Steven Kim1, Miklos Z Molnar2, Gregg C Fonarow3, Elani Streja4, Jiaxi Wang5, Daniel L Gillen6, Rajnish Mehrotra7, Steven M Brunelli8, Csaba P Kovesdy9, Kamyar Kalantar-Zadeh10, Connie M Rhee11. 1. Department of Mathematics and Statistics, California State University Monterey Bay, 100 Campus Center, Seaside, CA 93955, United States. Electronic address: stkim@csumb.edu. 2. Division of Nephrology, University of Tennessee Health Sciences Center, 956 Court Avenue, Memphis, TN 38163, United States. Electronic address: mzmolnar@uthsc.edu. 3. Division of Cardiology, David Geffen School of Medicine at University of California Los Angeles, 200 Medical Plaza Driveway, Room 247, Los Angeles, CA 90095, United States. Electronic address: gfonarow@mednet.ucla.edu. 4. Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, 101 The City Drive South, Suite 400, Orange, CA, United States. Electronic address: estreja@uci.edu. 5. Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, 101 The City Drive South, Suite 400, Orange, CA, United States. Electronic address: jiaxiw1@uci.edu. 6. Department of Statistics, University of California Irvine, 2226 Bren Hall, Irvine, CA 92697, United States. Electronic address: dgillen@uci.edu. 7. Harborview Medical Center and Kidney Research Institute, University of Washington, 325 9th Avenue, 3rd floor, NJB352, Seattle, WA 98104, United States. Electronic address: rmehrotra@nephrology.washington.edu. 8. DaVita Clinical Research, 825 South 8th Street, Suite 300, Minneapolis, MN 55404, United States. Electronic address: steven.brunelli@davita.com. 9. Division of Nephrology, University of Tennessee Health Sciences Center, 956 Court Avenue, Memphis, TN 38163, United States; Nephrology Section, Memphis Veterans Affairs Medical Center, Memphis, TN, United States. Electronic address: ckovesdy@uthsc.edu. 10. Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, 101 The City Drive South, Suite 400, Orange, CA, United States. Electronic address: kkz@uci.edu. 11. Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, 101 The City Drive South, Suite 400, Orange, CA, United States. Electronic address: crhee1@uci.edu.
Abstract
BACKGROUND: Higher mean platelet volume (MPV) is an indicator of larger, reactive platelets, and has been associated with a higher risk of thrombosis and cardiovascular events in the general population. Hemodialysis patients have a higher risk for cardiovascular death and predisposition to platelet dysfunction (thrombosis and bleeding diathesis), but the relationship between MPV and mortality in this population is unknown. METHODS: Among a 5-year cohort (1/2007-12/2011) of 149,118 incident hemodialysis patients from a large national dialysis organization, we examined the association between MPV and all-cause mortality. In primary analyses, we granularly analyzed MPV across five categories: 7.2-7.5, >7.5-9.5, >9.5-11.5, >11.5-13.5, and >13.5-15.0fL. In secondary analyses, we examined MPV categorized as low, normal, and high based on thresholds in the general population: 7.2-7.5, >7.5-11.5, and >11.5fL, respectively. Associations between baseline and time-dependent MPV with mortality were estimated using traditional and time-dependent Cox models in order to determine long-term and short-term exposure-mortality associations, respectively, using three adjustment levels: unadjusted, case-mix, and case-mix+laboratory models. RESULTS: In primary analyses, higher baseline and time-dependent MPV levels were associated with incrementally higher death risk in case-mix+laboratory analyses (reference: >9.5-11.5fL). In secondary analyses, high baseline and time-dependent MPV levels were associated with higher mortality, whereas low MPV was associated with lower death risk across all multivariable models (reference: normal MPV). CONCLUSIONS: Hemodialysis patients with higher MPV have heightened mortality risk. Further studies are needed to determine the pathophysiologic basis for the higher risk, and if modification of MPV ameliorates mortality in this population.
BACKGROUND: Higher mean platelet volume (MPV) is an indicator of larger, reactive platelets, and has been associated with a higher risk of thrombosis and cardiovascular events in the general population. Hemodialysis patients have a higher risk for cardiovascular death and predisposition to platelet dysfunction (thrombosis and bleeding diathesis), but the relationship between MPV and mortality in this population is unknown. METHODS: Among a 5-year cohort (1/2007-12/2011) of 149,118 incident hemodialysis patients from a large national dialysis organization, we examined the association between MPV and all-cause mortality. In primary analyses, we granularly analyzed MPV across five categories: 7.2-7.5, >7.5-9.5, >9.5-11.5, >11.5-13.5, and >13.5-15.0fL. In secondary analyses, we examined MPV categorized as low, normal, and high based on thresholds in the general population: 7.2-7.5, >7.5-11.5, and >11.5fL, respectively. Associations between baseline and time-dependent MPV with mortality were estimated using traditional and time-dependent Cox models in order to determine long-term and short-term exposure-mortality associations, respectively, using three adjustment levels: unadjusted, case-mix, and case-mix+laboratory models. RESULTS: In primary analyses, higher baseline and time-dependent MPV levels were associated with incrementally higher death risk in case-mix+laboratory analyses (reference: >9.5-11.5fL). In secondary analyses, high baseline and time-dependent MPV levels were associated with higher mortality, whereas low MPV was associated with lower death risk across all multivariable models (reference: normal MPV). CONCLUSIONS: Hemodialysis patients with higher MPV have heightened mortality risk. Further studies are needed to determine the pathophysiologic basis for the higher risk, and if modification of MPV ameliorates mortality in this population.
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