Massive tumoral calcifications in hemodialysis patients without severe hyperparathyroidism

Fernàndez, Elvira; Amoedo, Maria Luisa; Borràs, Mercè; Montolíu, J

doi:10.1016/8756-3282(93)90272-c

Cited by 10 publications

(19 citation statements)

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“…Epidemiological studies have shown that there is a variety of risk factors for ectopic calcification, including high serum levels of Ca, Pi and parathyroid hormone, the administration of VDR activator, alkalemia and the use of aluminum-based medicines (12,13). In the present case, both the serum Ca and Pi levels were increased.…”

Section: Discussionsupporting

confidence: 51%

Rapid Progression of Vascular and Soft Tissue Calcification while Being Managed for Severe and Persistent Hypocalcemia Induced by Denosumab Treatment in a Patient with Multiple Myeloma and Chronic Kidney Disease

et al. 2015

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We herein present the case of a patient with myeloma and chronic kidney disease (CKD) who developed rapidly progressive vascular and soft tissue calcification during the course of treatment for severe hypocalcemia induced by the administration of denosumab for myeloma and hypercalcemia. Because a large amount of supplementation with active vitamin D and calcium was required to correct the severe hypocalcemia, rapidly progressive vascular calcification developed. Seeing that patients with CKD are prone to developing severe and prolonged hypocalcemia after denosumab treatment, physicians should closely monitor the patients' serum calcium levels and manage their hypocalcemia appropriately so as to avoid the development of significant ectopic calcification.

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Section: Discussionsupporting

confidence: 51%

Rapid Progression of Vascular and Soft Tissue Calcification while Being Managed for Severe and Persistent Hypocalcemia Induced by Denosumab Treatment in a Patient with Multiple Myeloma and Chronic Kidney Disease

et al. 2015

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“…We believe that an unrestricted dietary P intake and overdosage of vitmain D 3 and Ca carbonate might lead to the formation of ectopic calcifications. According to earlier studies, there are infrequent tumoral calcifications in HD patients which are characterized by massive periarticular Ca deposition within multiple cavities formed by fibrous septae containing giant cells [3][4][5][6][7]. The present case may be explained by such tumoral calcinosis.…”

Section: Discussionmentioning

confidence: 99%

“…P product. Massive metastatic calcifications which resemble tumors are clinically defined as tumoral calcinosis [1][2][3][4]. Another type of so-called tumoral calcinosis character-…”

Section: Introductionmentioning

confidence: 99%

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Successful Treatment of Tumoral Calcinosis Using CAPD Combined with Hemodialysis with Low-Calcium Dialysate

et al. 1998

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Successful treatment of tumoral calcinosis using continuous ambulatory peritoneal dialysis (CAPD) combined with hemodialysis is described. A 32-year-old male patient with a 2-year history of CAPD rapidly developed multiple metastatic calcification (tumoral calcinosis) adjacent to his fingers, elbows, and knee joints. Tests showed severe hyperphosphatemia, moderate hypercalcemia, and increased Ca-P product without elevation of intact parathyroid hormone. An enlarged parathyroid gland was not found by echography. In order to rapidly lower the excessive Ca and P levels, a combined therapy with CAPD and vigorous transient hemodialysis using a low-Ca dialysate was performed. In parallel, the patient was given calcitonin, bisphosphonate, and short-term Al to ameliorate the metastatic calcifications more effectively. The result was dramatic with disappearance of the tumoral calcinosis as well as improvement in subjective symptoms within a few months. The present case suggests that combined therapy with hemodialysis and CAPD using a low-Ca dialysate, together with Ca-modulating agents, can be effective in ameliorating tumoral calcinosis in patients on CAPD.

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“…Secondary hyperparathyroidism plays a significant role in pathogenesis of extraskeletal calcification in con nection with uremia [2,3], Parathyroidectomy is per formed to decrease these Ca deposits [5,6], Other influencing factors are magnesium, vitamin D, aluminum (Al) [7,8], vitamin K. metabolic alkalosis dur ing and following dialysis as well as local tissue lesions [9,10], Tumoral calcifications are Ca-P deposits, most fre quently periarticular, which do not affect the joint or its capsule. The deposits are surrounded by a fibrous wall and they are multiocular [7.…”

Section: Introductionmentioning

confidence: 99%

Tumoral Calcinosis in Patients on Hemodialysis

Pečovnik-Balon¹,

Kramberger²

1997

Am J Nephrol

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Extraskeletal tumoral calcinoses occur in uremic patients with high calcium phosphorus (Ca × P) product and progressive secondary hyperparathyroidism. However, cases are also described in which this association cannot be confirmed. The influence of aluminum, vitamins D and K, alkalosis, magnesium and local lesions is described. The case of a female patient with tumoral calcinosis disappearing after parathyroidectomy is presented.

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Massive tumoral calcifications in hemodialysis patients without severe hyperparathyroidism

Cited by 10 publications

References 0 publications

Rapid Progression of Vascular and Soft Tissue Calcification while Being Managed for Severe and Persistent Hypocalcemia Induced by Denosumab Treatment in a Patient with Multiple Myeloma and Chronic Kidney Disease

Rapid Progression of Vascular and Soft Tissue Calcification while Being Managed for Severe and Persistent Hypocalcemia Induced by Denosumab Treatment in a Patient with Multiple Myeloma and Chronic Kidney Disease

Successful Treatment of Tumoral Calcinosis Using CAPD Combined with Hemodialysis with Low-Calcium Dialysate

Tumoral Calcinosis in Patients on Hemodialysis

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