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      Hypoparathyroidism Potentiates Cardiovascular Complications through Disturbed Calcium Metabolism: Possible Risk of Vitamin D 3 Analog Administration in Dialysis Patients with End-Stage Renal Disease

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          Abstract

          Background/Aim: Progressive cardiovascular calcification in dialysis patients with end-stage renal disease (ESRD) is a serious complication; however, the precise mechanism remains uncertain. We tested whether metabolic calcium abnormalities and hypoparathyroidism might have a correlation with cardiovascular complications in ESRD patients. Methods: A series of 48 ESRD patients with cardiovascular diseases and/or congestive heart failure, aged 36–82 (61 ± 12) years, 23 male and 25 female, were enrolled in this study. Serum total calcium (Ca, mmol/l), inorganic phosphate (mmol/l), and intact parathyroid hormone (iPTH, pg/ml) levels were determined in all cases. Results: Organic heart disease was confirmed in 28 patients (58.3%), including 15 with coronary artery disease: 8 with aortic aneurysm, 8 with stenotic valvular heart disease, 9 with excessive mitral annular calcification, 3 with dialysis cardiomyopathy, and 7 with obstructive arterial disease. Serum iPTH measurement revealed hypoparathyroidism (iPTH <60) in 20 of 48 (41.7%) and hyperthyroidism (iPTH ≧200) in 13 of 48 (27.1%) subjects. The 20 patients with low iPTH had a higher prevalence of valvular heart disease, a higher total Ca level corrected for serum albumin (2.70 ± 0.30 in low iPTH vs. 2.47 ± 0.30 in normal iPTH, 2.35 ± 0.20 in high iPTH, p = 0.003) and a higher tendency of vitamin D<sub>3</sub> analog use (65% in low iPTH vs. 33% in normal iPTH and 46% in high iPTH, p = 0.078). Moreover, corrected serum Ca exhibited a negative logarithmic correlation with serum iPTH: corrected Ca = –0.284× log (iPTH) + 3.021 (r = 0.637, p = 0.0001). Multiple logistic regression analysis revealed diabetes and hypoparathyroidism (iPTH <60) as risk factors for cardiovascular complications in ESRD. Conclusion: These results suggest that hypercalcemia and hypoparathyroidism in conjunction with vitamin D<sub>3</sub> use might play an important role in cardiovascular complications of chronic dialysis patients.

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          Most cited references 3

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          Intact parathyroid hormone overestimates the presence and severity of parathyroid-mediated osseous abnormalities in uremia

           L D Quarles (1992)
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            Rapidly progressing, massive mitral annular calcification. Occurrence in a patient with chronic renal failure.

            Calcification of the mitral annulus developed in a patient while undergoing dialysis. The rapid onset of events corresponded to the onset of end-stage renal failure and uncontrolled secondary hyperparathyroidism. Sequential echocardiograms verified the progression of calcification of the annulus as well as the valve. A new systolic and diastolic murmur and reduced valve orifice on two-dimensional echocardiography suggested acquired nonrheumatic mitral stenosis and insufficiency. We propose that metastatic calcium deposition rather than long-term hypertensive and degenerative effects was the predominant mechanism for massive calcification of the annulus and valve. It is suggested that M-mode echocardiography be used sequentially to follow both the occurrence and progression of calcification of the mitral annulus or valve in patients with chronic renal failure, secondary hyperparathyroidism, or both.
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              Calcium metabolism and osteodystrophy after renal transplantation

               C. L. HAMPERS (1969)
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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                2000
                January 2000
                19 January 2000
                : 84
                : 1
                : 13-20
                Affiliations
                2nd Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
                Article
                45533 Nephron 2000;84:13–20
                10.1159/000045533
                10644903
                © 2000 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 4, Tables: 2, References: 28, Pages: 8
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/45533
                Categories
                Original Paper

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