Circulating calcification inhibitors and vascular properties in children after renal transplantation.
Pediatric transplant patients are known to have vascular abnormalities. The calcification inhibitors matrix Gla protein (MGP) and fetuin-A play an important role in the pathophysiology of vascular calcification. In the cross-sectional study reported here, we examined the circulating levels of fetuin-A and MGP in children after renal transplantation compared to healthy children and the association of these factors with vascular properties of the carotid artery. Levels of MGP and fetuin-A together with vascular properties of the carotid artery were determined in 29 pediatric renal transplant recipients and 54 healthy controls. The level of fetuin-A was decreased in the transplant group relative to the control group (P=0.005), whereas the level of MGP (both non-phosphorylated MGP and non-carboxylated MGP) did not differ between groups. The intima-media thickness (P<0.001) and the elasticity (P=0.002) of the carotid artery were significantly increased in children after renal transplantation compared to healthy children. No associations between vascular parameters and calcification inhibitors were found in either group. Circulating levels of MGP and fetuin-A could not be identified as independent predictors of vascular stiffness or other carotid artery parameters in pediatric renal transplant recipients. Future prospective studies in pediatric ESRD and transplant patients are needed to learn more about the role of calcification inhibitors in relation to the prevention of vascular damage.
van Summeren
Marieke J H
MJ
Department of Pediatric Immunology, University Medical Centre Utrecht, Lundlaan 6, Room KE.04.133.1, 3584 EA Utrecht, The Netherlands. m.j.h.vansummeren@umcutrecht.nl
Hameleers
Jeroen M
JM
Schurgers
Leon J
LJ
Hoeks
Arnold P G
AP
Uiterwaal
Cuno S P M
CS
Krüger
Thilo
T
Vermeer
Cees
C
Kuis
Wietse
W
Lilien
Marc R
MR
D000293:Adolescent; D001794:Blood Pressure; D001798:Blood Proteins / Q000378:metabolism*; D002114:Calcinosis / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D002135:Calcium-Binding Proteins / Q000097:blood*; D002340:Carotid Artery Diseases / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D016022:Case-Control Studies; D002648:Child; D003430:Cross-Sectional Studies; D004548:Elasticity; D016326:Extracellular Matrix Proteins / Q000097:blood*; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism / Q000601:surgery*; D016030:Kidney Transplantation; D008297:Male; D060749:alpha-2-HS-Glycoprotein; D000097568:Matrix Gla Protein
D001798:Blood Proteins; D002135:Calcium-Binding Proteins; D016326:Extracellular Matrix Proteins; D060749:alpha-2-HS-Glycoprotein; D000097568:Matrix Gla Protein; C556354:AHSG protein, human