Figure 12. Schematic of CI-AKI.

1: Intravenous or intra-arterial contrast agents enter the renal circulation and peritubular capillaries and are taken up by resident renal phagocytes. 2: Contrast is filtered at the glomerulus and enters the urine and renal tubule. In the hydrated state, contrast is rapidly excreted. 3: Contrast uptake by the resident renal phagocytes activates the Nlrp3 inflammasome to generate IL-1β. 4: IL-1β mediates leukocyte recruitment from the circulation into the kidney. 5: Contrast in the urine is taken up by the tubular cell by the brush border enzyme DPEP-1. The tubular uptake of contrast is enhanced in the volume-depleted state. 6: Recruited leukocytes ingest contrast transported from the urine through a direct interaction with tubular cells that further activates the inflammasome. 7: The activation of resident renal phagocytes, tubular uptake of contrast, and leukocyte recruitment are all necessary, but none alone, is sufficient to induce AKI.