Veterinary Research Communications, 30(Suppl. 1) (2006) 337–339 DOI: 10.1007/s11259-006-0075-z C  Springer 2006 Bone Mineral Density in Two Boxer Dogs Affected by Moderate to End-stage Chronic Renal Failure A. Zotti 1,∗ , M. Caldin 2 , E. Vettorato 1 , V. Ferrari 1 , L. Cavicchioli 3 and D. Bernardini 1 1 Department of Veterinary Clinical Sciences, Faculty of Veterinary Medicine, University of Padua, Legnaro (PD), Italy; 2 “San Marco” Private Veterinary Clinic, Padua, Italy; 3 Department of Public Health, Comparative Pathology and Veterinary Hygiene, Faculty of Veterinary Medicine, University of Padua, Legnaro (PD), Italy ∗ Correspondence: E-mail: alessandro.zotti@unipd.it Zotti, A., Caldin, M., Vettorato, E., Ferrari, V., Cavicchioli, L. and Bernardini, D., 2006. Bone mineral density in two boxer dogs affected by moderate to end-stage chronic renal failure. Veterinary Research Communications, 30(Suppl. 1), 337–339 Keywords: bone mineral density, chronic renal failure, dog, dual-energy x-ray absorptiometry, radiology Abbreviations: BMD, bone mineral density; CRF, chronic renal failure; CV, coefficient of variation; DEXA, dual-energy X-ray absorptiometry; GFR, glomerular filtration rate; PTH, parathyroid hormone INTRODUCTION In human medicine there is an increasing interest in understanding and treating the con- sequences of CRF on bone patho-physiology. Moderate CRF can be defined as reduced GFR not requiring renal replacement therapy, whereas end-stage CRF is characterized by a GFR < 20% of the normal rate. In the latter stage individuals require hemodialysis (Lemann et al., 1966; Pitts et al., 1988; Chi-Yuan et al., 2002). A BMD decrease in moderate CRF-affected patients has been reported as the result of abnormalities in acid-base balance and vitamin D-PTH homeostasis (Lemann et al., 1966; Pitts et al., 1988). Chronic metabolic acidosis due to CRF may lead to bone buffering and slow dissolution of bone mineral. Moreover, many patients with moderate CRF also show decreased serum 1.25(OH) 2 vitamin D and increased PTH levels. Both of the above conditions may lead to bone demineralisation (Lemann et al., 1966; Pitts et al., 1988; Chi-Yuan et al., 2002). In moderate CRF, increased phosphaturia promoted by surviving nephrons maintains the plasma phosphate concentration toward normal. As soon as GFR drops below about 20% of the normal rate, renal adaptive effects are maximized and hyperphosphatemia en- sues, inducing a related degree of renal secondary hyperparathyroidism and consequent osteodystrophy (Lemann et al., 1966; Pitts et al., 1988; Osborne and Finco, 1995). Whether naturally occurring CRF can have these same adverse effects in dogs is unclear (Osborne and Finco, 1995). In our opinion, the lack of clinical studies on the effects of CRF on BMD in canine internal medicine could be due to: (1) the limited accuracy of conventional radiography, which requires at least 30–40% of the mineral content to be depleted from the bone to be detectable; (2) the lack of bone mineralisation reference data corrected for age, 337