“…6,15,27,49 Secondary or acquired oxalate nephrosis can be due to severe liver disease 46 or pyridoxine deficiency, 5,7,24,65 which results in compromised oxalate metabolism, or increased absorption of oxalates due to ingestion of oxalates (or their precursors) including plants, 2,3,11,40,58 ethylene glycol and other glycols, 1,10,11,31,50 xylitol, 13 ascorbic acid, 4,47,48,55 and collagen or feathers. 19,85 An altered intestinal microbiome, 43,69 excessive bile or long-chain fatty acids, 10,56 or low intestinal calcium content, 33 enterocolitis, 5,10 and intestinal surgical resection 9,32 can also increase oxalate absorption and result in oxalate crystal deposition in the kidney. Ethylene glycol toxicity was considered, although never proven, 72,76 in cheetah cases with large numbers of crystals but was thought unlikely in cases from the United Arab Emirates 37 and southern Africa, where ethylene glycol (antifreeze) is less widely utilized.…”