Association of Relatively Low Serum Parathyroid Hormone With Malnutrition-Inflammation Complex and Survival in Maintenance Hemodialysis Patients
published online 04 March 2010.
Background
Low serum parathyroid hormone (PTH) has been implicated as a primary biochemical marker of adynamic bone disease in individuals with chronic kidney disease (CKD) who undergo maintenance hemodialysis (MHD) treatment. We hypothesized that the malnutrition-inflammation complex is associated with low PTH levels in these patients and confounds the PTH-survival association.
Methods
We examined 748 stable MHD outpatients in southern California and followed them for up to 5 years (October 2001–December 2006).
Results
In 748 MHD patients, serum PTH <150pg/mL was more prevalent among non-blacks and diabetics. There was no association between serum PTH and coronary artery calcification score, bone mineral density, or dietary protein or calorie intake. Low serum PTH was associated with markers of protein-energy wasting and inflammation, and this association confounded the relationship between serum PTH and alkaline phosphatase. Although 5-year crude mortality rates were similar across PTH increments, after adjustment for the case-mix and surrogates of malnutrition and inflammation, a moderately low serum PTH in 100–150pg/mL range was associated with the greatest survival compared to other serum PTH levels, i.e., a death hazard ratio of 0.52 (95% confidence interval: 0.29–0.92, p<0.001) compared to PTH of 300–600pg/mL (reference).
Conclusions
Low serum PTH may be another facet of the malnutrition-inflammation complex in CKD, and after controlling for this confounder, a moderately low PTH in 100–150pg/mL range appears associated with the greatest survival. Limitations of observational studies should be considered.
∗Harold Simmons Center for Chronic Disease Research and Epidemiology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA 90502
†Salem Veteran Affairs Medical Center, Salem, VA 24153
§Division of Cardiology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA 90502
∗∗David Geffen UCLA School of Medicine, Los Angeles, CA 90095
††Northwestern University Feinberg School of Medicine, Evanston Northwestern Healthcare, Evanston, IL 60201
Address reprint requests to Kamyar Kalantar-Zadeh, MD, PhD, MPH, Harold Simmons Center for Kidney Disease Research and Epidemiology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, 1124 West Carson Street, C1-Annex, Torrance, CA 90502.
This study was supported by research grant DK61162 (for KKZ) from the National Institutes of Health, National Institute of Diabetes, Digestive and Kidney Disease, a research grant from DaVita, Inc (for KKZ), a philanthropist grant from Mr. Harold Simmons (for KKZ), and General Clinical Research Center (GCRC) grant M01-RR00425 from the National Centers for Research Resources, National Institutes of Health.
Drs. Kalantar-Zadeh, Kovesdy, Sprague, and/or Budoff have received grants and/or honoraria from Shire, Amgen, Abbott, Genzyme, or Fresenus.
The authors are thankful to Dr. Victor Goh, at Harbor-UCLA GCRC Core Laboratories, for the management of blood samples and measuring inflammatory markers, and to DaVita Clinical Research and DaVita dietitians for supporting the NIED Study in DaVita dialysis clinics in Los Angeles South Bay Area.
ABSTRACT