For over a century, serum creatinine has been used as the gold standard when assessing kidney function.1 However, as a filtration marker, creatinine does not distinguish between structural and functional causes of declines in glomerular filtration rate (GFR). Biomarkers of glomerular and tubular injury have been extensively studied in the inpatient setting and have demonstrated utility for distinguishing structural and functional etiologies of acute kidney injury (AKI), as well as for early detection and prognosis.