Original Research
Association of Relatively Low Serum Parathyroid Hormone With Malnutrition-Inflammation Complex and Survival in Maintenance Hemodialysis Patients

https://doi.org/10.1053/j.jrn.2009.10.006Get rights and content

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 <150 pg/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 100–150 pg/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 300–600 pg/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 100–150 pg/mL range appears associated with the greatest survival. Limitations of observational studies should be considered.

Section snippets

Patient Population

We studied maintenance hemodialysis (MHD) patients who participated in the Nutritional and Inflammatory Evaluation in Dialysis (NIED) Study (see the NIED Study website at www.NIEDStudy.org for more details, as well as previous publications).25, 26, 27, 28, 29, 30, 31 Subjects were randomly selected from a pool of over 3,000 MHD outpatients in eight DaVita chronic dialysis facilities in the South Bay Los Angeles area.32 Inclusion criteria were outpatients who had been undergoing MHD for at least

Results

The 748 MHD patients were 53.5 ± 18.6 years old (mean ± SD); 47% of patients (n = 351) were women, 50% (n = 373) were Hispanic, 32% (n = 239) were African American, and 55% (n = 413) were diabetic. The mean dialysis vintage was 32 ± 34 months (median, 21 months; interquartile range, 8–45 months). The average baseline serum intact PTH in the 748 MHD patients was 350 ± 351 pg/mL (median, 247; minimum, 2; maximum, 2,680; interquartile range, 159–408 ng/mL). Table 1 shows relevant variables in the three groups of

Discussion

In 748 MHD patients who were observed for up to 5 years in Southern California, we found that low serum PTH <150 pg/mL was more prevalent among non-blacks, Hispanics, and diabetics. There was no association between serum PTH and coronary artery calcification score, bone mineral density, or dietary protein or calorie intake. However, low PTH was associated with protein-energy wasting and inflammation, and this association appeared to overshadow and virtually nullify any possible relationship

Conclusions

Serum intact PTH below 150 pg/mL was associated with surrogates of malnutrition-inflammation complex in a cohort of 748 MHD patients. Among the subgroup of 167 randomly selected MHD patients who also underwent EBCT and DEXA, serum PTH was associated with neither coronary artery calcification nor bone mineral density. Despite the higher prevalence of death risk markers in patients with low PTH, patients with a serum intact PTH between 100 and 150 pg/mL had a greater chance of survival in

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    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.

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