Quote:
Well heck, that's just the first quote that came to hand. It's a well-known problem -- I didn't really expect you to argue about it!
Here's some more refs for ya, just a few that are easily accessible --
"Excess absorbed calcium is excreted through kidneys; high levels cause ureter and kidney impaction, resulting in nephrosis....High mortality from hyperuricemia with visceral urate deposits may result from kidney damage because of high dietary calcium. Lung pathology with damage to parenchyma from calcium deposits may also occur in young chicks."
-- p. 1138, Diseases of Poultry by YM Saif
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I'm including this next one because it specifically used layer ration --
"Experiments were designed to evaluate the effect of dietary acidification on the development of kidney lesions induced by excess dietary calcium (Ca) and Gray strain infectious bronchitis virus (IBV). Specific pathogen-free (SPF) chicks and SPF chicks inoculated with Gray strain IBV were fed one of three diets: a commercial pullet grower ration (1% Ca); a commercial layer ration (3.25% Ca); or layer ration plus .5% ammonium chloride (acidified layer ration). ....The layer ration induced a 60% incidence of kidney lesions, caused a significant increase in kidney weight asymmetry ratios, and caused a 25% reduction in the number of filtering nephrons....."
-- Poult Sci. 1987 Apr;66(4):626-33. Effect of dietary acidification on kidney damage induced in immature chickens by excess calcium and infectious bronchitis virus.
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"High calcium diet during rearing periods and increase
nitrogen intake in the form of urea; lead to degenerative
changes in various tissues, nephritis and the induction
of uroliths in chickens (Chandra et al., 1984 b, Beckman
1995).[....]
"Furthermore, Lent and Wideman, (1994) revealed that
excess calcium significantly reduced glomerular filtration
rate, affected renal plasma flow and phosphorous
excretion rates as well as significantly increased
calcium excretion and urine pH. It is believed that
mortality accompanied by visceral urate deposition
occurs when the amount of unobstructed renal tissues."
International Journal of Poultry Science 5 (10): 992-995, 2006. Association Between Serum Biochemistry of Leghorn Chickens and Changes in Renal Tissues Induced by High Calcium and High Urea Diets. Abdul-Rahman S. Al-Ankari
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"Most clinical cases of acute renal failure and urate deposition in commercial poultry are due to dehydration, ingestion of feed containing >3% calcium by nonlaying chickens, renal infection by nephrotropic strains of infectious bronchitis virus, or infection with avian nephritis virus.....Urolithiasis is common in older laying chickens. Brittle, white, staghorn calcium urate calculi form in one or both ureters. 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 acute urate deposition on visceral surfaces or less commonly in joint spaces. If blockage is incomplete or unilateral, chickens survive in compensated renal failure, and chronic urate deposits form in joint spaces. "
Merck Veterinary Manual --
http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/204606.htm
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I could keep going, but I hope you get the point!