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Fgf-23 and vascular calcification in a peritoneal dialysis population with residual renal function

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dc.contributor.authorSantos, S.
dc.contributor.authorCarlos Oliveira, José
dc.contributor.authorBarra, T.
dc.contributor.authorCampos, A.
dc.contributor.authorcarvalho, M.
dc.contributor.authorMalheiro, J.
dc.contributor.authorFonseca, Isabel
dc.contributor.authorCabrita, A.
dc.contributor.authorAdragão, T.
dc.contributor.authorRodrigues, Anabela
dc.date.accessioned2016-02-17T11:43:51Z
dc.date.available2016-02-17T11:43:51Z
dc.date.issued2015
dc.description.abstractIntroduction 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.pt_PT
dc.identifier.citationPort J Nephrol Hypert 2015; 29(3): 236-242pt_PT
dc.identifier.issn2183-1289
dc.identifier.urihttp://hdl.handle.net/10400.16/1904
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherSociedade Portuguesa de Nefrologiapt_PT
dc.relation.publisherversionhttp://www.bbg01.com/cdn/clientes/spnefro/pjnh/55/n3_2015_pjnh_08.pdfpt_PT
dc.subjectFGF-23pt_PT
dc.subjectfractional excretion of phosphoruspt_PT
dc.subjectperitoneal dialysispt_PT
dc.subjectphosphaturiapt_PT
dc.subjectresidual renal functionpt_PT
dc.subjectvascular calcificationpt_PT
dc.titleFgf-23 and vascular calcification in a peritoneal dialysis population with residual renal functionpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.conferencePlacePortugalpt_PT
oaire.citation.endPage242pt_PT
oaire.citation.issue3pt_PT
oaire.citation.startPage236pt_PT
oaire.citation.titlePortuguese Journal of Nephrology Hypertensionpt_PT
oaire.citation.volume29pt_PT
person.familyNameOliveira
person.familyNameFonseca
person.familyNameSoares Rodrigues
person.givenNameJosé Carlos
person.givenNameIsabel
person.givenNameAnabela
person.identifier806053
person.identifier415128
person.identifier.ciencia-id801F-D4FE-8694
person.identifier.ciencia-id6716-A5D1-FB3F
person.identifier.ciencia-id651F-A9D2-2136
person.identifier.orcid0000-0003-2142-6839
person.identifier.orcid0000-0001-8984-1751
person.identifier.orcid0000-0001-8818-2141
person.identifier.ridK-6339-2013
person.identifier.ridK-5226-2013
person.identifier.scopus-author-id55941495000
person.identifier.scopus-author-id7202269896
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicationbd6d8008-2622-4368-8ded-4ec1c1160c82
relation.isAuthorOfPublication2c7a2607-6376-486e-9ad5-490d0032946c
relation.isAuthorOfPublication2276a1c5-40fe-41e9-a369-a40049bf81e3
relation.isAuthorOfPublication.latestForDiscoverybd6d8008-2622-4368-8ded-4ec1c1160c82

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