Journal
JOURNAL OF RENAL NUTRITION
Volume 21, Issue 1, Pages 100-104Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/j.jrn.2010.10.006
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Funding
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R21DK077341, K23DK061162, R01DK078106, R21DK078012] Funding Source: NIH RePORTER
- NIDDK NIH HHS [K23 DK061162, R01 DK078106-05, R21 DK078012-02, K23 DK061162-05, R21 DK077341, R21 DK078012, R01 DK078106] Funding Source: Medline
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In individuals with advanced chronic kidney disease, secondary hyperparathyroidism is known to be associated with high turnover bone disease. Low serum parathyroid hormone (PTH) levels may not necessarily be because of hypodynamic bone, but could be another facet of the malnutrition-inflammation-cachexia syndrome (MICS). A recent 5-year cohort study in 748 stable hemodialysis outpatients showed that after the confounding effect by the MICS was removed, the moderately low levels of PTH in the 100 to 150 pg/mL range was associated with the greatest survival rate. Data from Japanese dialysis patients show similar survival advantages of having a lower PTH range. Low levels of serum PTH seem to be associated with markers of protein-energy wasting and inflammation, and this association may confound the relationship between serum PTH and alkaline phosphatase. PTH stimulates lipogenesis through influx of calcium into the adipocytes. PTH secretion is suppressed by interleukin-1 beta and interleukin-6, which are proinflammatory cytokines that are associated with poor outcome in dialysis patients. These cytokines inhibits PTH secretion in cultured parathyroid tissue slices. In this article, we review the association of a low serum PTH level with the MICS in patients with chronic kidney disease and suggest avoiding over-interpretation of low serum PTH level as an indicator of low turnover bone disease. (C) 2011 by the National Kidney Foundation, Inc. All rights reserved.
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