Abstract
Renal oxalosis has been reported in New and Old-World monkeys. Occasional reports describe a low prevalence of subclinical renal oxalosis, but these typically lack supporting evidence of primary oxalosis or toxicity and may be a natural background lesion. In a retrospective cross-sectional postmortem observation study, 12 of 156 (7.7%) African green monkeys (AGMs) (Chlorocebus sabaeus) from the Behavioural Science Foundation (St. Kitts) colony had histological evidence of oxalate-induced nephrosis (renal oxalosis). Histologically, affected tubules from both the cortex and medulla were ectatic; expanded several times normal size; and lined by attenuated, degenerative, regenerative, or necrotic epithelium with intraluminal, pale yellow, translucent, variably shaped, crystals that were birefringent under polarized light (calcium oxalate). The tubules were often surrounded by multinucleated macrophages. To identify independent predictors of renal oxalosis, we fit a multivariable logistic regression model with robust (“sandwich”) standard errors, including sex, age, and birth origin, as categorical covariates. Several enrichment food items were found to be oxalate-rich: sweet potato (95.9 mg/100 g), pumpkin (64.6 mg/100 g), and bananas (169 mg/100 g). There was a significant increase in the prevalence of calcium oxalate concretions with age, from 0% in young monkeys to 18.6% in aged individuals, likely due to longer exposure to oxalate-rich produce and a cumulative effect. Due to the large ingestion of oxalate-rich foods, diet is suspected to be a major cause of subclinical oxalosis in the St. Kitts AGM, raising awareness of this potential background finding during their use as laboratory animals in toxicologic and other research studies.
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