TL;DR: It is suggested that dietary oxalate makes a much greater contribution to urinaryOxalate excretion than previously recognized, that dietary calcium influences the bioavailability of ingested oxalATE, and that the absorption of dietary oxAlate may be an important factor in calcium oxalates stone formation.
TL;DR: Five of 18 patients with ileal resection, two of seven with bacterial over-growth, and six of 15 with miscellaneous conditions, including nontropical sprue and cirrhosis, had hyperoxaluria.
Abstract: In seven patients with resection of the distal ileum, calcium oxalate nephrolithiasis and increased urinary excretion of oxalate (64 to 135 mg per 24 hours) developed. Cholestyramine therapy (4 g four times a day) lowered the 24-hour urinary excretion of oxalate to normal in the four patients in whom it was used. Urinary excretion of oxalate was measured in an additional 42 patients with various types of intestinal disorders without evidence of nephrolithiasis. Five of 18 patients with ileal resection, two of seven with bacterial over-growth, and six of 15 with miscellaneous conditions, including nontropical sprue and cirrhosis, had hyperoxaluria.
TL;DR: Cholestyramine therapy (4 g four times a day) lowered the 24-hour urinary excretion of oxalate to normal in the four patients in which it was used as mentioned in this paper.
Abstract: Abstract In seven patients with resection of the distal ileum, calcium oxalate nephrolithiasis and increased urinary excretion of oxalate (64 to 135 mg per 24 hours) developed. Cholestyramine therapy (4 g four times a day) lowered the 24-hour urinary excretion of oxalate to normal in the four patients in whom it was used. Urinary excretion of oxalate was measured in an additional 42 patients with various types of intestinal disorders without evidence of nephrolithiasis. Five of 18 patients with ileal resection, two of seven with bacterial over-growth, and six of 15 with miscellaneous conditions, including nontropical sprue and cirrhosis, had hyperoxaluria.
TL;DR: In this paper, the authors describe a case series of 60 patients seen at Mayo Clinic-Rochester that developed nephrolithiasis after Roux-en-Y gastric bypass (RYGB), including a subset of 31 patients who had undergone metabolic evaluation in the Mayo Stone Clinic.
TL;DR: Progressive renal failure in oxalate nephropathy results primarily from NALP3-mediated inflammation, thereby excluding differences in intestinal oxalates handling to explain the observed phenotype.