Acute renal disease remains challenging to diagnose in avian species due to their ability to hide illness, an absence of specific clinical signs, and a lack of validated sensitive markers of glomerular and tubular dysfunction or damage. Acute avian renal disease occurs in response to a range of nephron-damaging events, including severe dehydration, high protein load, vitamin A deficiency, nephrotoxin exposure, and renal adenocarcinoma.1
Mammalian renal indices are of limited value.1-3 For example, birds make predominately creatine, not creatinine; they are more uricotelic than ureotelic, and BUN when produced is strongly influenced by dietary protein intake and differential handling by functionally discrete nephron populations.1,2,4 The purpose of the present study was to determine tissue levels of creatine and Nacetyl-b-D-glucosaminidase (NAG) as a prelude to renal disposition and disease studies.
A modified two-step creatinine assay procedure (Boehringer-Mannheim, now Roche) was previously adapted and validated and used to measure creatine, using a Hitachi 917 clinical chemistry autoanalyzer. NAG was similarly assayed using a standard commercial kit (Roche). Selected tissue samples (pancreas, liver, skeletal muscle, kidney and small/large intestine from four captive-bred homing pigeons fed a standard diet and humanely euthanatized as a part of flock culling were rapidly collected, snap frozen, powdered in liquid nitrogen and stored at -80°C. At the time of assay, aliquots of frozen powdered tissues were resuspended in cold Tris buffer (pH 8.0), vortexed 30 seconds, centrifuged at 10,000 rpm, and assayed for creatine and NAG. Analysis employed one-way ANOVA using tissues as factors.
Results indicated that creatine was significantly (p<00001) elevated in skeletal muscle as compared to other tissues examined, and that NAG was significantly (p<00001) elevated in renal tissue as compared to the other tissues.
These results were promising in that creatine shares the same relationship with avian muscle that creatinine does in mammals; likewise, NAG appears specific for renal parenchyma. Thus, both these potential acute renal disease markers warrant further investigation as indices of renal dysfunction.
Funding was provided by a grant from the Morris Animal Foundation.
1. Lumeij, J.T. 1994. Nephrology. In: Avian Medicine. G.J. Harrison, B.W. Ritchie, L.R. Harrison, eds. Wingers Publishing: Lake Worth, FL. Pp. 538–555.
2. Braun, E.J. 1998. Comparative renal function in reptiles, birds, and mammals. Semin Avian Exotic Pet Med. 7: 62–71.
3. Hochleithner, M. 1994. Biochemistries. In: Avian Medicine. G.J. Harrison, B.W. Ritchie, L.R. Harrison (eds). Wingers Publishing: Lake Worth, FL. Pp. 223–227.
4. Wimsatt, J. 1998. Comparative aspects of nitrogen excretion, and visceral and articular gout deposition in nonhuman species. In: Gout, Hyperuricemia and the Crystal-associated Arthropathies. C. Smyth, and V.M. Holers, eds. Marcel Dekker: New York, NY. Pp. 59–101.