AGXT and primary hyperoxaluria: Mice with a deficiency in the hepatic alanine-glyoxylate aminotransferase (Agxt−/−, mouse model for primary hyperoxaluria) and wild-type mice after probiotic treatment, who were fed an oxalate-supplemented diet, showed increased ability to degrade dietary oxalate, thus limiting its absorption across the intestine and reducing urinary oxalate excretion.