Avian species excrete nitrogenous wastes as urates bound in colloidal form with mucus in their urine. Renal dysfunction decreases the clearance of uric acid from the blood, which results in hyperuricemia with precipitation of insoluble products within the kidney itself or other organs, causing urate deposition or urolithiasis (gout). Urate deposits are white and semisolid and must be differentiated from yellow fibrinous or purulent inflammatory exudates that are secondary to infectious causes such as synovitis, peritonitis, perihepatitis, and pericarditis.

Visceral urate deposition occurs after rapidly progressing renal failure, or as a terminal event with acute decompensation of chronic renal disease. Deposits develop most commonly on the pericardium, peritoneum, and liver capsule, and rarely on synovial surfaces of joints and tendons. Microscopically, urate deposits are often seen as feathery crystals or basophilic spherical masses, usually with little inflammation due to the rapid course. Infectious causes of acute renal failure and visceral urate deposition in commercial poultry include infectious bronchitis virus, avian nephritis virus, and cryptosporidiosis. Noninfectious causes include dehydration, ingestion of feed containing >3% calcium by nonlaying chickens, vitamin A deficiency, urolithiasis, and exposure to myotoxins (eg, oosporein). Other avian species commonly develop visceral deposits secondary to nephrotoxin exposure, most commonly aminoglycoside antibiotics or heavy metals.

Articular urate deposition is less common and occurs after longterm increases in serum levels of uric acid. Deposits develop on synovial membranes in the toes and wing joints and incite a chronic granulomatous reaction to urate crystals (tophi). Articular urate deposition may be seen in chickens that have hereditary defects in uric acid metabolism or that are fed excessive protein.

Urolithiasis is common in older laying chickens. It is characterized by severe atrophy of one or both kidneys with distended ureters often containing brittle, white, staghorn calcium urate calculi or uroliths. Most cases are due to feeding high-calcium laying feed to hens not in egg production, infection with infectious bronchitis virus, or severe vitamin A deficiency. If blockage is complete, acute postrenal failure develops, and birds die with visceral urate deposition. If blockage is incomplete or unilateral, chickens survive in compensated renal failure, and articular urate deposits may develop.

Last full review/revision March 2012 by Rocio Crespo