Abstract
Dear Sir
I have recently read an article on feline primary oxaluria (De Lorenzi et al 2005) which appeared in your journal and I feel obliged to make some comments.
It is well known that oxalate urolithiasis is common in the domestic cat and much work has been done on reducing the renal oxalate load by dietary manipulation (Lulich et al 2004). Naturally occurring genetic disorders of oxalate metabolism are rare, but have been reported in the Tibetan Spaniel (Danpure et al 1991) and the domestic cat (Blakemore et al 1988).
The authors describe a patient with glyceric aciduria, neurological involvement and oxalate crystalluria and classified this patient as having primary hyperoxaluria. Here caution should be advised, particularly with the classification of the genetic oxalurias. The term ‘primary hyperoxaluria’ is reserved for type 1 oxalosis due to alanine:glyoxalate/serine:pyruvate aminotransferase deficiency which is a hepatic peroxisomal enzyme. The term type II oxalosis refers to recurrent oxaluria with concomitant urinary l-glyceric aciduria.
The clinical description of the patient (De Lorenzi et al 2005) is consistent with that of the previously described patients; however, I would have liked to seen the urinary oxalate levels. We routinely assay urinary oxalate, not only in humans, but also in canine and feline patients and quantitative results would be useful. Likewise, I am not sure about the level of l-glyceric acid. Unfortunately, the value is not related either to urinary creatinine or kg body weight/24 h and there is no reference range given. We also routinely measure urinary organic acid excretion in felines and we have seen increased urinary glycerate levels raised secondary to glycerate-containing medication.
Finally, the authors have erroneously cited one of our papers referring to d(+)-glyceric acid in an Afghan hound (Sewell et al 1997) as ‘primary hyperoxaluria’. Here again, caution should be exercised. d(+)-glyceric aciduria is not a primary oxaluria as only d(+)-glyceric acid is excreted with no oxaluria and can only be diagnosed using sophisticated technology to distinguish between d- and l-forms of glyceric acid.