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Sidney M Kobrin, MD
Section Editor
Gary C Curhan, MD, ScD
Deputy Editor
Albert Q Lam, MD


Nephrocalcinosis is characterized by the deposition of calcium in the kidney parenchyma and tubules [1]. Nephrocalcinosis may cause acute or chronic kidney injury, or be incidentally detected radiographically in a patient with normal renal function. Nephrocalcinosis is caused by multiple different conditions and the renal prognosis is determined by the underlying cause; whereas most patients with nephrocalcinosis do not progress to end-stage renal disease, certain underlying conditions, if not effectively treated, may be associated with progressive kidney dysfunction. The pathogenesis, clinical presentation, causes and treatment of nephrocalcinosis are discussed here.


The term nephrocalcinosis is used to describe the deposition of both calcium oxalate and calcium phosphate [1,2]. Some experts limit the definition of nephrocalcinosis to the deposition of calcium phosphate and refer to the deposition of calcium oxalate as oxalosis [3,4]. For the purposes of this review, we retain the broader definition of nephrocalcinosis to include both calcium phosphate and calcium oxalate. The term oxalosis will refer exclusively to calcium oxalate deposition.

The defining characteristic of nephrocalcinosis is generalized calcium deposition in the kidney [1,2]. Localized calcium deposition that occurs with focal renal injury is not included in this definition.

Nephrocalcinosis is classified as follows [1,2]:

Molecular or chemical – A measurable increase in intracellular calcium concentration exists but is not visible microscopically or via radiographic imaging.

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Literature review current through: Nov 2017. | This topic last updated: Apr 07, 2017.
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