12 May 2026
Lotfi El Bahri DVM, MSc, PhD discusses the different types of this plant and the toxicity issues they can cause.
Lotfi El Bahri
Job Title
Image: Cyrustr / Adobe Stock
Many plants are given the generic classification of lily, making identifying poisonous plants a challenge.
Plants with “lily” in their names, such as peace lily (Spathiphyllum wallisli), calla lily (Zantedeschia aethiopica), lily of the valley (Convallaria majalis) and Peruvian lily (Alstroemeria species), are not of the lilies group, and do not cause kidney failure in cats, but still can be harmful, creating confusion when evaluating and diagnosing the feline patient. Only Lilium and Hemerocallis species are considered true lilies, and they are also highly toxic to cats.
The Lilium genus contains more than 100 species and hundreds of hybrids, and is a herbaceous perennial flowering plant of the Liliaceae family. Most species of true lilies are native to Europe, Asia and North America. The species highly toxic to cats include Easter lily (Lilium longiflorum); tiger lily (L tigrinum or L lancifolium); Asiatic lily (L asiatica or L orientalis); Japanese show lily (L speciosum); rubrum lily (L rubrum); stargazer lily – a hybrid; western lily (L occidentale); wood lily (L philadelphicum or L umbellatum), and Madonna lily (L candidum).
The Hemerocallis genus (Asphodelaceae family) has fewer species, including day lily (H dumortieri), and orange day lily (H graminea), toxic to cats.
Lilies are present in the home as gifts, during Christmas or Easter time, wedding celebrations and funerals, or in ornamental flower arrangements. This allows house cats easy access for plant ingestion. Also, most pet owners know little about the potentially life-threatening issues these plants pose to cats.
Lilium is an erect plant with scaly bulbs consisting of overlapping fleshy scales that do not encircle the bulb, as in the onion-type bulb. Leaves are arranged in spirals or whorls on the erect stems, and vary from grass-like, linear to lanceolate, usually bright green and quite sessile.
The inflorescences consist of solitary flowers, racemes or umbels, with flowers being held erect, horizontal or pendent, and are generally large, showy and cup-shaped or funnel-shaped. Flower colours include white, yellow, orange and red, with frequent spotting on the inner surfaces of the petals.
Hemerocallis is characterised by its clump-forming habit, arching strap-like leaves, and showy funnel-shaped or bell-shaped flowers that typically last for only one day.
Cats – known to be particularly sensitive to lilies toxicity – are the only species known to be affected. The mortality rate from Easter lily toxicosis is as high as 50% to 60%.
According to the US Animal Poison Control Center, lilies topped the list of the plants most toxic to cats in 2024. In the UK, a total of 118 cases of lily exposure in cats were reported by the VPIS database in 2022. Westgate reported in March 2025 that Petplan, a leading UK pet insurer, had paid out more than €1.5 million (£1.29 million) for lily poisoning, accounting for 45% of all cat poisoning claims. Ingestion of plant material from Lilium and Hemerocallis genera causes acute kidney injury (AKI) in cats. No age, sex or breed predilection exists.
Ingestion of any part of the plant, including leaves, stems, flowers or pollen, can result in toxicosis in cats. Even a small amount of plant material (petals or one leaf), or drinking water in a vase containing cut lilies, is enough to cause severe poisoning in a cat. Flowers are more toxic than the leaves.
Cats have an increased sensitivity to toxins compared to dogs due to differences in certain xenobiotic metabolism.
In dogs, only vomiting and other mild gastrointestinal signs can be observed following lily ingestion, even when fed large amounts of plant.
However, it is recommended that bulbs of lilies be kept out of reach of the inquisitive paws of dogs. True lilies do not pose a problem for other pets or humans.
Lilium and Hemerocallis genera contain a multiple-component mixture, including saponins, polysaccharides, glycoalkaloids and flavonoids.
True lilies exerts toxic effects through several mechanisms:
Ingestion of steroid glycoalkaloids may lead to nausea, vomiting, diarrhoea and dehydration.
Several species of Lilium and Hemerocallis are nephrotoxic to cats, with rapid loss of nephron function, leading to AKI.
The microscopic lesions consist of severe epithelial cell degeneration and necrosis of the proximal tubules of the kidney. Bioassay-guided fractionation of methanol extract from Easter lily flowers has identified a complex mixture of different steroid glycoalkaloids of the solasodine type, containing a nitrogen atom (C27H43NO2) responsible for the cytotoxic effects on a feline kidney cell line model.
The oral median lethal dose of solasodine is 300mg/kg in rats.
Hydrolysis of steroidal glycoalkaloids in the gastrointestinal tract produces solasodine, the aglycone portion (sugar moiety is dissociated). Solasodine is a small molecule (molecular weight of 413 daltons) and is lipid soluble.
