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2016 ; 20
(3
): 378-87
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Fibroblast growth factor-23 and chronic allograft injury in pediatric renal
transplant recipients: a Midwest Pediatric Nephrology Consortium study
#MMPMID26880121
Seifert ME
; Ashoor IF
; Chiang ML
; Chishti AS
; Dietzen DJ
; Gipson DS
; Janjua HS
; Selewski DT
; Hruska KA
Pediatr Transplant
2016[May]; 20
(3
): 378-87
PMID26880121
show ga
The chronic kidney disease-mineral bone disorder (CKD-MBD) produces fibroblast
growth factor-23 (FGF-23) and related circulating pathogenic factors that are
strongly associated with vascular injury and declining kidney function in native
CKD. Similarly, chronic renal allograft injury (CRAI) is characterized by
vascular injury and declining allograft function in transplant CKD. We
hypothesized that circulating CKD-MBD factors could serve as non-invasive
biomarkers of CRAI. We conducted a cross-sectional, multicenter case-control
study. Cases (n = 31) had transplant function >20 mL/min/1.73 m(2) and
biopsy-proven CRAI. Controls (n = 31) had transplant function >90 mL/min/1.73
m(2) and/or a biopsy with no detectable abnormality in the previous six months.
We measured plasma CKD-MBD factors at a single time point using ELISA. Median
(range) FGF23 levels were over twofold higher in CRAI vs. controls [106 (10-475)
pg/mL vs. 45 (8-91) pg/mL; p < 0.001]. FGF23 levels were inversely correlated
with transplant function (r(2) = -0.617, p < 0.001). Higher FGF23 levels were
associated with increased odds of biopsy-proven CRAI after adjusting for
transplant function, clinical, and demographic factors [OR (95% CI) 1.43 (1.23,
1.67)]. Relationships between additional CKD-MBD factors and CRAI were attenuated
in multivariable models. Higher FGF23 levels were independently associated with
biopsy-proven CRAI in children.