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This study explored the relationship between adenine nucleotide levels in canine renal cortex and renal function following: (a) graded periods of warm ischemia; (b) 48 hours' flush cooling with electrolyte solutions and ice storage; and (c) continuous hypothermic perfusion. Exposure to normothermic ischemia resulted in a rapid (within 15 minutes) degradation of ATP to ADP and AMP as well as a slow decline in total adenine nucleotide (TAN) to levels which were proportional to the duration of the ischemie injury. No functional impairment was evident after 15 minutes' ischemia, but with longer times, both the extent of decline in TAN and the degree of recovery following restoration of blood flow could be used to predict the quality of renal function.The relationship between TAN levels and function was of less predictive value following cold storage or continuous perfusion. The efficacy of intracellular flush solutions could not be attributed solely to conservation of TAN, nor did the well-maintained TAN levels during continuous perfusion necessarily lead to significantly better 48-hour storage than flush cooling with C2 solution.

Since first described by Starzl in 1964 (1), acute pancreatitis following renal homotransplantation has been the subject of sporadic reports and reviews (2-5). The generally reported incidence has been around 2%, with a mortality rate of 50-60%. A recent experience with such a patient caused us to retrospectively analyze our own series of renal transplant recipients. In an eight-year period, there were six patients who had documented pancreatitis out of a total 120 renal homograft recipients, an incidence of 5%. The mortality was distressingly high; five out of the six succumbed directly to this complication, a rate of 83%. The purpose of this paper is to review these six patients in detail, with special attention to the protean etiologies and manifestations of this lethal complication.