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Sudden onset of parathyroid hormone-independent severe hypercalcemia from reversal of tumoral calcinosis in a dialysis patient


Background:
Tumoral calcinosis is a rare manifestation of extraskeletal calcification, featuring large calcified cystic masses in the periarticular regions of large joints. In chronic kidney disease (CKD), this disorder is thought to evolve through a chronically elevated calcium-phosphorus solubility product leading to calcium precipitation in soft tissue. Treating tumoral calcinosis in these patients involves interventions to lower the calcium-phosphorus product such as reduction in vitamin D therapy and intensive hemodialysis regimens.

Case Presentation:
We report the case of a 54-year old woman with polycystic kidney disease on peritoneal dialysis with widespread tumoral calcinosis in the context of hypercalcemic tertiary hyperparathyroidism who had been on long-term alfacalcidol therapy. After withdrawal of the vitamin D analogue and initiation of daily hemodialysis, there was rapid dissolution of her tumoral calcium deposits with the abrupt onset of parathyroid hormone (PTH)-independent transient hypercalcemia that resolved once the soft tissue deposits disappeared.

Conclusions:
Resorption of soft tissue calcific deposits may result in transient parathyroid hormone (PTH)-independent hypercalcemia. In CKD patients, this hypercalcemia causes a decrease in the PTH level, distinguishing it from tertiary hyperparathyroidism, though PTH may not be totally suppressed, the way it is seen in PTH-independent hypercalcemia in non-CKD patients.

Keywords:
Hypercalcemia, Parathyroid hormone, Hyperparathyroidism, Tumoral calcinosis, Metastatic calcification, Chronic kidney disease, Peritoneal dialysis, Hemodialysis


Autoři: Fareed B. Kamar 1*;  Bikaramjit Mann 1,2;  Gregory Kline 1
Působiště autorů: Department of Medicine, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. 1;  Department of Critical Care Medicine, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. 2
Vyšlo v časopise: BMC Nefrol 2016, 17:137
Kategorie: Case report
prolekare.web.journal.doi_sk: https://doi.org/10.1186/s12882-016-0355-y

© 2016 The Author(s).

Open access
This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
The electronic version of this article is the complete one and can be found online at: http://bmcnephrol.biomedcentral.com/articles/10.1186/s12882-016-0355-y

Souhrn

Background:
Tumoral calcinosis is a rare manifestation of extraskeletal calcification, featuring large calcified cystic masses in the periarticular regions of large joints. In chronic kidney disease (CKD), this disorder is thought to evolve through a chronically elevated calcium-phosphorus solubility product leading to calcium precipitation in soft tissue. Treating tumoral calcinosis in these patients involves interventions to lower the calcium-phosphorus product such as reduction in vitamin D therapy and intensive hemodialysis regimens.

Case Presentation:
We report the case of a 54-year old woman with polycystic kidney disease on peritoneal dialysis with widespread tumoral calcinosis in the context of hypercalcemic tertiary hyperparathyroidism who had been on long-term alfacalcidol therapy. After withdrawal of the vitamin D analogue and initiation of daily hemodialysis, there was rapid dissolution of her tumoral calcium deposits with the abrupt onset of parathyroid hormone (PTH)-independent transient hypercalcemia that resolved once the soft tissue deposits disappeared.

Conclusions:
Resorption of soft tissue calcific deposits may result in transient parathyroid hormone (PTH)-independent hypercalcemia. In CKD patients, this hypercalcemia causes a decrease in the PTH level, distinguishing it from tertiary hyperparathyroidism, though PTH may not be totally suppressed, the way it is seen in PTH-independent hypercalcemia in non-CKD patients.

Keywords:
Hypercalcemia, Parathyroid hormone, Hyperparathyroidism, Tumoral calcinosis, Metastatic calcification, Chronic kidney disease, Peritoneal dialysis, Hemodialysis


Zdroje

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2. Eisenberg B, Tzamaloukas AH, Hartshorne MF, Listrom MB, Arrington ER, Sherrard DJ. Periarticular tumoral calcinosis and hypercalcemia in a hemodialysis patient without hyperparathyroidism: a case report. J Nucl Med. 1990;31(6):1099–103.

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8. Goldsmith DJ, Covic A, Fouque D, Locatelli F, Olgaard K, Rodriguez M, et al. Endorsement of the Kidney Disease Improving Global Outcomes (KDIGO) Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guidelines: a European Renal Best Practice (ERBP) commentary statement. Nephrol Dial Transplant. 2010;25(12):3823–31.

9. Bover J, Urena P, Brandenburg V, Goldsmith D, Ruiz C, Dasilva I, et al. Adynamic bone disease: from bone to vessels in chronic kidney disease. Semin Nephrol. 2014;34(6):626–40.

10. Fernandez E, Amoedo ML, Borras M, Pais B, Montoliu J. Tumoral calcinosis in haemodialysis patients without severe hyperparathyroidism. Nephrol Dial Transplant. 1993;8(11):1270–3.

11. Foundation NK. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis. 2003;42(4 Suppl 3): S1–S201.

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Detská nefrológia Nefrológia
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