Complete Resorption of Massive Soft Tissue Calcification in a Hemodialysis Patient after Parathyroidectomy

Sabeel, A; Al-Homrany, Mohammed

doi:10.1159/000013630

Cited by 14 publications

(9 citation statements)

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“…In contrast, massive soft tissue calcification resorption was observed in hemodialysis patients after PTX. [ 27 , 28 ] We have also found that phosphorus excretion in the dialysis solution and stool of post-PTX patients is not increased (data not shown). Therefore, we focused on bone as the target organ of phosphorus deposition.…”

Section: Discussionmentioning

confidence: 75%

The Effect of Bovine Parathyroid Hormone Withdrawal on MC3T3-E1 Cell Proliferation and Phosphorus Metabolism

Liu

Zhu

et al. 2015

PLoS ONE

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Hypocalcemia and hypophosphatemia are common complications after parathyroidectomy (PTX). Sudden removal of high circulating levels of parathyroid hormone (PTH) causes decreased osteoclastic resorption resulting in a decreased bone remodeling space. These phenomena are likely due to an increased influx of calcium and phosphorus into bone. However, there are currently no data to support this hypothesis. In this study, we found that PTX significantly reduced levels of PTH, calcium and phosphate. Compared with preoperative levels, after 1 year, postoperative PTH, calcium and phosphate levels were 295.6 ± 173.7 pg/mL (P < 0.05), 86.62 ± 15.98 mg/dL (P < 0.05) and 5.56 ± 2.03 mg/dL (P < 0.05), respectively. We investigated continuous bovine PTH administration as well as withdrawal of bovine PTH stimulation in the mouse osteoblast precursor cell line MC3T3-E1. MC3T3-E1 cells were cultured with continuous bovine PTH treatment for 20 days or with transient bovine PTH treatment for 10 days. High doses of continuous bovine PTH exposure strongly reduced cell proliferation, alkaline phosphatase activity and the number of mineralized calcium nodules. However, withdrawal of bovine PTH (100 ng/mL) significantly increased the number of mineralized calcium nodules and caused a rapid decline in calcium and phosphorus content of culture medium. In conclusion, continuous exposure to bovine PTH inhibited osteoblast differentiation and reduced the formation of mineralized nodules. However, this inhibition was removed and mineralized nodule formation resumed with withdrawal of bovine PTH. According to the results of our clinical examinations and in vitro experiments, we hypothesize that the sudden removal of high levels of PTH may cause an increased influx of calcium and phosphorus into bone after PTX.

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Section: Discussionmentioning

confidence: 75%

The Effect of Bovine Parathyroid Hormone Withdrawal on MC3T3-E1 Cell Proliferation and Phosphorus Metabolism

Liu

Zhu

et al. 2015

PLoS ONE

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“…In addition to the indications mentioned above, PTx should be considered more readily in the presence of the following features: (i) symptoms of severe secondary hyperparathyroidism, (i) increased serum markers of bone turnover (such as ALP), (iii) radiological signs of bone lesions (such as salt and pepper skull, rugger jersey spine, and subperiosteal resorption in the phalanges), and (iv) progressive ectopic calcifications (vascular calcification, cardiac valve calcification, and tumoral calcinosis). Several studies reported attenuation of progressive vascular calcification , regression of tumoral calcinosis , and amelioration of anemia , hypertension and cardiac function in patients who underwent PTx for severe secondary hyperparathyroidism. Surgical series also reported clinical improvement of calciphylaxis following PTx .…”

Section: Rationalementioning

confidence: 99%

Clinical Practice Guideline for the Management of Chronic Kidney Disease‐Mineral and Bone Disorder

et al. 2013

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“…Low serum levels of Klotho cannot be demonstrated in ESRD because of technical problems related to measurements. Severe elevations of PTH that lead to increased Ca ϫ P are also associated with uremic tumoral calcinosis, and marked improvement has been reported after parathyroidectomy and lowering for calciumphosphate product (77).…”

Section: Acquired Disordersmentioning

confidence: 99%

How Fibroblast Growth Factor 23 Works

Liu

Quarles

2007

Journal of the American Society of Nephrology

366

341

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There is a discontinuum of hereditary and acquired disorders of phosphate homeostasis that are caused by either high or low circulating levels of the novel phosphaturic hormone fibroblastic growth factor 23 (FGF23). Disorders that are caused by high circulating levels of FGF23 are characterized by hypophosphatemia, decreased production of 1,25-dihydroxyvitamin D, and rickets/osteomalacia. On the other end of the spectrum are disorders that are caused by low circulating levels of FGF23, which are characterized by hyperphosphatemia, elevated production of 1 Fibroblast Growth Factor 23 Gene and Protein StructureThe fibroblast growth factor (FGF) family consists of 22 members with varied functions (2). FGF23 is an approximately 32-kD (251 amino acids) protein with an N-terminal region that contains the FGF homology domain and a novel 71-amino acid C-terminus that was originally discovered by homology-based PCR screening of a mouse embryonic cDNA library (3). The FGF23 gene is located on Chr 12p13 and is phylogenetically grouped with FGF19 and 21 gene products (2,3), with which it has approximately 24% and approximately 22% amino acid identities, respectively. FGF23 principally acts as a phosphaturic factor and suppressor of 1␣-hydroxylase activity in the kidney (4,5), making it functionally distinct from other members of this family. Tissue Expression and Function: Evidence for a Bone-Kidney AxisFGF23 is predominately expressed in osteocytes in bone (6,7), but it is also expressed in pericyte-like cells that surround the venous sinuses in the bone marrow, in the ventrolateral thalamic nucleus, and in thymus and lymph nodes (Figure 1). The relative contribution of these sites to circulating FGF23 levels is not known, but the high levels of expression in the osteocyte and that osteocytes are the most abundant cell in bone suggest that the serum levels of FGF23 are derived mainly from bone. In addition, the production of FGF23 by osteocytes, cells that are central to the regulation of osteoblast function and mineralization, likely has functional significance (8). In this regard, osteocytes secrete sclerostin, an inhibitor of bone formation and the phosphaturic factor FGF23, as well as other gene products, such as phosphate-regulating endopeptidase homolog, X-linked (Phex), dentin matrix protein 1 (DMP1), and matrix extracellular phosphoglycoprotein (MEPE), that regulate bone mineralization and FGF23 expression. Phex is a type I cell surface zinc metalloprotease that is involved in the regulation of FGF23 levels and is mutated in X-linked hypophosphatemic rickets (9). Both DMP1 and MEPE are glycophosphoproteins that belong to the small integrin-binding ligand N-linked glycoprotein (SIBLING) family of proteins. MEPE and DMP1 are predominately expressed in bones and/or teeth, where they respectively inhibit and induce mineralization of extracellular matrix (10). These associations suggest that osteocytes coordinate osteoblast-mediated bone formation with renal regulation of systemic phosphate homeostasis through the regu...

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Complete Resorption of Massive Soft Tissue Calcification in a Hemodialysis Patient after Parathyroidectomy

Cited by 14 publications

References 14 publications

The Effect of Bovine Parathyroid Hormone Withdrawal on MC3T3-E1 Cell Proliferation and Phosphorus Metabolism

The Effect of Bovine Parathyroid Hormone Withdrawal on MC3T3-E1 Cell Proliferation and Phosphorus Metabolism

Clinical Practice Guideline for the Management of Chronic Kidney Disease‐Mineral and Bone Disorder

How Fibroblast Growth Factor 23 Works

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