In the 1990 s, diclofenac was responsible for the inadvertent deaths of over ten million vultures on the Asian subcontinent. While the pathology associated with their deaths was clearly evident as visceral and articular gout, the mechanism behind their death remains an enigma. In one of the supposition proposed on a potential mechanism of toxicity, it was postulated that the acute necrosis of the proximal convoluted tubules was caused by ischaemia. More specifically, toxicity was related to the avian renal vascular anatomy, whereby a renal portal blood supply exists viz. venous blood originating from the hind-quarters co-perfuses the kidney with arterial blood from the aorta. A further uniqueness of this system, is the presence of the renal portal valve in the v. iliaca communis, which appears to control the shunting of venous blood from the hind limbs to the vena cava, thereby bypassing the cranial renal lobe in times of stress.
In the theory put forward, it was suggested that the valve could be under prostaglandin control and that diclofenac (a potent cyclooxygenase inhibitor) would potentially induce a change in the valve functionality with the net effect being the shunting of blood away from the cranial renal lobe resulting in hypoperfusion, ischaemia and necrosis of this lobe. While the theory appears plausible, the valva renalis portalis has only been described in a small number of other bird species such as the chicken (Gallus domesticus) and ostrich (Struthio camelus), which actually has six valvae renales (de Carvalho, et al. 2007). The aim of this study was to evaluate the renal anatomy and related vasculature of the Cape griffon vulture (Gyps coprotheres) (CGV), which is senstive to the toxic effects of diclofenac. Special attention is also being given to comparisons with the anatomy of the domestic chicken.
This study made use of 13 CGVs. Six specimens were freshly perfused with formalin within minutes of being euthansed. In all cases, the birds were euthanised on the recommendation of the treating veterinarian due severe orthopaedic injuries. The birds were otherwise deemed to be healthy. For the histological portion of the study, evaluations were made of both stored samples in the bank at the Section of veterinary pathology of the University of Pretoria, while renal and associated vascular tissue from two of the freshly fixed birds were prepared using standard H&E techniques. The other seven were recovered dead in the field. Of these four were prepared for skeletal evaluation, and the remainder used for vascular casting. The kidneys of the CGV were present within the fossae renales and were well attached to the synsacrum and the ilium, and was trilobular. While this was similar to the chicken, the divisions with their connective tissue capsule in the vulture was much more prominent than in the chicken. The vasculature was also almost identical to the domestic chicken, with the only differences being at the entrance of the v. portalis renalis caudalis and the exit of the v. renalis caudalis into the v. iliaca communis on the right. The valva renalis portalis was also present in same location described in the chicken with a similar appearance viz. the valve was present in the v. iliaca communis between the v. renalis caudalis and the v. renalis cranialis and appeared as conical shaped, with finger-like processes.
Histologically, the CGV kidney was similar to that to other avian spp, with reptilian, mammalian and intermediate nephrons being evident. The kidney also had the expected appearance with the cortex consisting of the glomeruli and the medulla being made up of medullary cones. On cross-section the renal portal valve was composed of smooth muscle finger-like projections that protruded into the lumen of the lumen of the v. iliaca communis. The valve was well vascularised and was associated with a nerve plexus. While the plexus could not be conclusively associated with the valve, the renal portal valve is the only intravascular smooth muscle structure that has been described to have sympathetic and parasympathetic innervation.
Based on the findings of this study, the proposed mechanism of toxicity of diclofenac is anatomically possible. The similarity of the chicken and vulture in their anatomical structure may also explain previous finding that the chicken could serve as a physiological model of the study of the pathophysiology of diclofenac s toxicity.