CKD), being coupled with vascular calcification and mortality. Residual renal function (RRF) is associated with significant capacity to excrete phosphate in peri- toneal dialysis (PD). Besides testing whether FGF-23 is still related with glomerular filtration rate (GFR) and phosphate excretion in this late stage of CKD (5d), we aimed to explore its link with vascular calcification.Subjects and Methods: FGF-23 (C terminal) was measured in forty prevalent PD patients with RRF, aged 61.5 (51.0-67.0) years old, in renal replacement therapy (RRT) for 43.5 (23-80.0) months; 36.6% were female, 19.5% had diabetes mellitus and 37.5% were under automated PD regimen; 80% were on PD first, and only 20% had previous RRT. Relevant variables including dietary phosphate (P) intake, CKD-bone laboratory parameters, serum 25-hydroxyvitamin D, magnesium (Mg) levels, GFR, urinary phosphate, fractional excretion of phosphorus (FEP), albumin, proBNP and Adragão vascular calcification score were explored. Results: Median levels (25-75% range) of serum variables were: FGF-23 1997 (1623-2149) RU/mL, Mg 0.94 (0.8-1.0) mmol/L, 25-hydroxyvitamin D 30 (18-47) nmol/L, calcium 2.2 (2.0-2.37) mmol/L, phosphorus 1.69 (1.30-1.90) mmol/L, PTH 429 (309-626) pg/mL. FGF-23 correlated positively with serum phosphate (r = 0.39, p = 0.013) and negatively with urine volume (r = -0.48, p = 0.001), phosphaturia (r = -0.594, p < 0.0001) and GFR (r =-0.61,p < 0.0001). However, FGF-23 was not significantly correlated with age, total time of RRT, dietary P, FEP, Mg, nor 25-hydroxyvitamin D. High FGF-23 group had higher FEP. GFR was the single inde- pendent predictor of increased FGF-23. On the other hand, neither FGF-23 nor low FEP/FGF-23 ratio were significantly associated with the vascular calcification score. Only albumin (lower), magnesium (lower) and proBNP (higher) levels significantly differed in calcified versus non-calcified patients (all with p < 0.05). Conclusions: In our population, FGF-23 was not associated with vascular calcification. GFR was the single independent predictor of increased FGF-23 in patients with diuresis. Increment of FGF-23 in PD patients signalizes an active endocrine phosphaturic process compensating renal function loss, as expressed by higher fractional excretion of phosphorus. It alerts for dietetic and therapy optimization. However, its link with vascular calcification still lacks validation.Sociedade Portuguesa de NefrologiaRepositório Científico do Centro Hospitalar Universitário de Santo AntónioSantos, S.Carlos Oliveira, JoséBarra, T.Campos, A.carvalho, M.Malheiro, J.Fonseca, IsabelCabrita, A.Adragão, T.Rodrigues, Anabela2016-02-17T11:43:51Z20152015-01-01T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10400.16/1904engPort J Nephrol Hypert 2015; 29(3): 236-2422183-1289info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-10-20T10:58:05Zoai:repositorio.chporto.pt:10400.16/1904Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T20:38:13.335425Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
Fgf-23 and vascular calcification in a peritoneal dialysis population with residual renal function |
title |
Fgf-23 and vascular calcification in a peritoneal dialysis population with residual renal function |
spellingShingle |
Fgf-23 and vascular calcification in a peritoneal dialysis population with residual renal function Santos, S. FGF-23 fractional excretion of phosphorus peritoneal dialysis phosphaturia residual renal function vascular calcification |
title_short |
Fgf-23 and vascular calcification in a peritoneal dialysis population with residual renal function |
title_full |
Fgf-23 and vascular calcification in a peritoneal dialysis population with residual renal function |
title_fullStr |
Fgf-23 and vascular calcification in a peritoneal dialysis population with residual renal function |
title_full_unstemmed |
Fgf-23 and vascular calcification in a peritoneal dialysis population with residual renal function |
title_sort |
Fgf-23 and vascular calcification in a peritoneal dialysis population with residual renal function |
author |
Santos, S. |
author_facet |
Santos, S. Carlos Oliveira, José Barra, T. Campos, A. carvalho, M. Malheiro, J. Fonseca, Isabel Cabrita, A. Adragão, T. Rodrigues, Anabela |
author_role |
author |
