We speculate that if the marked effects of COXI on renal vascular resistance such as we observed with acute indomethacin administration to conscious lambs, persist in the absence of the rapid buffering capacity observed in the healthy newborn animal, the perfusion of the kidney would decrease, resulting in a decreased capacity to filter the blood, and leading eventually to acute kidney injury, and death if the kidney perfusion is not restored. The gene discussed is MT-CO1; the disease is acute kidney injury.