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Nutritional status, dietary intake, and body composition |
1 From the Harold Simmons Center for Kidney Disease Research and Epidemiology (CSS and KK-Z) and the Division of Nephrology and Hypertension (JDK, RM, and KK-Z), Los Angeles Biomedical Research Institute at Harbor–UCLA Medical Center, Torrance, CA; and the David Geffen School of Medicine at UCLA, Los Angeles, CA (JDK, RM, and KK-Z); the Departments of Epidemiology (CSS, KK-Z, and SG) and Family Health (JDK), UCLA School of Public Health, Los Angeles, CA; the Salem VA Medical Center, Salem, VA (CPK); DaVita, Inc, El Segundo, CA (DVW); and the Arizona Center on Aging, Arizona Health Sciences Center, Tucson, AZ (DVW)
2 The abstract for this article was presented orally at the International Society of Renal Nutrition and Metabolism conference, June 10–14, 2008, in Marseilles, France. The data in this report are part of the doctoral dissertation of the first author (CSS) in the Department of Epidemiology at the UCLA School of Public Health, Los Angeles, CA. 3 Supported by grants no. R01DK078106 from the National Institutes of Health and 0655776Y from the American Heart Association (to KK-Z), by DaVita Clinical Research, and by a grant from Harold Simmons (to KK-Z). 4 Address reprint requests to K Kalantar-Zadeh, Harold Simmons Center for Kidney Disease Research & Epidemiology, Los Angeles Biomedical Research Institute at Harbor–UCLA Medical Center, 1124 West Carson Street, C1-Annex, Torrance, CA 90509-2910. E-mail: kamkal{at}ucla.edu.
Background: Dietary restrictions to control serum phosphorus, which are routinely recommended to persons with chronic kidney disease, are usually associated with a reduction in protein intake. This may lead to protein-energy wasting and poor survival.
Objective: We aimed to ascertain whether a decline in serum phosphorus and a concomitant decline in protein intake are associated with an increase in the risk of death.
Design: In a 3-y study (7/2001–6/2004) of 30 075 prevalent maintenance hemodialysis (MHD) patients, we examined changes in serum phosphorus and in normalized protein nitrogen appearance (nPNA), a surrogate of dietary protein intake, during the first 6 mo and the subsequent mortality. Four groups of MHD patients were defined on the basis of the direction of the changes in serum phosphorus and nPNA.
Results: Baseline phosphorus had a J-shaped association with mortality, whereas higher baseline nPNA was linearly associated with greater survival. Compared with MHD patients whose serum phosphorus and nPNA both rose over 6 mo, those whose serum phosphorus decreased but whose nPNA increased had greater survival, with a case mix–adjusted death risk ratio of 0.90 (95% confidence limits: 0.86, 0.95; P < 0.001), whereas those whose phosphorus increased but whose nPNA decreased or those whose phosphorus and nPNA both decreased had worse mortality with a risk ratio of 1.11 (1.05,1.17; P < 0.001) and 1.06 (1.01,1.12; P = 0.02), respectively.
Conclusions: The risk of controlling serum phosphorus by restricting dietary protein intake may outweigh the benefit of controlled phosphorus and may lead to greater mortality. Additional studies including randomized controlled trials should examine whether nondietary control of phosphorus or restriction of nonprotein sources of phosphorus is safer and more effective.
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