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      Detection of Cardiac Calcinosis in Hemodialysis Patients by Whole-Body Scintigraphy with 99m-Technetium Methylene Diphosphonate

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          A noninvasive method for the diagnosis of cardiac calcinosis, a life-threatening complication in hemodialysis patients with end-stage renal disease (ESRD), has not, as yet, been firmly established. We tested whether whole body scanning with 99m-technetium methylene diphosphonate (MDP) might visualize cardiac calcinosis. In 19 consecutive chronic hemodialysis ESRD patients (13 males and 6 females, aged 40–81, mean 63 ± 8 years) with cardiovascular disease [mitral annular calcinosis and/or calcified aortic valve (n = 4), hemodialysis cardiomyopathy (n = 1), coronary artery disease (n = 9) and peripheral artery atherosclerotic disease (n = 6)], MDP uptake in the heart was compared to that in 7 non-ESRD controls with hyperparathyroidism due to adenoma. Cardiac and lung field MDP uptake was confirmed in only 3 (16%) and 5 (26%) of the 19 ESRD subjects, respectively, but was absent in controls. Positive cardiac uptake was related to cardiac calcified complications (mobile intracardiac calcinosis, myocardial calcinosis and mitral annular calcification) and the duration of hemodialysis (p = 0.015). While it was statistically insignificant, subjects showing MDP uptake were elder and had higher serum Ca or Ca × P product and lower intact parathyroid hormone levels. These results suggest that cardiac calcinosis in ESRD patients can be detected noninvasively by myocardial scintigraphy with 99m-technetium MDP.

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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

          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 3 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 3 use might play an important role in cardiovascular complications of chronic dialysis patients.
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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)

                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                August 2000
                01 September 2000
                : 20
                : 4
                : 278-282
                aSecond Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, and bObihiro Kyohkai Hospital, Obihiro, Japan
                13601 Am J Nephrol 2000;20:278–282
                © 2000 S. Karger AG, Basel

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                Figures: 1, Tables: 1, References: 11, Pages: 5
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