These results suggest that the increase in PGD2 in the Alox15−/− CKD mouse kidneys was not due to an increase in synthases but due to the increased substrate availability or an inhibition of degradation, and in fact, we have revealed a reduction in 15-PGDH, one of the major PGD2 metabolizing enzymes [29], in the Alox15−/− CKD mouse kidneys (Fig. 8b). This evidence concerns the gene PTGDS and chronic kidney disease.