Hyperoxaluria, hyperglycoluria and renal oxalosis in Gilbert's potoroos (Potorous gilbertii)

Case report Six Gilbert's potoroos (Potorous gilbertii) in a captive colony, five of which were closely related, died or were euthanased with severe renal disease. Clinical signs were mostly non‐specific. Renal calculi were seen on ultrasound of two affected potoroos and oxalate crystalluria was seen in two of three affected potoroos that had urine samples examined. Necropsies revealed extensive severe renal oxalosis in all affected potoroos. These findings and markedly increased concentrations of glycolate in the urine of the four affected potoroos for which it was measured, confirmed a disorder of oxalate metabolism and suggested a condition similar to primary hyperoxaluria type 1 in humans. Liver alanine : glyoxylate aminotransferase activity and intracellular location were assessed as normal in one affected potoroo, which is inconsistent with human primary hyperoxaluria type 1. Although a condition similar to human primary hyperoxaluria type 2 or 3 was not ruled out, other clinicopathological findings were not consistent with those seen in humans with these conditions. A lack of faecal oxalate‐degrading activity was observed in two affected potoroos in which it was measured, whereas oxalate‐degrading activity was variably present in healthy captive and wild potoroos. Conclusion Although the pathogenesis of renal oxalosis in these cases was not clear, the biochemical findings of elevated urinary oxalate and glycolate excretion indicate an abnormality of oxalate metabolism. The familial pattern of disease suggests it could be an inherited condition.