The lipophilicity of solasodine (logP6.83) interacts with the phospholipid (dimyristoyl phosphatidylcholine) bilayer (logP2) of the cell membrane leading to high structural disorders in the lipid molecules and inducing cell membrane fluidisation.
Disruption of cell membrane leads to fluidisation of the lipid systems in the nerve cell membrane of CNS (neurotoxicity) and erythrocytes (decreased blood flow, loss of oxygen).
Functions of ion channels, receptors and enzymes immersed in cell membrane lipid moieties also might be affected. The lipid environment of ion channels, transporters and receptors is of great importance for their function.
Clinical features usually develop within one to six hours following plant ingestion, although some reports indicate onset of these signs can occur from one and five days after exposure.
The GI signs first observed manifest as:
Neurologic signs manifest as:
Death is due to AKI.
Laboratory abnormalities – detectable early, 12 hours post-ingestion – indicate:
No specific antidote exists. Supportive care and specific treatment for AKI are required. Feline lilies toxicosis is a life-threatening emergency. A delay of treatment of more than 18 hours after exposure results in AKI and death.
Intravenous fluid therapy is indicated to rehydrate, restore intravascular volume and induce diuresis using isotonic saline sodium chloride 0.9% at least 48 hours at twice usual maintenance rate over 12 to 24 hours.
The volume of fluid to be administered should be calculated based on the percentage dehydration and the animal’s bodyweight from the following formula:
Fluid deficit (L) = bodyweight (kg)
x % dehydration (as a decimal)
Percentage dehydration can be estimated by examining mucous membrane moisture, skin turgor, eye position and corneal moisture, as described in Table 1.
Administering an increased fluid volume may not increase toxin excretion and can result in fluid overload.
If fluid therapy alone fails to promote an adequate urine output (1ml/kg/hour to 2ml/kg/hour), furosemide, a loop diuretic, increases urine output by acting on proximal renal tubules (1mg/kg to 2mg/kg IV bolus).
If no substantial diuresis develops in one hour, the dose may be doubled to 4mg/kg IV. If furosemide successfully induces diuresis, it may be repeated at eight-hour intervals as needed to sustain diuresis. If furosemide administration fails to increase urine production, osmotic diuresis may be considered. Mannitol, an osmotic diuretic, improves urine output in an oliguric renal failure patient (less than 0.25ml urine/kg/hour). Administer 0.25g/kg to 0.5g/kg slow bolus over 5 to 10 minutes (20% to 25% solution).
If substantial diuresis occurs, it may repeated every four to six hours or administered as a CRI (8% to 10 % solution) for first 12 to 24 hours of therapy.
Mannitol has three advantages:
The disadvantage of mannitol is a vascular overload if oliguria persists. Mannitol should be avoided in anuric patients. Potassium-sparing diuretics such as sodium channel blockers (for example, triamterene or amiloride) and aldosterone antagonists (for example, spironolactone) are contraindicated because they cause diuresis without causing potassium loss in the urine.
Mannitol solutions are recommended to be stored at room temperature; avoid freezing. At low temperatures in concentrations greater than 15%, crystallisation may occur.
Frequent monitoring of renal function, BUN, creatinine and electrolytes is imperative.
Metabolic acidosis may occur in animals with AKI. Alkalinising therapy is not recommended unless the blood pH level is less than 7.2 (reference range in cats 7.32 to 7.44) and standardised base excess less than -5mmol/L. Severe acidosis should be managed with sodium bicarbonate 8.4% solution: 2ml/kg to 5ml/kg CRI, depending on the severity of the acidosis, every four to eight hours.
The treatment of hyperkalaemia requires a combined treatment approach.
Calcium gluconate. Calcium gluconate 10% (0.5ml/kg to 1.5ml/kg slow IV over 10 minutes) antagonises the effect of hyperkalaemia on the heart without lowering serum potassium concentrations and may be effective in rhythm disturbances. It usually starts working within minutes and should last about 30 to 60 minutes. Repeat doses over 5 to 10 minutes until a desired effect is noted. The heart rate should be monitored via ECG to ensure rapid administration does not cause bradycardia. If bradycardia develops, halt infusion.
Insulin with glucose. Insulin and glucose shift the intracellular potassium from the blood into cells. Administer rapid insulin zinc (0.25unit/kg to 0.5unit/kg; withdraw with an insulin syringe) via slow IV injection, always with 2g of glucose per unit of insulin, followed by a CRI of 2.5% glucose at maintenance rates for six to eight hours. The onset of the hypokalaemic action occurs within 15 minutes and lasts at least four to six hours. Monitor blood glucose and potassium levels.
