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Other Names: Visceral Gout, Articular Gout, Renal Gout, Urate Deposition

Gout occurs when there is too much uric acid in the bird's body. Uric acid is regularly produced in the liver and excreted through the kidneys into the urine. However, birds with impaired renal function may not be able to get rid of uric acid as efficiently, leading to a build up within the blood which is called hyperuricemia. Hyperuricemia can result in uric acid deposits within the joints (articular gout) and in visceral organs or other extra-visceral sites (visceral gout). Over time, these deposits will grow to form tophi (nodular masses of uric acid crystals).

What are the Different Forms of Gout?

  • Articular Gout: The accumulation of urates within the synovial capsules and tendon sheaths of the joints, including the toes of the feet.
  • Visceral Gout: The precipitation of uric acid crystals along the surface of internal visceral organs and other sites within the body.
Articular Gout Versus Visceral Gout

Typical Onset:AcuteChronic
Gender:BothMostly roosters
Percent of flock affected:Can be up to 100% of the flockIndividual birds
Gross lesions observed in organs after death
Kidneys:Almost always involved. Abnormally sized and covered w/ white chalky depositsMay become involved. Usually appears normal unless the bird was dehydrated.
Joints:May or may not be involvedAlways, especially the feet
Possible causes:Dehydration

Sodium bicarbonate

Infectious agents

Vitamin A deficiency

Secondary to urolithiasis


Immune mediated glomerulonephritis

Exposure to toxic substances
High protein diet

Excess dietary calcium in diet

Low-phosphorus diet

High energy diet

Genetic defect


What Causes Gout?

Goat is caused by kidney damage or malnutrition, often related to the following factors:

Diet-Related Risk Factors:
  • Excess dietary calcium: Feeding non-laying chickens (such as chicks, pullets, roosters, and aged hens that don't lay eggs anymore) a high calcium diet for an extended period of time can cause kidney damage. This is most commonly related to feeding all flock members commercial laying hen feed. It can also be caused by a feed mill error, feeding an abundance of table scraps or treats that contain high amounts of calcium, and by providing low-quality poultry feed that contains large particles of calcium carbonate (CaCO3).
  • High protein diet: When chickens are fed protein in excess of their nutritional requirements, the additional protein is converted into uric acid. This puts them at a higher risk of developing gout.
  • Vitamin A deficiency: Vitamin A is an essential vitamin for chickens, and if they are receiving a vitamin A-deficient diet for any length of time, it can cause damage to the lining of the ureters (the ducts by which urine passes from the kidneys to the cloaca), leading to gout. Not all commercial chicken feeds contain vitamin A, and in those that do, the amount degrades over time, especially when it is exposed to sunlight. This is because vitamin A is very sensitive to sunlight. Chickens that do not have regular access to pasture grass are at a high risk of vitamin A deficiency, as grasses and various weeds (such as dandelion) are a good source.
  • Low-Phosphorus diet: Chickens receiving a diet low in phosphorus are more at risk of developing gout, as phosphorus acts as a urine acidifier which helps in the prevention of kidney stones.
  • High cholesterol diet: Chickens fed a diet high in cholesterol are more prone to developing renal disease.
  • Dehydration: If chickens become dehydrated, this puts them at risk of kidney damage. Dehydration is usually caused by lack of water, which most often is a risk during hot weather with increased water intake or during cold weather from lack of water access due to the formation of ice along the surface of the water source.
Viral infectionsToxins
  • Mycotoxins: Mycotoxins are toxins produced by molds that are commonly found in commercial poultry feeds worldwide, in addition to bedding materials, and other feedstuff. Ingestion of certain types of mycotoxins are known to cause kidney damage.
  • Aminoglycoside Antibiotics: Aminoglycosides (Amikacin, Tobramycin, Gentamicin) have nephrotoxic side effects.
  • Disinfectants and insecticides: Are safe and effective when used properly in accordance to manufacturer recommendations, however they can cause kidney damage when the dosage is miscalculated.
  • Sodium bicarbonate (baking soda): Giving chickens sodium bicarbonate (which is sometimes administered during periods of hot weather and/or to improve egg shell quality) can contribute to the onset of gout by disrupting the pH of the urine, making it more alkaline, and putting chickens more at risk of kidney stones.

Clinical Signs

Shifting leg lameness
Swelling of feet and/or joints
Inability to flex certain joints
White raised nodules on feet and lower legs
Difficulty perching or walking


  • History
  • Clinical signs
  • Physical Exam
  • Urinalysis
  • Blood chemistry
  • Radiography
  • Biopsy
  • Cytology

Reported Cases

  • Case 1: Amyloidosis and Gout in a Flamingo On presentation, a flamingo was weak and thin. Supportive care was given, but bird was found dead two days later. The plantar aspects of both feet have thickened/calloused 1-1.5 cm diameter lesions with a small central crater over the proximal joints of digits one, two, and three. Associated joints contain cloudy, viscous fluid. Ref

  • Case 2: Visceral gout and Cryptosporidiosis in a Commercial laying hens Formalin-fixed kidney tissues from adult egg-laying chickens in two houses of an egg-production complex in the upper Midwest were submitted to Iowa State University for histopathologic examination. An increased incidence of visceral gout, average daily mortality 1%-2% higher than expected, and egg production within normal limits were observed in both houses. Numerous developing stages of Cryptosporidium were observed on the apical surface of epithelial cells lining renal collecting tubules and ureters. Scanning and transmission electron microscopy were used to visualize colonization of cryptosporidia, disruption of microvilli, and exfoliation of parasitized epithelial cells. Lymphoplasmacytic infiltration in the wall of ureters and hyperplasia of parasitized epithelial cells resulted in partial obstruction of ureters, which may have induced visceral gout in affected hens. Ref


Supportive careIsolate the bird from the flock and place in a safe, comfortable, warm location (your own chicken "intensive care unit") with easy access to water and food. Limit stress. Call your veterinarian.
Allopurinol10-15 mg/kg administered IM or orally, once a day. Take caution as this drug has been linked to liver damage with long term use.S Echols, K Marx
Supplemental vitamin A< 20 KIU/kg IM added to the diet may be of benefitS Echols, 2013
Probenecid and colchicineFor up to 10 weeks, in conjunction with a low protein dietTufts University
Moringa oleifera leaf powderSupplementing the diet with 10 gm/kg may be beneficial.



  • Make sure that all flock members always have access to a fresh, clean water source, even in the winter with ice formation (use heated waterers or buckets)
  • Ensure chickens receive proper daily amounts of vitamin A
  • Feed a balanced diet with recommended protein levels
  • Do not feed pullets feed intended for egg laying hens until they lay their first egg
  • Provide regular access to pasture grass
  • Purine-free diet

Scientific References

Risk Factors

  • Dehydration
  • Older birds
  • Receiving excess vitamin D3
  • High protein or cholesterol diet
  • Vitamin A deficiency
  • Mycotoxins present in feed
  • Feeding high calcium diets to non-laying hens
  • Diets high in fructose - increases the risk of gout and causes phosphate depletion.
  • Nephrotoxic drugs (aminoglycosides, sulfonamides) decrease urate excretion by damaging the renal tissue.
  • Genetics - certain chicken breeds have been identified to have a simple autosomal recessive gene that causes a defect in the renal tubular secretion of urate.
  • Ingestion of certain nephrotoxic plants.