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Avian Urolithiasis (Gout)

Avian urolithiasis, or gout, is not a single disease entity, but rather the result of kidney damage from any of a number of potential causes. Kidney damage can be caused by infectious disease, nutritional issues, toxic substances, or a combination of factors.
Visceral gout is a condition of chickens that has been recognized for more than 30 years. Due to its striking lesions, many names have been used to describe visceral gout, such as acute toxic nephritis, renal gout, kidney stones, nutritional gout, nephrosis, and others. Visceral gout is readily recognized by its distinctive lesions which are characterized by white chalk-like deposits covering the surface of various abdominal organs as well as the pericardial (heart) sac.
Pathology and Clinical Signs
Gout occurs when kidney function has decreased to the point where uric acid (a nitrogenous waste) accumulates in the blood and body fluids. The uric acid subsequently precipitates as calcium sodium urate crystals in a variety of locations, particularly in the kidneys and on the serous membranes of the liver, heart, air sacs, and joints. The damaged kidneys are characterized by atrophied or missing portions of kidney lobes, kidney and ureter stones, and remaining kidney tissue that is swollen and white with urates. Compensatory enlargement of remaining normal kidney tissue takes place in an attempt to maintain adequate renal function.

Although gout has been recognized for some time as a cause of excessive pullet and layer mortality, it continues to be a diagnostic challenge. Chickens affected by renal damage can continue to be productive until less than one third of kidney mass remains functional. As a result, birds can be in full production and exhibit few external symptoms until shortly before death.

Figure 1. Gout lesions: White chalky deposits over the heart, liver, and abdominal cavity.


Figure 2. Kidney degeneration, leaving swollen ureter on the right side. Compensatory hypertrophy in lower lobes on the left side.

Figure 3. Normal kidneys.

Kidney Anatomy and Function
The long, paired kidneys of the chicken are located in depressions in the pelvis bone in the abdominal cavity. They are normally reddish-brown in color and have 3 distinct lobes or divisions.

The primary function of the kidney is to maintain the chemical composition of body fluids (blood). The kidney serves a variety of other functions in the body; removal of metabolic waste and toxic products, conserving fluids and vital electrolytes, regulation of blood volume, and production of hormones that regulate blood pressure and production of red blood cells. The kidney is truly a vital organ. When renal function stops, uric acid, normally excreted by the kidney in the urine, is then deposited any place that blood is circulated. A bird with no renal function will likely die within 36 hours.
Causes of Gout
The cause of gout is often difficult to determine. The original kidney damage may occur long before the onset of gout mortality. Possible factors that can cause or contribute to gout are nutritional, infectious, and toxic.
Nutritional or metabolic factors known to affect the kidneys are:

  • Excess dietary calcium fed to immature pullets over a period of time will result in kidney damage that may lead to gout. This could result from a feed milling error, accidental delivery of layer feed to a growing house, or excessively early use of pre-lay diet (i.e., before 15-16 weeks of age).
  • Grower diets that contain large particle-size CaCO3 (i.e., greater than 1-2 mm mean diameter) that allows individuals to selectively pick out and consume these particles, in turn resulting in excessive intake of calcium. To ensure correct calcium intake, grower diets should contain CaCO3 only in a fine-powder form (i.e, 1 mm mean diameter or less). Larger particle size CaCO3 may be used beginning with the pre-lay diet, after 15-16 weeks of age.
  • Phosphorus has been shown to partially protect the kidney against calcium-induced damage. Phosphorus acts as a urinary acidifier and helps prevent kidney stones from forming. Marginally low available phosphorus in grower diets has been associated with higher gout incidence.
  • Sodium bicarbonate is sometimes used to improve egg shell quality or combat the effects of heat stress. Sodium bicarbonate can contribute to gout by making the urine more alkaline, which, with high levels of calcium, is an ideal medium for formation of kidney stones.
  • Water deprivation, due to mechanical malfunction, may affect kidney function, but research has not demonstrated a direct result in gout.
  • Vitamin A deficiency over a long period of time can cause damage to the lining of the ureters, but should be rare with modern vitamin formulation.

Viral agents known to be involved in gout are infectious bronchitis (IB) and avian nephritis virus (ANV). Infectious bronchitis is a highly contagious virus that normally involves the respiratory tract, but can also affect the reproductive and urinary systems. Certain strains of bronchitis, termed nephropathogenic, have a special predilection for the kidneys.
One mechanism by which bronchitis may affect the kidneys is chronic viral persistence leading to nephritis and renal failure over time. As young birds are most susceptible to bronchitis kidney damage, the initial infection may occur long before renal function is critically reduced and mortality occurs. When pullets sexually mature, they are placed on higher calcium diets to meet the demands of egg production. If the kidneys were previously damaged, they may no longer function normally with the higher level of calcium excretion, and the result is likely to be gout.
Avian nephritis virus, an enterovirus that affects the kidneys, has been associated with kidney disease and serious outbreaks of mortality in Europe and Asia. Serological surveys show that antibodies to avian nephritis virus can be detected in chicken and turkey sera from around the world. Although most information at this time suggests only a subclinical role for avian nephritis virus, research has shown avian nephritis virus inoculated into healthy chickens will cause inflammation of the kidneys and could lead to gout.
Poisonous substances (toxins), while widely distributed in nature, are not considered major causes of production loss or disease in poultry in most countries. There are, however, problems that can arise from nephrotoxic substances. Some potentially toxic substances are used on a routine basis, while others are the result of accidental exposure.
Products used on a routine basis that have potential for human error and resulting toxicity are antibiotics, anticoccidials, minerals, vitamins, manufactured chemicals, and pesticides.

