perfusion. In Cohen's study there was a progressive increase in urinary protein concentration during 8 day preservation until the protein content of the urine equalled that of the perfusate. This may have been related to the swelling of the glomerular basement membranes and the progressive fusion of epithelial cell foot processes that was also observed during the same period of perfusion storage. Mechanisms of injury The mechanisms that damage kidneys during hypothermic storage can be sub-divided as follows: Injury to the metabolic processes of the cell caused by: Cold Anoxia when the kidney is warm both before and after the period of hypothermic storage. Failure to supply the correct nutrients. Toxin accumulation in the perfusate. Toxic damage from the storage fluid. Washout of essential substrates from the kidney cells. Injury to nuclear DNA. Mechanical injury to the vascular system of the kidney during hypothermic perfusion. Post reimplantation injury. Metabolic injury Cold At normal temperatures pumping mechanisms in cell walls retain intracellular potassium at high levels and extrude sodium. If these pumps fail sodium is taken up by the cell and potassium lost. Water follows the sodium passively and results in swelling of the cells. The importance of this control of cell swelling was demonstrated by McLoughlin who found a significant correlation between canine renal cortical water content and the ability of kidneys to support life after 36-hour storage. The pumping mechanism is driven by the enzyme system known as Na+K+- activated ATPase and is inhibited by cold. Levy found that metabolic activity at 10 °C, as indicated by oxygen consumption measurements, was reduced to about 5% of normal and, because all enzyme systems are affected in a similar way by hypothermia, ATPase activity is markedly reduced at 10 °C. There are, however, tissue and species differences in the cold sensitivity of this ATPase which may account for the differences in the ability of tissues to withstand hypothermia. Martin has shown that in dog kidney cortical cells some ATPase activity is still present at 10 °C but not at 0 °C. In liver and heart cells activity was completely inhibited at 10 °C and this difference in the cold sensitivity of ATPase correlated with the greater difficulty in controlling cell swelling during hypothermic storage of liver and heart cells. A distinct ATPase is found in vessel walls, and this was shown by Belzer to be completely inhibited at 10 °C, when