The consumption of grapes and raisins presents a potential health threat to dogs. Their toxicity to dogs can cause the animal to develop acute kidney injury (the sudden development of kidney failure) with anuria (a lack of urine production). The phenomenon was first identified by the Animal Poison Control Center (APCC), run by the American Society for the Prevention of Cruelty to Animals (ASPCA). Approximately 140 cases were seen by the APCC in the one year from April 2003 to April 2004, with 50 developing symptoms and seven dying.
It is not clear that the observed cases of renal failure following ingestion are due to grapes only. Clinical findings suggest raisin and grape ingestion can be fatal, but the mechanism of toxicity is still considered unknown.
The reason some dogs develop renal failure following ingestion of grapes and raisins is not known. Types of grapes involved include both seedless and seeded, store-bought and homegrown, and grape pressings from wineries. A mycotoxin is suspected to be involved, but none has been found in grapes or raisins ingested by affected dogs. The dose-response relationship has not been determined, but one study estimated ≥3 g/kg for grapes or raisins. The most common pathological finding is proximal renal tubular necrosis. In some cases, an accumulation of an unidentified golden-brown pigment was found within renal epithelial cells.
Vomiting and diarrhea are often the first clinical signs of grape or raisin toxicity. They often develop within a few hours of ingestion. Pieces of grapes or raisins may be present in the vomitus or stool. Further symptoms include weakness, not eating, increased drinking, and abdominal pain. Acute renal failure develops within 48 hours of ingestion. A blood test may reveal increases in blood urea nitrogen (BUN), creatinine, phosphorus, and calcium.
Emesis (induction of vomiting) is the generally recommended treatment if a dog has eaten grapes or raisins within the past two hours. A veterinarian may use an emetic such as apomorphine to cause the dog to vomit. Further treatment may involve the use of activated charcoal to adsorb remaining toxins in the gastrointestinal tract and intravenous fluid therapy in the first 48 hours following ingestion to induce diuresis and help to prevent acute renal failure. Vomiting is treated with antiemetics and the stomach is protected from uremic gastritis (damage to the stomach from increased BUN) with H2 receptor antagonists. BUN, creatinine, calcium, phosphorus, sodium, and potassium levels are closely monitored. Dialysis of the blood (hemodialysis) and peritoneal dialysis can be used to support the kidneys if anuria develops. Oliguria (decreased urine production) can be treated with dopamine or furosemide to stimulate urine production.
The prognosis is guarded in any dog developing symptoms of toxicosis. A negative prognosis has been associated with oliguria or anuria, weakness, difficulty walking, and severe hypercalcemia (increased blood calcium levels).