Tumoral calcinosis due to severe hyperphosphatemia and secondary hyperparathyroidism without vascular calcification in a hemodialysis patient
- 1 March 2021
- journal article
- research article
- Published by Dustri-Verlgag Dr. Karl Feistle in Clinical Nephrology
- Vol. 95 (3), 166-170
- https://doi.org/10.5414/cn110201
Abstract
We report a case of a 32-year-old man who was undergoing chronic hemodialysis and had hyperphosphatemia and secondary hyperparathyroidism (SHPT) with multiple tumoral calcinosis (TC) lesions refractory to drug therapy. Total parathyroidectomy and autotransplantation were performed, and he recovered from TC within 3 months. Several soft-tissue calcifications were present, but neither computed tomography (CT) before diagnosis nor CT performed 12 months after surgery detected evidence of vascular calcification (VC), despite persistence of hyperphosphatemia. This patient had a high calcium (Ca) x phosphate (P) product and calciprotein particles, and high serum Ca and P levels are important risk factors for both TC and VC. P plays a crucial role in regulation of VC, but the absence of VC in our case suggests a specific circumstance in which VC does not progress even under a high phosphatemic state, and that P alone may be insufficient for VC progression. TC in our patient was probably due to severe SHPT and continuous high serum P and Ca x P product levels, but the absence of VC suggests that the pathophysiologic process leading to VC requires further investigation, particularly in chronic kidney disease.Keywords
This publication has 15 references indexed in Scilit:
- Arterial ageing: from endothelial dysfunction to vascular calcificationJournal of Internal Medicine, 2017
- Calcification of vascular smooth muscle cells is induced by secondary calciprotein particles and enhanced by tumor necrosis factor-αAtherosclerosis, 2016
- Vascular calcification: Mechanisms of vascular smooth muscle cell calcificationTrends in Cardiovascular Medicine, 2014
- Medial vascular calcification revisited: review and perspectivesEuropean Heart Journal, 2014
- Tumoral Calcinosis—A Pathogenetic OverviewInternational Journal of Surgical Pathology, 2012
- Replicative senescence of vascular smooth muscle cells enhances the calcification through initiating the osteoblastic transitionAmerican Journal of Physiology-Heart and Circulatory Physiology, 2009
- A homozygous missense mutation in human KLOTHO causes severe tumoral calcinosisJCI Insight, 2007
- Tumoral Calcinosis: Pearls, Polemics, and Alternative PossibilitiesRadioGraphics, 2006
- An FGF23 missense mutation causes familial tumoral calcinosis with hyperphosphatemiaHuman Molecular Genetics, 2004
- Mutations in GALNT3, encoding a protein involved in O-linked glycosylation, cause familial tumoral calcinosisNature Genetics, 2004