Nephrol Dial Transplant (2003) 18: 2479-2482
© 2003 European Renal Association-European Dialysis and Transplant Association
Editorial Comment
Left ventricular hypertrophy: a surrogate end point or correlate of cardiovascular events in kidney disease?
1Duke Institute of Renal Outcomes Research and Health Policy, Department of Medicine, Duke University Medical Center, Durham, NC and 2Baxter International Healthcare, Waukegan, IL, USA
Correspondence and offprint requests to: Todd F. Griffith, MD, MHS, Metrolina Nephrology Associates, PA, 928 Baxter Street, Charlotte, NC 28204, USA 3646, Durham, NC 27710, USA. Email: todd.griffith@alumni.duke.edu
Keywords: anaemia; cardiovascular disease; end-stage renal disease; left ventricular hypertrophy; mortality
| The first 150 words of the full text of this article appear below. |
| Surrogate endpoints vs clinical correlates |
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Prentice [1] offered a statistical definition of a surrogate endpoint as a response variable for which a test of the null hypothesis of no relationship to the treatment groups under comparison is also a valid test of the corresponding null hypothesis based on the true endpoint. A National Institutes of Health (NIH) working group generated less quantitatively rigorous definitions that contrasted clinical and surrogate endpoints [2]. A clinical endpoint is [a] characteristic or variable that reflects how a patient feels, functions, or survives, and so is related to the surrogate, [a] biomarker that is intended to substitute for a clinical endpoint. Moreover, [a] surrogate endpoint is expected to predict clinical benefit (or harm or lack of benefit or harm) based on epidemiologic, therapeutic, pathophysiologic, or other scientific evidence [2]. While Prentices definition of surrogate requires the surrogate to account for the entirety of the
| Anaemia, left ventricular hypertrophy and mortality |
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| Anaemia treatment and clinical outcomes |
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| LVH as a surrogate outcome in anaemia correction |
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| Conclusions |
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