Serum ionic calcium is associated with a nondipping blood pressure pattern in hypertensive patients with chronic kidney disease, and advanced CKD increases the risk of nondipping.
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Should not yet change practice in hypertensive CKD; leaves open whether ionic calcium or eGFR causally influences nondipping.
A nondipping BP pattern has been shown to be predictive of end-organ damage, cardiovascular events, and mortality. The mechanisms of blunted nocturnal BP fall are multifactorial. We assessed whether total corrected serum calcium and ionic calcium (iCa) are associated with a blunted nocturnal BP fall in both treated and untreated hypertensive patients with stages 1-3 of the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI). Clinical data and 24-hour ambulatory blood pressure monitoring were obtained in a cohort of 231 essential hypertensive patients. Among the entire cohort, 107 were nondippers and 124 were dippers. Only in nondippers, we found significant correlations between iCa and 24-hour systolic blood pressure (SBP; r = 0.21, P < .03), diurnal SBP (r = 0.21, P < .03), and 24-hour pulse pressure (PP; r = 0.23, P < .02). The ambulatory arterial stiffness index (AASI) was significantly related with 24-hour PP in both dippers and nondippers after adjusting for age. Both AASI and 24-hour PP were higher in nondippers than in dippers. In addition, in nondippers, the prevalence of estimated glomerular filtration rate (eGFR) < 60 mL/minute/1.73 m2 was higher than in dippers (50% vs. 33.7%, P < .02). Logistic regression showed that patients with eGFR ≥ 60 mL/minute/1.73 m2 had lower risk of nondipper status than patients with eGFR < 60 mL/minute/1.73 m2 (odds ratio = 2.445; 95% confidence interval = 1.398-4.277, P < .002). In conclusion, serum iCa could participate in the pathogenesis of nondipping pattern. Increased large artery stiffness may be a mechanism of the deleterious influence of nondipping on cardiovascular outcome. Hypertensive subjects with stage 3 of NKF KDOQI had a greater loss of circadian BP rhythm than those in stages 1 and 2.
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Feldstein et al. (2012) studied this question.
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