Therefore, to investigate whether SLC26A1 activity is a major determinant of sulfate homeostasis in humans, we searched for associations between rare, coding SLC26A1 variants that were predicted to be damaging (see Supplemental Table 2) and plasma sulfate levels among 4,708 participants of the prospective German Chronic Kidney Disease (GCKD) study that enrolled a total of 5,217 patients with moderate chronic kidney disease (22). This evidence concerns the gene SLC26A1 and chronic kidney disease.