LRP2 and acute kidney injury: Since heme injury to PTECs is also the dominant mechanism of injury in Rhabdo-AKI (78, 79), increased reabsorption of CFH and myoglobin from the tubular filtrate in by Megalin-mediated uptake in S1 and S2 PTEC segments that are found throughout the renal cortex (80–83); this may explain the more widespread activation of RAR signaling in SA- and Rhabdo-AKI compared with IRI-AKI, where PTEC injury and RAR activation is more restricted to PTECs in the OSOM (14).