author2 |
Carlos Oliveira, José Barra, T. Campos, A. carvalho, M. Malheiro, J. Fonseca, Isabel Cabrita, A. Adragão, T. Rodrigues, Anabela |
author2_role |
author author author author author author author author author |
dc.contributor.none.fl_str_mv |
Repositório Científico do Centro Hospitalar Universitário de Santo António |
dc.contributor.author.fl_str_mv |
Santos, S. Carlos Oliveira, José Barra, T. Campos, A. carvalho, M. Malheiro, J. Fonseca, Isabel Cabrita, A. Adragão, T. Rodrigues, Anabela |
dc.subject.por.fl_str_mv |
FGF-23 fractional excretion of phosphorus peritoneal dialysis phosphaturia residual renal function vascular calcification |
topic |
FGF-23 fractional excretion of phosphorus peritoneal dialysis phosphaturia residual renal function vascular calcification |
description |
Introduction and Aims: Fibroblast growth factor 23 (FGF-23) induces phosphaturia. Its clinical impact is beyond mineral bone disease in chronic kidney disease (CKD), being coupled with vascular calcification and mortality. Residual renal function (RRF) is associated with significant capacity to excrete phosphate in peri- toneal dialysis (PD). Besides testing whether FGF-23 is still related with glomerular filtration rate (GFR) and phosphate excretion in this late stage of CKD (5d), we aimed to explore its link with vascular calcification.Subjects and Methods: FGF-23 (C terminal) was measured in forty prevalent PD patients with RRF, aged 61.5 (51.0-67.0) years old, in renal replacement therapy (RRT) for 43.5 (23-80.0) months; 36.6% were female, 19.5% had diabetes mellitus and 37.5% were under automated PD regimen; 80% were on PD first, and only 20% had previous RRT. Relevant variables including dietary phosphate (P) intake, CKD-bone laboratory parameters, serum 25-hydroxyvitamin D, magnesium (Mg) levels, GFR, urinary phosphate, fractional excretion of phosphorus (FEP), albumin, proBNP and Adragão vascular calcification score were explored. Results: Median levels (25-75% range) of serum variables were: FGF-23 1997 (1623-2149) RU/mL, Mg 0.94 (0.8-1.0) mmol/L, 25-hydroxyvitamin D 30 (18-47) nmol/L, calcium 2.2 (2.0-2.37) mmol/L, phosphorus 1.69 (1.30-1.90) mmol/L, PTH 429 (309-626) pg/mL. FGF-23 correlated positively with serum phosphate (r = 0.39, p = 0.013) and negatively with urine volume (r = -0.48, p = 0.001), phosphaturia (r = -0.594, p < 0.0001) and GFR (r =-0.61,p < 0.0001). However, FGF-23 was not significantly correlated with age, total time of RRT, dietary P, FEP, Mg, nor 25-hydroxyvitamin D. High FGF-23 group had higher FEP. GFR was the single inde- pendent predictor of increased FGF-23. On the other hand, neither FGF-23 nor low FEP/FGF-23 ratio were significantly associated with the vascular calcification score. Only albumin (lower), magnesium (lower) and proBNP (higher) levels significantly differed in calcified versus non-calcified patients (all with p < 0.05). Conclusions: In our population, FGF-23 was not associated with vascular calcification. GFR was the single independent predictor of increased FGF-23 in patients with diuresis. Increment of FGF-23 in PD patients signalizes an active endocrine phosphaturic process compensating renal function loss, as expressed by higher fractional excretion of phosphorus. It alerts for dietetic and therapy optimization. However, its link with vascular calcification still lacks validation. |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015 2015-01-01T00:00:00Z 2016-02-17T11:43:51Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10400.16/1904 |
url |
http://hdl.handle.net/10400.16/1904 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Port J Nephrol Hypert 2015; 29(3): 236-242 2183-1289 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Sociedade Portuguesa de Nefrologia |
publisher.none.fl_str_mv |
Sociedade Portuguesa de Nefrologia |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
instname_str |
Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
instacron_str |
RCAAP |
institution |
RCAAP |
reponame_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
collection |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
repository.name.fl_str_mv |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
repository.mail.fl_str_mv |
|
_version_ |
1799133643522703360 |