Oxalosis

Oxalosis is a systemic condition in which calcium oxalate crystals accumulate in body tissues due to chronically elevated oxalate levels. It is most often associated with end-stage kidney disease, where reduced renal clearance allows oxalate to deposit in multiple organs, but it can also occur with primary or secondary hyperoxaluria that produces or absorbs excess oxalate. Oxalosis is distinct from oxaluria, which refers to high urinary oxalate excretion without widespread tissue deposition.

Causes fall into several categories. Primary hyperoxaluria comprises genetic disorders that overproduce oxalate, most commonly PH type 1 (AGXT), PH type 2 (GRHPR), and PH type 3 (HOGA1). Secondary or enteric hyperoxaluria results from fat malabsorption disorders (such as inflammatory bowel disease, bariatric surgery, celiac disease) that increase intestinal oxalate absorption. External toxins such as ethylene glycol can also raise oxalate levels. In advanced kidney disease, even moderate oxalate production can lead to tissue deposition.

Oxalate crystals precipitate with calcium to form calcium oxalate, which can deposit in kidneys causing nephrocalcinosis and stones, and disseminate to bones, joints, vasculature, heart, lungs, sclera, and skin. This systemic deposition contributes to progressive organ dysfunction and complicates management.

Diagnosis relies on showing elevated oxalate burdens: increased urine oxalate excretion, elevated plasma oxalate in advanced disease, genetic testing for PH types, imaging revealing nephrocalcinosis, and tissue biopsy showing calcium oxalate crystals when indicated.

Treatment focuses on reducing oxalate burden and protecting renal function. This includes adequate hydration, dietary oxalate restriction, and calcium binding of oxalate with meals; pyridoxine may help in PH1. Emerging disease-modifying therapies (for example, RNA interference approaches) and, in selected cases, liver transplantation to correct the metabolic defect, sometimes combined with kidney transplantation for established renal failure, are used. Management of secondary oxalosis centers on treating malabsorption and reducing intestinal oxalate absorption.