title: Phosphocalcic Markers and Calcification Propensity for Assessment of Interstitial Fibrosis and Vascular Lesions in Kidney Allograft Recipients.
abstract: Renal interstitial fibrosis and arterial lesions predict loss of function in chronic kidney disease. Noninvasive estimation of interstitial fibrosis and vascular lesions is currently not available. The aim of the study was to determine whether phosphocalcic markers are associated with, and can predict, renal chronic histological changes. We included 129 kidney allograft recipients with an available transplant biopsy in a retrospective study. We analyzed the associations and predictive values of phosphocalcic markers and serum calcification propensity (T50) for chronic histological changes (interstitial fibrosis and vascular lesions). PTH, T50 and vitamin D levels were independently associated to interstitial fibrosis. PTH elevation was associated with increasing interstitial fibrosis severity (r = 0.29, p = 0.001), while T50 and vitamin D were protective (r = -0.20, p = 0.025 and r = -0.23, p = 0.009 respectively). On the contrary, fibroblast growth factor 23 (FGF23) and Klotho correlated only modestly with interstitial fibrosis (p = 0.045) whereas calcium and phosphate did not. PTH, vitamin D and T50 were predictors of extensive fibrosis (AUC: 0.73, 0.72 and 0.68 respectively), but did not add to renal function prediction. PTH, FGF23 and T50 were modestly predictive of low fibrosis (AUC: 0.63, 0.63 and 0.61) but did not add to renal function prediction. T50 decreased with increasing arterial lesions (r = -0.21, p = 0.038). The discriminative performance of T50 in predicting significant vascular lesions was modest (AUC 0.61). In summary, we demonstrated that PTH, vitamin D and T50 are associated to interstitial fibrosis and vascular lesions in kidney allograft recipients independently of renal function. Despite these associations, mineral metabolism indices do not show superiority or additive value to fibrosis prediction by eGFR and proteinuria in kidney allograft recipients, except for vascular lesions where T50 could be of relevance.
authors.affiliation: Service of Internal Medicine, Department of Internal Medicine, University Hospital of Geneva, Geneva, Switzerland.|Service of Nephrology, Department of Internal Medicine Specialities, University Hospital of Geneva, Geneva, Switzerland.
authors.forename: Lena
authors.initials: L
authors.lastname: Berchtold
authors.affiliation: Service of Nephrology, Department of Internal Medicine Specialities, University Hospital of Geneva, Geneva, Switzerland.
authors.forename: Belen
authors.initials: B
authors.lastname: Ponte
authors.affiliation: Institute of Clinical Pathology, Departement of Clinical Pathology, University Hospital of Geneva, Geneva, Switzerland.
authors.forename: Solange
authors.initials: S
authors.lastname: Moll
authors.affiliation: Service of Nephrology, Department of Internal Medicine Specialities, University Hospital of Geneva, Geneva, Switzerland.
authors.forename: Karine
authors.initials: K
authors.lastname: Hadaya
authors.affiliation: Institute of Clinical Pathology, Departement of Clinical Pathology, University Hospital of Geneva, Geneva, Switzerland.
authors.forename: Olivia
authors.initials: O
authors.lastname: Seyde
authors.affiliation: Service of Clinical Research, Department of Clinical Research, University of Bern, Bern, Switzerland.
authors.forename: Matthias
authors.initials: M
authors.lastname: Bachtler
authors.affiliation: Service of Radiology, Department of Radiology and Medical Informatics, University Hospital of Geneva, Geneva, Switzerland.
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Vallée
authors.affiliation: Service of Nephrology, Department of Internal Medicine Specialities, University Hospital of Geneva, Geneva, Switzerland.
authors.forename: Pierre-Yves
authors.initials: PY
authors.lastname: Martin
authors.affiliation: Service of Clinical Research, Department of Clinical Research, University of Bern, Bern, Switzerland.
authors.forename: Andreas
authors.initials: A
authors.lastname: Pasch
authors.affiliation: Service of Nephrology, Department of Internal Medicine Specialities, University Hospital of Geneva, Geneva, Switzerland.
authors.forename: Sophie
authors.initials: S
authors.lastname: de Seigneux
mesh_terms: D000293:Adolescent; D064591:Allografts / Q000378:metabolism* / Q000473:pathology*; D015415:Biomarkers / Q000378:metabolism*; D002113:Calcification, Physiologic / Q000502:physiology*; D002114:Calcinosis / Q000378:metabolism / Q000473:pathology; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000378:metabolism; D005355:Fibrosis / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000473:pathology; D007676:Kidney Failure, Chronic / Q000378:metabolism / Q000473:pathology; D016030:Kidney Transplantation / Q000379:methods; D008297:Male; D010710:Phosphates / Q000378:metabolism*; D051436:Renal Insufficiency, Chronic / Q000378:metabolism / Q000473:pathology; D012189:Retrospective Studies; D014807:Vitamin D / Q000378:metabolism
chemical_list: D015415:Biomarkers; C000717427:FGF23 protein, human; D010710:Phosphates; D014807:Vitamin D; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23