Renal function evaluations were conducted on pullets and laying hens during outbreaks of urolithiasis. The following parameters were measured: kidney weights; hematocrits; plasma concentrations of uric acid, calcium, inorganic phosphate, magnesium, sodium, and potassium; urine flow rates; glomerular filtration rates; renal plasma flow rates; urine pH; and relative clearances of inorganic phosphate, calcium, magnesium, sodium, potassium, and para-amino hippuric acid. The adequacy of renal portal perfusion was estimated by timed phenol red extraction. Considerable interindividual variability was noted, presumably due to differences in age and reproductive status. Intraindividual left versus right kidney comparisons also were made, since urolithiasis often is associated with macroscopic lesions of one kidney but not the other. The results indicate that even when gross lesions of only one kidney were present, specific tubular transport processes were similar in both kidneys. Urolithiasis did cause significant alterations in urine flow rates, glomerular filtration rates and renal plasma flow rates. it was concluded that the changes associated with urolithiasis reflect the expected compensatory hypertrophic responses of surviving kidney tissue to a reduction of renal mass. The physiological impact of this form of kidney damage appears to arise from reduced renal mass rather than from inappropriate renal handling of minerals or electrolytes.

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Infectious tenosynovitis was diagnosed in three separate outbreaks in a commercial White Leghorn hens, though not previously reported in adult White Leghorns (3). Clinically affected flocks had decreased production and increased daily mortality, with many hens showing signs of the so called "cage-fatigue bluecomb" syndrome. Most sick birds had lesions typical of infectious tenosynovitis, with pronounced cyanosis and dehydration. Dead birds had signs of acute septicemia. The course of the disease (about 8 weeks) was not altered by the medicinal regimens tried. Young laying-age flocks were most seriously affected. Production losses averaged 15 to 20%, and mortality reached 5% per month during the recovery phase.

A significant outbreak of avian urolithiasis was observed on a large commercial egg farm. From the initial outbreak site (a single laying house), the incidence of urolithiasis slowly spread in the ensuing months to numerous other laying houses. Increasing mortality associated with urolithiasis commenced during late growout to early lay and then leveled off when egg production peaked. At the height of the outbreak, mortality was typically 0.5% per week; 75% of this mortality was due to urolithiasis. The clinical and pathologic features of this condition are described. Both infectious bronchitis virus (IBV) and fowl adenoviruses were isolated from organ homogenates of sampled birds. A clone of the IBV strain was found to induce nephritis in specific-pathogen-free white leghorns.