Glomerulosclerosis in Captive Cheetahs (Acinonyx jubatus)

Abstract

Abstract. The cheetah (Acinonyx jubatus) is an endangered species with low fecundity and premature death in captivity. A previous survey determined that renal failure as a result of glomerulosclerosis was a major cause of death in captive populations. This study characterizes the morphologic, histochemical, and epidemiologic properties of glomerulosclerosis in this population. Kidneys from 87 cheetahs were examined by light microscopy; kidneys from six of those cheetahs were examined by electron and fluorescent microscopy using special stains specific for collagen, glycoproteins, reticulin, and fibrin. Immunohistochemistry for the advanced glycosylation end products (AGEs), pyrraline and pentosidine, also was performed on these cases. Glomerulosclerosis was present to some degree in 82% of the population, and in 30% of cheetahs the sclerosis was moderate to severe. Affected cheetah kidneys had thickened glomerular and tubular basement membranes, culminating in glomerulosclerosis. Thickened basement membranes were positive for collagen, glycoproteins, reticulin, and AGEs. Ultrastructurally, membrane material was homogeneous and fibrillar without electron-dense deposits. This glomerular lesion in cheetahs resembles diabetic glomerulopathy in humans and chronic progressive nephropathy in rats. No cheetahs had lesions of diabetes. However, adrenal cortical hyperplasia was prevalent and highly correlated with glomerulosclerosis in this population. If cheetahs with glomerulosclerosis had hypercorticoidism, then hyperglycemia and glomerular hypertension could lead to progressive AGE and plasma protein accumulations in membrane lesions. As in rats, daily feeding of high-protein diets and lack of genetic variation in the population may further contribute to the high prevalence of glomerulosclerosis in captive cheetahs.

Extrinsic Factors Significantly Affect Patterns of Disease in Free-Ranging and Captive Cheetah (Acinonyx Jubatus) Populations

“…A subset of this data has been published previously. (Munson, 1993;Papendick et al, 1997;Bolton and Munson, 1999). b Prevalences are expressed as the proportion (%) of tissues available.…”

“…The propensity for cheetahs to maintain persistent viral infections and develop atypical immune responses to common pathogens (Evermann et al, 1988;Junge et al, 1991;Eaton et al, 1993;Steinel et al, 2000;Munson et al, 2003) may also have a genetic basis, although modulation of the immune response by chronic stress has also been proposed . In light of these suspected inherent vulnerabilities to viral agents, we were surprised to find that morbidity and mortality in North American (NA) cheetahs were principally due to chronic degenerative diseases, such as veno-occlusive disease, glomerulosclerosis, and amyloidosis, rather than infectious disease (Munson, 1993;Papendick et al, 1997;Bolton and Munson, 1999). Furthermore, the prevalence and severity of these diseases in both captive populations differed among facilities, suggesting an environmental effect.…”

Inherited Podocytopathies

“…For example, a very high percentage of cheetahs, a species with minimal genetic diversity, develop glomerulosclerosis and renal failure (91).…”

Evidence for Chronic Stress in Captive but Not Free-Ranging Cheetahs (Acinonyx Jubatus) Based on Adrenal Morphology and Function

“…Captive cheetahs have a high prevalence of unusual diseases, such as veno-occlusive disease and glomerulosclerosis, that rarely occur in other species (Munson, 1993;Bolton and Munson, 1999). Also, common infectious agents, such as Helicobacter and feline infectious peritonitis (FIP), cause persistent and severe inflammatory disease in cheetahs (Eaton et al, 1993;Munson, 1993).…”