β2 agonists. Selective β2 adrenoceptor agonists (for example, terbutaline, salbutamol) can be administered as an adjunct therapy for the treatment of hyperkalaemia: terbutaline 0.01mg/kg IM or SC twice daily or salbutamol 0.02mg/kg to 0.05mg/kg once every 8 to 12 hours. β2 agonists binds to β2 receptors in erythrocytes, the liver, and muscle cells, stimulating adenylate cyclase that converts adenosine triphosphate (ATP) to adenosine monophosphate. This stimulates the sodium-potassium ATP pumps, resulting in intracellular K+ uptake.
Administer diuretics such as acetazolamide, a potent inhibitor of the enzyme carbonic anhydrase, that works on the proximal tubules to promote renal phosphate excretion: 50mg/kg IV one time. Reconstitute 500mg vial with at least 5ml of sterile water for injection; use within 24 hours after reconstitution. Acetazolamide is associated with relatively potential adverse effects (for example, GI disturbances, CNS effects).
Severe vomiting should be treated by antiemetic serotonin antagonists with powerful activity such as ondansetron 0.5mg/kg IV slow bolus, followed by 0.5mg/kg/hour CRI for 6 hours; or dolasetron 1mg/kg IV slow bolus every 24 hours. Alternatively, administer maropitant (neurokinin-1 antagonist) 1mg/kg IV, once a day, for up to five consecutive days. Metoclopramide (dopamine antagonist) is contraindicated (excitatory effects can occur).
Hypergastrinaemia occurs in animals with decreased renal function and may contribute to increased gastric acidity. Drugs that inhibit gastric acid production may be beneficial. Administer proton pump inhibitors omeprazole 0.7mg/kg IV every 24 hours, or pantoprazole 1mg/kg IV or lansoprazole 0.6mg/kg to 1mg/kg IV every 24 hours.
Correction of metabolic acidosis (lactic acidosis), which occurs in animals with AKI, depends on the severity of the acidosis. Administer sodium bicarbonate 8.4% solution at 2ml/kg to 5ml/kg bodyweight CRI, depending on the severity of the acidosis, over a four-hour period. Alkalinising therapy is not recommended unless the blood pH level is less than 7.2 (reference range in cats 7.32 to 7.44) and standardised base excess less than -5mmol/L.
Arterial hypertension is common abnormality in animals with AKI due to the activation of the renin-angiotensin-aldosterone system. Maintaining systolic blood pressure less than 160mmHg is recommended in cats. If not controlled, hypertension can lead to worsening glomerular disease.
Administer amlodipine (calcium channel blocker) with an initial starting dose of 0.625mg/cat to 1.25mg/cat orally once daily. Blood pressure should be rechecked one to two weeks after starting dose. Angiotensin-converting enzyme inhibitors (for example, benazepril, enalapril), antihypertensive drugs, are contraindicated (as potassium sparing can contribute to hyperkalaemia).
Wash pollen from the cat’s fur and face with water. Many cats will vomit on their own after lily ingestion, but attempting to induce vomiting is recommended if a cat is known to have eaten or chewed on a lily and has not vomited.
Dexmedetomidine is the emetic agent of choice in cats (high concentrations an alpha-2 adrenergic receptors in the chemoreceptor trigger zone): 3.5µg/kg IV or 7µg/kg to 10µg/kg IM (up to 18µg/kg). The most common adverse effect to be expected is sedation, which can be reversed using a α2-adrenergic antagonist (for example, yohimbine 0.1 mg/kg IV, or atipamezole 0.2 mg/kg IM, IV). Alternatively administer xylazine 0.44mg/kg IV, 1.1mg/kg to 2.2mg/kg IM, SC (limited effectiveness in cats). Apomorphine is not recommended for inducing emesis in cats.
Administering one dose of activated charcoal (AC; 1g/kg to 2g/kg) mixed with water to make a 20% slurry (1g/5ml water) via a nasogastric tube as soon as possible post-ingestion, and after the airway is secured, is recommended.
AC admitted orally is contraindicated in convulsing or comatose animals, and should be used with caution in the vomiting patient due to the risk of aspiration pneumonia.
Nutrition is a very important treatment tool in animals with AKI. Dietary therapy can help to slow down the progression of kidney disease and improve laboratory values.
Feline renal diets in cats should have the following characteristics.
Use of some of the drugs in this article is under the veterinary medicine cascade.
Lotfi El Bahri qualified as a doctor in veterinary medicine in Toulouse in 1969. In 1976, he joined the National Veterinary School at Sidi-Thabet in Tunisia. He gained a master in veterinary science in 1977 and, in 1981, a PhD in Alfort, France. Lotfi is a professor of pharmacology and toxicology, an analyst and a pharmacotoxicology expert in veterinary drugs.