Urolithiasis is one of the most common urologic diseases in industrialized societies. More than 80% of renal stones are composed of calcium oxalate, and small changes in urinary oxalate concentrations affect the risk of stone formation. Elucidation of the source of oxalate and its mechanism of transport is crucial for understanding the etiology of urolithiasis. Sources of oxalate can be both endogenous and exogenous. With regard to oxalate transport, tests were carried out to prove the function of solute-linked carrier 4 (SLC4) and SLC26. The molecular mechanism of urolithiasis caused by SLC4 and SLC26 is still unclear. The growing number of studies on the molecular physiology of SLC4 and SLC26, together with knockout genetic mouse model experiments, suggest that SLC4 and SLC26 may be a contributing element to urolithiasis. This review summarizes recent research on the sources of oxalate and characterization of the oxalate transport ionic exchangers SLC4 and SLC26, with an emphasis on different physiological defects in knockout mouse models including kidney stone formation. Furthermore, SLC4 and SLC26 exchangers provide new insight into urolithiasis and may be a novel therapeutic target for modification of urinary oxalate excretion.