Choline deficiency and the reversibility of renal lesions in rats.
A transient choline deficiency was induced in young rats subsequently fed a nutritionally complete purified diet during recovery periods of 0 to 119 days. The purpose was to investigate the pathomorphology of the renal lesions and relate this to observed biochemical changes. Acute renal lesions consisting of tubular epithelial cell necrosis and tubulorrhexis were observed in rats immediately after the insult. Chronic renal lesions consisting of interstitial nephritis and scarring were observed 28 to 119 days after the insult; these lesions were qualitatively similar at all times but showed a healing trend as the recovery period lengthened. Kidney and liver weights, liver fat concentration, and serum urea nitrogen concentration were higher in treated rats than in control rats at 0 days (no recovery period allowed) but treatment effects at all other times were minor. Significant changes occurred in serum phenylalanine and tyrosine concentrations and in the phenylalanine to tyrosine ratios after recovery periods of 0, 42 and 84 days. It was concluded that the proximal convoluted tubule was most seriously affected and that the chronic lesions represent a potential threat to kidney function in a stress situation. Some implications for human nutrition are discussed.
D000818:Animals; D001806:Blood Urea Nitrogen; D002794:Choline / Q000627:therapeutic use; D002796:Choline Deficiency / Q000150:complications* / Q000188:drug therapy / Q000473:pathology; D007672:Kidney Cortex / Q000473:pathology; D007674:Kidney Diseases / Q000209:etiology* / Q000473:pathology; D007684:Kidney Tubules / Q000473:pathology; D008099:Liver / Q000473:pathology; D008297:Male; D009393:Nephritis / Q000209:etiology; D051381:Rats
D002794:Choline