Notably, sequencing of a specimen from a patient with severe renal calcinosis revealed a substitution of a non-conserved amino acid (M132T) in the transmembrane structural domain of SLC26A1 (DAWSON et al., 2013), thus altering the structure of the hydrophobic region of the third segment, suggesting that the loss of SLC26A1 protein function may lead to hyperoxaluria and urolithiasis. Here, SLC26A1 is linked to Hyperoxaluria.