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Kidney Blood Press Res. 2007;30(6):416-20. Epub 2007 Apr 26.

Relation between serum thyroid hormone and 'nondipper' circadian blood pressure variability.

Author information

1
Department of Internal Medicine, Section of Nephrology, Fatih University School of Medicine, Ankara, Turkey. mkanbay@fatih.edu.tr or drkanbay@yahoo.com

Abstract

Currently, the pathogenesis of nondipper hypertension remains largely unclear in patients without any renal or endocrine pathology. It is well known that overt hypothyroidism is strongly associated with diastolic hypertension. However, no study has addressed the pathogenic role of TSH, free T3 (FT3), and free T4 (FT4) in nondipper hypertension. The aim of the present investigation is to evaluate if higher TSH, low FT3 and FT4 would be associated with a nondipper hypertension profile, in patients with normal renal function and without any overt thyroid hormone disorder. 131 subjects were screened and those who met the following inclusion criteria were enrolled: (1) glomerular filtration rate (GFR) >60 ml/min; (2) no history of thyroid disorders; (3) no history of thyroid hormone medication. All subjects underwent 24-hour ambulatory blood pressure monitoring on a usual working day. Of the total population, 59 patients (45%) were classified as dippers and 72 (55%) were classified as nondippers. The only significant differences between dipper and nondipper patients appear to be related to FT3 levels and GFR. Nondipper patients had lower FT3 levels (4.5 +/- 0.6 vs. 4.0 +/- 0.9 pmol/l, p = 0.02) and low GFR (80.5 +/- 12.2 vs. 86.9 +/- 16.9 ml/min, p = 0.03), compared to dipper patients. The final regression model included serum TSH, FT3 levels, and GFR; the only independent predictor of nondipper hypertension was FT3 (p = 0.04). In conclusion, even if the mechanisms of our findings remain incompletely understood, we demonstrate a graded independent relation between lower level of FT3 and the risk of nondipping. Further studies are warranted to confirm this relationship and to elucidate the pathogenetic mechanisms of this relationship.

PMID:
17960070
DOI:
10.1159/000110082
[Indexed for MEDLINE]
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