Acute tubular necrosis.  An experimental model detailing the biochemical events accompanying renal injury and recovery.
Male Charles River mice, divided into control or experimental groups, received on Day 0 either sterile 0.3 MNaHCO3 in 0.9 per cent saline (pH7.4) intraperitoneal injection or pteroylglutamic acid (200 mug per body weight), similarly buffered to pH7.6, and were sacrificed on Days 0, 1/4, 1/2, 1,2,3,4,7, and 14. The experimental kidneys demonstrated intratubular deposits of pteroylglutamic acid with edema between  Days 1 and 4 with cortical scarring by Day 14. The experimental kidneys reached maximal increases in weight (+90 per cent) on Day 2, RNA (+61 per cent, protein (+67 per cent) on Day 3, and DNA (+25 per cent) on Day 4 before falling to below control levels on Day 14. The control kidneys demonstrated the gradual incremental increases of normal renal growth throughout this period. No change in renal size, protein, RNA, or DNA could be detected in those animals who failed to demonstrate renal tubular damage. It is postulated that the response of the kidney to folic acid administration is a reparative response and not a response directed toward accelerated renal growth.
Acute tubular necrosis.  An experimental model detailing the biochemical events accompanying renal injury and recovery. Male Charles River mice, divided into control or experimental groups, received on Day 0 either sterile 0.3 MNaHCO3 in 0.9 per cent saline (pH7.4) intraperitoneal injection or pteroylglutamic acid (200 mug per body weight), similarly buffered to pH7.6, and were sacrificed on Days 0, 1/4, 1/2, 1,2,3,4,7, and 14. The experimental kidneys demonstrated intratubular deposits of pteroylglutamic acid with edema between  Days 1 and 4 with cortical scarring by Day 14. The experimental kidneys reached maximal increases in weight (+90 per cent) on Day 2, RNA (+61 per cent, protein (+67 per cent) on Day 3, and DNA (+25 per cent) on Day 4 before falling to below control levels on Day 14. The control kidneys demonstrated the gradual incremental increases of normal renal growth throughout this period. No change in renal size, protein, RNA, or DNA could be detected in those animals who failed to demonstrate renal tubular damage. It is postulated that the response of the kidney to folic acid administration is a reparative response and not a response directed toward accelerated renal growth.