Abstract MP30: Chronic Kidney Disease Progression and Risk of End-Stage Renal Disease: The Use of Change in Novel Kidney Filtration Markers
Introduction: Chronic kidney disease (CKD) progression assessed by estimated GFR from creatinine (eGFR-Cr) is a risk factor for cardiovascular disease and end-stage renal disease (ESRD) and has been proposed as a surrogate endpoint for clinical trials. It is unclear if CKD progression assessed by change in different filtration markers has similar risk associations with ESRD.
Hypothesis: We hypothesized that percent change in novel kidney filtration markers (β2-microglobulin and cystatin C) over a 6-year period would be independently associated with increased risk of ESRD during 15 years of follow-up, similar to the risk seen with change in eGFR-Cr.
Methods: We conducted prospective analyses of the ARIC study (N=9,703). β2-microglobulin, cystatin C, and creatinine were measured at study visits 1 (1990-92) and 2 (1996-98). Incident ESRD (kidney dialysis or transplant) was defined as entry into the U.S. Renal Data System registry between study visit 2 and September 30, 2011. Cox proportional hazards regression was used to estimate the association between percent change in filtration marker and incident ESRD, adjusting for demographics, kidney disease risk factors, and 1st measurement of the filtration marker.
Results: During a median follow-up of 13.1 years, there were 142 incident ESRD cases. Median eGFR-Cr was 97.3 mL/min/1.73 m2 at 1st measurement and 89.0 mL/min/1.73 m2 at 2nd measurement. Percent change in eGFR-Cr was moderately correlated with percent change in the inverse of β2-microglobulin (r = 0.34) and the inverse of cystatin C (r = 0.36). Progression of CKD (10-25% and >25% decline in filtration function) was associated with increased ESRD risk, with novel markers (β2-microglobulin, cystatin C) showing an association at least as strong as the creatinine and eGFR-Cr estimates (Table).
Conclusions: CKD progression assessed using novel filtration markers is independently associated with ESRD risk, suggesting the potential utility of measuring change in β2-microglobulin and cystatin C in clinical trials.
Author Disclosures: C.M. Rebholz: None. K. Matsushita: None. E. Selvin: None. M.E. Grams: None. J. Coresh: None.
- © 2014 by American Heart Association, Inc.