Injected exogenous cysC binds to megalin and is reabsorbed by a megalin dependent process in the PT [23]; however, the molecular mechanisms regulating the reabsorption of endogenous cysC have not been fully characterized, and while it has been hypothesized that in both AKI and CKD the increased urinary excretion of cysC (and other biomarkers) is due to decreased reabsorption of cysC in the PT [24], the exact mechanism and role of megalin and cubilin has not been fully characterized. Here, LRP2 is linked to chronic kidney disease.