Format

Send to

Choose Destination
See comment in PubMed Commons below
Clin J Am Soc Nephrol. 2012 Oct;7(10):1722-9. doi: 10.2215/CJN.02470312. Epub 2012 Aug 9.

Onco-nephrology: the pathophysiology and treatment of malignancy-associated hypercalcemia.

Author information

1
Division of Nephrology, University of Virginia Health System, Charlottesville, VA 22908, USA. mhr9r@virginia.edu

Abstract

Hypercalcemia complicates the course of 10%-30% of all patients with malignancies and can be a sign of very poor prognosis and advanced malignancy. Prompt recognition of the nonspecific signs and symptoms of hypercalcemia and institution of therapy can be lifesaving, affording the opportunity to address the underlying etiology. The mechanisms of malignancy-associated hypercalcemia generally fall into three categories: humoral hypercalcemia due to secreted factors (such as parathyroid-related hormone), local osteolysis due to tumor invasion of bone, and absorptive hypercalcemia due to excess vitamin D produced by malignancies. The mainstays of therapy for hypercalcemia are aggressive intravenous volume expansion with saline, bisphosphonate therapy, and perhaps loop diuretics. Adjunctive therapy may include calcitonin and corticosteroids. In refractory cases, gallium nitrate and perhaps denosumab are alternatives. In patients presenting with severe AKI, hemodialysis with a low-calcium bath can be effective. In most cases, therapy normalizes calcium levels and allows for palliation or curative therapy of the malignancy.

PMID:
22879438
DOI:
10.2215/CJN.02470312
[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Support Center