학술논문

Urinary Markers of Fibrosis and Risk of Cardiovascular Events and Death in Kidney Transplant Recipients: The FAVORIT Trial
Document Type
article
Source
American Journal of Transplantation. 17(10)
Subject
Organ Transplantation
Cardiovascular
Kidney Disease
Transplantation
Prevention
Heart Disease
Detection
screening and diagnosis
4.1 Discovery and preclinical testing of markers and technologies
Renal and urogenital
Good Health and Well Being
Aged
Biomarkers
Cardiovascular Diseases
Case-Control Studies
Female
Fibrosis
Folic Acid
Humans
Kidney Transplantation
Male
Middle Aged
Nephritis
Interstitial
Risk Factors
biomarker
cardiovascular disease
clinical research/practice
kidney disease
kidney transplantation/nephrology
Medical and Health Sciences
Surgery
Language
Abstract
Cardiovascular risk remains high in kidney transplant recipients (KTRs) despite improved kidney function after transplant. Urinary markers of kidney fibrosis and injury may help to reveal mechanisms of this risk. In a case-cohort study among stable KTRs who participated in the FAVORIT trial, we measured four urinary proteins known to correlate with kidney tubulointerstitial fibrosis on biopsy (urine alpha 1 microglobulin [α1m], monocyte chemoattractant protein-1 [MCP-1], procollagen type I [PINP] and type III [PIIINP] N-terminal amino peptide) and evaluated associations with cardiovascular disease (CVD) events (n = 300) and death (n = 371). In adjusted models, higher urine α1m (hazard ratio [HR] per doubling of biomarker 1.40 [95% confidence interval [CI] 1.21, 1.62]), MCP-1 (HR 1.18 [1.03, 1.36]), and PINP (HR 1.13 [95% CI 1.03, 1.23]) were associated with CVD events. These three markers were also associated with death (HR per doubling α1m 1.51 [95% CI 1.32, 1.72]; MCP-1 1.31 [95% CI 1.13, 1.51]; PINP 1.11 [95% CI 1.03, 1.20]). Higher concentrations of urine α1m, MCP-1, and PINP may identify KTRs at higher risk for CVD events and death. These markers may identify a systemic process of fibrosis involving both the kidney and cardiovascular system, and give new insights into mechanisms linking the kidney with CVD.