|
| Slc26a1-/- mice exhibit hyposulfatemia, hypersulfaturia, calcium oxalate urolithiasis, and nephrocalcinosis in the setting of hyperoxalemia and hyperoxaluria | |
Sat1-deficient mice also have a phenotype of hyperoxalemia, hyperoxaluria, and calcium oxalate stones  |
|
Slc36a1 loss in mice leads to hyperoxaluria and calcium oxalate renal stones |
|
hyperoxalemia in Slc26a1-/- mice was most likely caused by reduced intestinal secretion of oxalate, based on reduced oxalate transport in basolateral membrane vesicles from the distal ileum, cecum, and proximal colon |