SOURCES

The first report of Lilium sp. nephrotoxicity was presented in 1992 and based on data generated at the ASPCA Animal Poison Control Center (ASPCA-APCC) in Urbana, Ill.¹ The first report involved Lilium longiflorum (Easter lily), but further observations now suggest that all species of the Lilium genera and plants in the Hemerocallis genera (day lilies) should be viewed as potentially nephrotoxic in cats.^1–7 It is of special note that the only animal to date that is known to be susceptible to the nephrotoxicity of these plants is the domestic cat.

The principal source of Lilium sp. and Hemerocallis sp. exposure in cats is via household entry of potted ornamental plants and floral arrangements. And since both the leaves and the flowers are associated with poisoning, corsages of these flowers also pose a risk. Although outdoor cats could be exposed to these plants in flowerbeds, currently there have only been reports of lethal indoor ingestions.

The key in first identifying the Lilium sp. as being toxic stemmed from the fact that some of these plants are more commonly introduced into houses during specific holiday seasons. The Easter lily is a common plant introduced into houses from 1 week before to 3 weeks after Easter and has resulted in clusters of cases being reported to the APCC. Following these clusters, using past years’ data, and following-up on past reported exposures from previous years, it was found that this plant had a high risk of causing renal damage.

TOXIC DOSE

Species susceptibility to the toxic effects of Lilium sp. and Hemerocallis sp. lilies is quite distinct. The toxic effects of these plants have only been manifest in cats. After the original identification of suspected toxicity, rats, mice, and rabbits were fed plant material at up to 1.5% of their body weight without any adverse effects. In addition, cases of ingestion by dogs have only resulted in gastrointestinal upset, without any renal effects.

Small amounts of plant ingestion can be toxic to cats. Ingestion of as little as 2 to 3 leaves or part of a flower has resulted in lethal effects in cats. The rapid onset of clinical signs, especially vomiting, likely limits the amount of plant ingestion. It has been found that the toxin(s) in the Easter lily is in the water-soluble fraction of the plant.⁸

TOXICOKINETICS

No true kinetic data are available for the toxin(s) in the Lilium sp. and Hemerocallis sp., since the toxin(s) have yet to be identified. However, it is likely that the toxic constituent of the plants is rapidly absorbed. This observation is based on the common finding that early emesis of the plant material may lessen the clinical effects, but renal damage still occurs without other supportive treatment. In addition, clinical signs can begin as early as 5 to 10 minutes postingestion.

The elimination of the toxin(s) from the body likely occurs within the first 48 hours, although the duration of clinical effects can last for several days. The longer duration of effects after the toxin(s) are eliminated is the result of acute renal tissue damage and secondary effects from the renal failure. Early fluid diuresis initiated before the onset of renal shutdown and continued for 24 to 72 hours can significantly prevent renal failure—associated death. These data suggest a relatively rapid elimination of the toxin(s), especially in the presence of fluid diuresis.

Metabolism of the toxin(s) of Lilium sp. and Hemerocallis sp. is unknown. But one potential cause for the sensitivity of cats could be a differing metabolism of the toxin(s), as compared with dogs, rats, mice, and rabbits, resulting in a toxic metabolite. This would be supported by the fact that direct application of the water soluble plant components was not toxic to cultured feline renal tubular epithelial cells (unpublished data).