Abnormalities of mineral metabolism, including those of calcium (Ca), phosphorus (P), and parathyroid hormone (PTH) in patients on maintenance hemodialysis induce severe bone involvement, which manifests as renal osteodystrophy. Recently, vascular calcification caused by abnormal mineral metabolism has been attracting attention because cardiovascular diseases (CVD) are a major cause of death in hemodialysis patients. Since 2000, the treatment standard for overt secondary hyperparathyroidism (SHPT) in our facilities has shifted from conventional or pulse therapy with oral vitamin D3 (VitD) to intravenous pulse therapy with maxacalcitriol or calcitriol. After selecting the criterion of overt SHPT as intact-PTH>500 pg/mL, the proportion of overt SHPT cases among all hemodialysis patients decreased from 12% at the start of intravenous pulse treatment to 6.4% after 4 years' treatment. However, the number of patients who had an interruption to pulse treatment because of hypercalcemia and/or hyperphosphatemia was high and it became a bottleneck for the continuation of the therapy. The major cause of hypercalcemia is considered to be Ca load derived from oral calcium carbonate. In Japan, sevelamer hydrochrolide (SH), which does not contain Ca, has been available commercially since 2003 and potentially should enable a reduction in the incidence of overt SHPT during long-term intravenous treatment when combined with careful adjustment of the dose of VitD and strict monitoring of Ca and P level concentrations. In this study, we found that the proportion of patients who satisfy the recommended serum concentrations of Ca and P reported by K/DOQI guideline was low irrespective of the serum concentration of intact-PTH. The aortic calcification index was high in the patient group with lower intact-PTH level concentration, probably because of reduced Ca and P buffering ability associated with reduced bone turnover. We consider that VitD treatment with SH might give better control of the intact-PTH level concentration within the range recommended by the K/DOQI guideline.
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http://dx.doi.org/10.1111/j.1744-9987.2005.00325.x | DOI Listing |
Curr Vasc Pharmacol
June 2024
Department of Vascular Disease, University Medical Centre, Ljubljana, Slovenia.
Primary hyperparathyroidism (PHPT) is presented in various forms, including classic PHPT, characterised by increased parathyroid hormone (PTH) secretion, normohormonal PHPT, and normocalcaemic PHPT. Secondary hyperparathyroidism is characterised by increased PTH secretion triggered by factors such as vitamin D deficiency and kidney failure. This review aims to discuss the involvement of hyperparathyroidism (HPT) in atherosclerosis, including peripheral arterial disease (PAD).
View Article and Find Full Text PDFEndocr Connect
September 2015
Endocrine Unit 2University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, ItalyDepartment of Clinical and Experimental MedicineUniversity of Pisa, Pisa, ItalyLaboratory of Chemistry and EndocrinologyUniversity Hospital of Pisa, Pisa, Italy Endocrine Unit 2University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, ItalyDepartment of Clinical and Experimental MedicineUniversity of Pisa, Pisa, ItalyLaboratory of Chemistry and EndocrinologyUniversity Hospital of Pisa, Pisa, Italy
We investigated the prevalence of normocalcemic primary hyperparathyroidism (NPHPT) in the adult population living in a village in Southern Italy. All residents in 2010 (n=2045) were invited by calls and 1046 individuals accepted to participate. Medical history, calcium intake, calcium, albumin, creatinine, parathyroid hormone (PTH) and 25OHD were evaluated.
View Article and Find Full Text PDFNephrol Dial Transplant
July 2012
Stanford University School of Medicine, Palo Alto, CA, USA.
Background: Secondary hyperparathyroidism (sHPT) and other abnormalities associated with chronic kidney disease-mineral bone disorder can contribute to dystrophic (including vascular) calcification. Dietary modification and variety of medications can be used to attenuate the severity of sHPT. However, it is unknown whether any of these approaches can reduce the high risks of death and cardiovascular disease in patients with end-stage renal disease.
View Article and Find Full Text PDFTher Apher Dial
August 2005
Jinyukai Kitasaito Hospital, Asahikawa City, Hokkaido, Japan.
Abnormalities of mineral metabolism, including those of calcium (Ca), phosphorus (P), and parathyroid hormone (PTH) in patients on maintenance hemodialysis induce severe bone involvement, which manifests as renal osteodystrophy. Recently, vascular calcification caused by abnormal mineral metabolism has been attracting attention because cardiovascular diseases (CVD) are a major cause of death in hemodialysis patients. Since 2000, the treatment standard for overt secondary hyperparathyroidism (SHPT) in our facilities has shifted from conventional or pulse therapy with oral vitamin D3 (VitD) to intravenous pulse therapy with maxacalcitriol or calcitriol.
View Article and Find Full Text PDFNephrol Dial Transplant
May 1995
Nagoya University School of Medicine, Third Department of Internal Medicine, Japan.
In order to evaluate the clinical outcome as well as the effect of vitamin D3 treatment on secondary hyperparathyroidism (SHPT) in the patients undergoing long-term dialysis therapy, we conducted a long-term follow-up survey on the demographic characteristics of 425 patients who were observed for more than 3 years. All patients were treated with daily 1 alpha (OH)D3 treatment after the initiation of dialysis. Among them the percentage of patients needing parathyroidectomy was 4.
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