The fractional excretion of urate increased after inosine loading; increased urate excretion in the setting of uricosuric therapy and genetic deficiencies in URAT1 or GLUT9 has also been implicated in the genesis of acute kidney injury and/or nephrolithiasis, likely due to the uricosuria with intra-tubular crystallization of monosodium urate16–18. Here, SLC2A9 is linked to acute kidney injury.