Visceral Urate Deposition Research Articles

Pathogenesis of renal dysfunction in chicks experimentally induced by avian nephritis virus

Renal dysfunction in chicks infected with avian nephritis virus (ANV) at 1 day or 1 week of age was studied. Two chicks inoculated per os and one inoculated intraperitoneally, both infected at 1 day of age, died with visceral urate deposits within 10 to 13 dpi, and the surviving infected chicks showed a markedly reduced weight gain. In a chronological study, ANV was consistently isolated from the kidney irrespective of the route of infection or age of chick. Fluorescent antigen to ANV was also detected as cytoplasmic granules in the tubular cells, accompanied by necrosis of tubular cells. A high concentration of serum uric acid was detected 4 to 13 dpi in chicks infected at 1 day of age and was frequently coincident with detection of the tubular cell necrosis. These results suggest that the increased serum uric acid concentration is caused by viral damage of kidney tubular cells.

Visceral urate deposits in chicks inoculated with avian nephritis virus

Avian nephritis virus, G-4260 strain, was inoculated orally into one-day-old specific-pathogen-free chicks of two lines. Approximately 20 per cent of the chicks of both lines died with visceral urate deposits from eight to 12 days after infection, and the virus was isolated from the kidneys of the dead chicks. At 14 or 15 days of age the mean liveweight of the surviving infected chicks was approximately 16 per cent less than that of the uninfected control chicks.

Renal Pathology in Chicks following Water Deprivation

Total water deprivation of 2-day-old broiler chicks for 24, 48, 72, 96, and 120 hours did not result in visceral urate deposits. Renal tubular changes consisted of increased spaces between membrane infoldings of the distal convoluted tubular epithelium, increased number of cytoplasmic vacuoles in proximal convoluted tubules, and increased mucin production and dilation of collecting ducts.

Microscopic and Ultrastructural Renal Pathology of Oosporein-Induced Toxicosis in Broiler Chicks

Kidneys from broiler chicks receiving 300 micrograms of oosporein K salt per gram of feed continuously from 0 to 21 days of age were examined by light and electron microscopy. Chicks that died at 3 days had nephrosis of initial proximal tubular segments with an early pyogranulomatous interstitial response. Macula densa cells had cytoplasmic accumulations of periodic-acid-Schiff-positive granules. Kidneys from chicks surviving 21 days had hypercellular or atrophic glomeruli and hyperplastic dilated proximal tubules. Centrilobular distal tubules were dilated and filled with hyaline basophilic casts. Interstitial fibrosis was prominent in cortical and medullary zones. These findings indicate that oral oosporein is a severe nephrotoxin which can cause visceral urate deposition and severe nephrosis of initial proximal tubular segments. The histopathology of this mycotoxicosis was compared with those of infectious-bronchitis-induced nephrosis and avian urolithiasis syndrome.

Epizootiology, Pathology, and Microbiology of an Outbreak of Urolithiasis in Chickens

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.

The effects of estradiol-17β and/or progesterone on nitrogen balance values in studies on the castrated rooster

The effects of estradiol-17β (E), progesterone (P), and E plus P (BOTH) on N balance and N constituents of the urine and plasma were investigated in 9- to 10-week old castrated cocks. Birds were subjected to surgical trauma by exteriorizing the ureters in order to obtain feces-free urine. Statistically significant increases were observed in food consumption and body weight gain of E- and BOTH-treated chickens. These increases were suppressed by the stress of the exteriorization. However, treated birds remained in a positive N balance after the operation, whereas the control animals went into a negative N balance with one-third of them dying prior to the termination of the experiment. None of the hormones utilized produced significant changes in the percentage composition of the nitrogenous waste products. Daily fluctuations occurred but were probably within normal variations. Treatments of E and BOTH resulted in statistically significant increases in the plasma total N and protein N, the urine volume, and a decreased plasma concentration of sodium and uric acid in the E-treated group. Progesterone had an inhibitory influence on the estrogen stimulated variables and had no effect alone. Untreated controls which died showed statistically significant increases in the percentage of sodium retained, and in plasma sodium, uric acid, and glucose concentrations. They also were characterized by adrenal hypertrophy, visceral urate deposits on various thoracic and abdominal organs and damaged kidneys. It was hypothesized that an increased secretion of corticosterone occurred due to the exteriorization stress, causing a negative N balance. E and P seemed to protect the birds from these effects.