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Oxalosis

Last revised by Henry Knipe on 21 Nov 2023

Oxalosis is supersaturation of calcium oxalate in the urine (hyperoxaluria), which in turn results in nephrolithiasis and cortical nephrocalcinosis

This article focus on the secondary oxalosis, please refer to primary oxalosis for a specific discussion on this entity. 

Calcium oxalate deposition most commonly affects the bone, bone marrow, blood vessels, central nervous system, peripheral nerves, retina, skin, and thyroid. There are two forms of this condition:

  • primary: an autosomal recessive disease that is expressed in childhood

  • secondary: usually related to an over-ingestion of oxalic acids or its precursors (e.g. vitamin C) in patients with kidney or hepatic chronic diseases, especially during long-term dialysis

Foods that are high in oxalic acids include rhubarb, spinach, celery and cocoa 2.

In individuals with secondary (enteric) hyperoxaluria, a complex interplay between oxalate, calcium, and fatty acids occurs, resulting in the formation of calcium oxalate stones. Typically, oxalate is sequestered by calcium, rendering it insoluble and easily eliminated through feces. However, in those individuals with steatorrhea, calcium is diverted towards binding with fatty acids, allowing oxalate to be absorbed into the bloodstream for excretion by the kidneys. Unfortunately, the scarcity of fatty acids in the filtrate leads to the recrystallization of oxalate with calcium, rendering it insoluble and ultimately culminating in the formation of a calcified mass (calcium oxalate stones) within the urinary tract 4.

A few causes of secondary hyperoxaluria include Crohn disease, cystic fibrosis, chronic biliary disease, pancreatic pathologies, and short bowel syndrome 4.

The typical radiographic finding is cortical nephrocalcinosis.

When left untreated, hyperoxaluria will ultimately lead to renal failure, which in turn results in oxalosis: a condition in which calcium oxalate crystals are deposited in extrarenal organs.

Renal transplant is the only treatment for patients with renal failure and systemic oxalosis as dialysis is not sufficient to prevent disease progression.

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