We retrospectively examined plasma uric acid concentrations of swift parrots (Lathamus discolor) in samples collected during a period when a suspected toxin was causing renal tubular pathologic changes. The primary aim of this study was to investigate plasma uric acid concentrations from birds with existing renal compromise on 2 levels of dietary protein. There was a significant difference in the monthly pattern of plasma uric acid concentration between the birds that died and those that remained clinically normal. Birds that were fed a high-protein ration had a significantly different monthly pattern of plasma uric acid concentration than those birds fed a low-protein ration. We then evaluated the effects of an overnight fast and subsequent feeding on plasma uric acid concentrations in swift parrots. The preprandial plasma uric acid concentration, taken after a 14-hour fast, was not significantly different from the 2- and 6-hour postprandial concentrations. To further examine the effect of diet on plasma uric acid concentration, we examined the plasma of wild swift parrots feeding on nectar, pollen, and insects and of swift parrots from a private aviculturist feeding seed and commercial lorikeet nectar food. The highest levels of plasma uric acid were those of the captive swift parrots fed the mixed nectar and seed diet; plasma uric acid concentrations of the wild birds were lower than preprandial concentrations of captive parrots. It remains unclear whether increases in plasma uric acid concentrations were a consequence of renal tubular damage or of high dietary protein levels. However, the finding of low plasma uric acid concentrations in wild birds and high concentrations in captive birds provide support for the hypothesis that dietary protein levels provided to captive birds were in excess of requirements. As nectarivores, swift parrots might have lower protein requirements than granivorous parrots. However, confirmation of this hypothesis will requirenitrogen balance studies as a direct assessment of protein metabolism. We hypothesize that dietary protein levels did not induce the renal disease but might have contributed to ongoing pathologic changes in the damaged kidneys.