Nutritional Management of Hyperoxaluria

Abstract

Urine oxalate is derived both from the ingestion of foods that contain oxalate and its precursors (exogenous sources) and from biosynthesis (endogenous source). Oxalate biosynthesis occurs as an end-product of metabolism, by the degradation of dietary carbohydrates, ascorbate (vitamin C), and amino acids (hydroxyproline, phenylalanine, tryptophan). The relative contribution of exogenous and endogenous oxalate in urine varies greatly between individuals owing to metabolic, physiologic, and environmental factors. Patients with primary hyperoxaluria (there are three types) produce excessive oxalate due to enzyme deficiencies that would otherwise divert oxalate production to less toxic metabolites. Patients with altered gastrointestinal physiology (such as short bowel) or with inflammatory bowel disorders (such as Crohns or Celiac) absorb excessive oxalate from the gastrointestinal tract due to malabsorption and/or dysbiosis. Finally, patients with insufficient intakes of dietary factors that regulate oxalate absorption or its solubility in urine are at risk for higher urinary concentrations of oxalate and, thus, calcium oxalate stones. This chapter provides guidance on the management of high urine oxalate with dietary recommendations aimed at these challenges: controlling oxalate biosynthesis, controlling oxalate absorption, and controlling oxalate concentration in the gastrointestinal tract.