Kidney fibrosis is the common final pathway to kidney failure. Experimental data mechanistically link decreased kidney perfusion with resultant hypoxia and inflammation to kidney fibrosis and subsequent loss of kidney function.1 Unfortunately, these fibrotic changes are irreversible without any approved anti-fibrotic therapies for patients with kidney diseases. Non-invasive quantification of kidney fibrosis remains a major barrier to drug development. The only method to quantify kidney fibrosis is to perform a kidney biopsy, which carries risks and is not performed in all patients with kidney diseases.