The renin-angiotensin system, blood pressure, and heart structure in patients with hereditary vitamin D–resistance rickets (HVDRR)

Authors

  • Dov Tiosano,

    Corresponding author
    1. Division of Pediatric Endocrinology, Meyer Children's Hospital, Rambam Health Care Campus, Haifa, Israel
    2. The Rappaport Faculty of Medicine, The Technion–Israel Institute of Technology, Haifa, Israel
    • Division of Pediatric Endocrinology, Meyer Children's Hospital, Rambam Health Care Campus, Haifa, Israel.
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  • Yitzchak Schwartz,

    1. Institute of Pediatric Cardiology and Adults with Congenital Heart Disease, Meyer Children's Hospital, Rambam Health Care Campus, Haifa, Israel
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  • Yulia Braver,

    1. Institute of Pediatric Cardiology and Adults with Congenital Heart Disease, Meyer Children's Hospital, Rambam Health Care Campus, Haifa, Israel
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  • Amir Hadash,

    1. Division of Pediatric Endocrinology, Meyer Children's Hospital, Rambam Health Care Campus, Haifa, Israel
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  • Vardit Gepstein,

    1. Division of Pediatric Endocrinology, Meyer Children's Hospital, Rambam Health Care Campus, Haifa, Israel
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  • Yosef Weisman,

    1. Bone Disease Unit, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
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  • Avraham Lorber

    1. Institute of Pediatric Cardiology and Adults with Congenital Heart Disease, Meyer Children's Hospital, Rambam Health Care Campus, Haifa, Israel
    2. The Rappaport Faculty of Medicine, The Technion–Israel Institute of Technology, Haifa, Israel
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Abstract

Vitamin D deficiency has been linked to hypertension and an increased prevalence of cardiovascular risk factors and disease. Studies in vitamin D receptor knockout (VDR KO) mice revealed an overstimulated renin-angiotensin system (RAS) and consequent high blood pressure and cardiac hypertrophy. VDR KO mice correspond phenotypically and metabolically to humans with hereditary 1,25-dihydroxyvitamin D–resistant rickets (HVDRR). There are no data on the cardiovascular system in human HVDRR. To better understand the effects of vitamin D on the human cardiovascular system, the RAS, blood pressure levels, and cardiac structures were examined in HVDRR patients. Seventeen patients (9 males, 8 females, aged 6 to 36 years) with hereditary HVDRR were enrolled. The control group included age- and gender-matched healthy subjects. Serum calcium, phosphorous, creatinine, 25-hydroxyvitamin D [25(OH)D],1,25-dihydroxyvitamin D3 [1,25(OH)2D3], parathyroid hormone (PTH), plasma rennin activity (PRA), aldosterone, angiotensin II (AT-II), and angiotensin-converting enzyme (ACE) levels were determined. Ambulatory 24-hour blood pressure measurements and echocardiographic examinations were performed. Serum calcium, phosphorus, and alkaline phosphatase values were normal. Serum 1,25(OH)2D3 and PTH but not PRA and ACE levels were elevated in the HVDRR patients. AT-II levels were higher than normal in the HVDRR patients but not significantly different from those of the controls. Aldosterone levels were normal in all HVDRR patients. No HVDRR patient had hypertension or echocardiographic pathology. These findings reveal that 6- to 36-year-old humans with HVDRR have normal renin and ACE activity, mild but nonsignificant elevation of AT-II, normal aldosterone levels, and no hypertension or gross heart abnormalities. © 2011 American Society for Bone and Mineral Research

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