Excess Oxalate Can Result in a Spectrum of Disease Pathology
Oxalate is a two-carbon carboxylic acid found in food, especially fruits and vegetables such as spinach, as well as nuts, chocolate and tea. Oxalate is also a normal byproduct of digestion and cellular metabolism, and is normally excreted by the kidneys as waste in the urine. Individuals with hyperoxaluria have elevated levels of oxalate in their urine.
When there is too much oxalate in the urine, it can accumulate and bind with other ions such as calcium to form crystals. These crystals may trigger an inflammatory response, and can grow into calcium oxalate kidney stones (nephrolithiasis). As a result, patients with hyperoxaluria are at increased risk for calcium oxalate kidney stones and other adverse renal outcomes.
There are two types of hyperoxaluria: primary hyperoxaluria, which is a genetic disorder resulting in excess endogenous hepatic oxalate production, and secondary hyperoxaluria, which can be idiopathic (no identifiable cause) or enteric. Enteric hyperoxaluria is caused by excess absorption of oxalate from the gastrointestinal tract due to underlying gastrointestinal conditions such as gastric bypass, Crohn’s Disease, short bowel syndrome or other malabsorption disorders.
Patients with hyperoxaluria are at risk of adverse renal outcomes including recurrent kidney stones, chronic kidney disease, acute kidney injury, and end-stage renal disease requiring dialysis. Patients with underlying renal disease may be at particularly high risk of renal complications associated with hyperoxaluria.
Unfortunately, hyperoxaluria is most often asymptomatic until the clinical manifestation of kidney stones or kidney dysfunction.
There are no pharmacological agents currently approved to treat hyperoxaluria.