  • Antibiotics, such as sulfas and aminoglycosides, are eliminated from the body via the kidneys and are potentially nephrotoxic, particularly when water intake is restricted.
  • Minerals and vitamins such as calcium, phosphorus, sodium, and vitamin D3 are potentially toxic to chickens. Chicks, however, are much more sensitive to toxicity, probably because their kidneys are not fully developed.
  • Disinfectants and insecticides, when used according to manufacturers' recommendations, are safe and effective, but a miscalculation of dosage can result in toxicity.
  • There are several mycotoxins that are nephrotoxic and/or hepatotoxic in laying hens, including ochratoxin A, oosporein, and deoxynivalenol (DON). The kidney and liver damage caused by ingesting these mycotoxins can cause gout among other clinical signs.

Gout, when recognized as a problem in field cases, is likely to be a multi-factorial problem and identifying a specific cause is often difficult. Another reason for diagnostic difficulty is that kidney damage occurring during the growing period often has no apparent signs until the birds later come into egg production and are fed high calcium diets.
Field cases and research have demonstrated the importance of interactions between 2 or more contributing factors, especially nutrition and infectious bronchitis.

  • The grower diets should contain no more than about 1% calcium (see the nutritional recommendations) in powder (i.e., less than 1 mm mean diameter) form up to 15-16 weeks of age. A high calcium intake in immature pullets can cause serious kidney damage.
  • The dietary content of available phosphorus levels should be adequate, typically 0.45-0.50% in grower diets, see the nutritional recommendations for each individual Hy-Line variety. Insufficient phosphorus predisposes the kidneys to calcium damage.The pre-lay diet should not be used before 15-16 weeks of age, and should not be fed until the flock shows signs of sexual maturity (blooming of the combs and wattles). Do not supply more than the recommended 2.50-2.75% calcium in the pre-lay diet.
  • If sodium bicarbonate is used, use only enough to supply 20-30% of the diet's recommended sodium content (with the remainder coming from salt, NaCl). A flock with gout should not be medicated with sodium bicarbonate or fed a diet that is highly alkaline (i.e., high levels of sodium or potassium).
  • Review all calcium and available phosphorous levels in the feeding program and follow the recommendations for the age and variety. Pullet and layer feeds should be routinely analyzed for calcium and phosphorus.
  • Feed samples could be assayed for the presence of the mycotoxins citrinin, ochratoxin, and oosporein.
    • Water deprivation should be avoided in growing and laying flocks.

Infectious bronchitis
Bronchitis alone has not been shown to trigger gout under research conditions, but in the presence of calcium-induced kidney damage, bronchitis greatly amplifies gout mortality. Due to the possible role of infectious bronchitis, the following should be considered.

  • Infectious bronchitis vaccines should be administered according to the manufacturers' directions and recommendations. To provide optimum protection, the vaccination program should include several live vaccinations of bronchitis (can be in combination with Newcastle) at about 3 weeks, 8 weeks, and 14 weeks of age by spray or drinking water. The degree of reactivity of the vaccinations starts low and then is gradually increased each succeeding time by using either a less attenuated virus or by giving it by a more reactive method, such as spray instead of water. Killed vaccines or live boosters throughout lay help keep bronchitis immunity high.
  • The vaccine strains used should be those known to be endemic in the area. Use of several serotypes of bronchitis vaccine will generally improve cross-protection against other field variants and possibly against nephropathogenic strains.
  • Due to the complex clinical signs associated with infectious bronchitis, a diagnostic laboratory should be enlisted to help in diagnosis and in virus isolation. Routine serological testing can provide initial indications of bronchitis challenges. Virus isolation may be facilitated with the use of specific-pathogen free (SPF) sentinel birds placed in the house and isolation attempts from them after 5 to 10 days of exposure.

Experimental diets containing ammonium chloride, ammonium sulfate, DL-methionine, and methionine hydroxy analog all successfully acidify the urine. Please check with a local veterinarian if these treatments are approved for treatment in the specific country where the flock is located.
The presence of gout mortality in pullets or layers indicates some form of kidney damage has occurred at an earlier time in the flock's life. Research supports a strong link for bronchitis and calcium-phosphorus imbalance as major causes of gout mortality. While this is likely to be the underlying cause for most cases of gout, other factors such as electrolyte balance, mycotoxins, and water deprivation need to be recognized as possible contributing factors.
Likewise, any diet that increases urine alkalinity in combination with high calcium can contribute to gout mortality in pullets and layers. If gout does occur in a flock, mortality can be reduced by increasing the acidity of the urine to dissolve existing kidney stones or to prevent additional kidney stones from forming.

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