Traditionally, oxalate has been relegated to the status of a metabolic by-product, the role of which in stone disease is limited to the physical chemistry of crystallization. Recent investigations indicate, however, that oxalate can increase chloride, water, and sodium reabsorption in the proximal tubule and activate multiple signaling pathways in renal epithelial cells. By contrast, little is known about the partitioning of oxalate between urinary excretion, fecal excretion, and accumulation in tissues and organs. Until the factors that control this partitioning are understood, preventive medical therapies will elude patients with idiopathic hyperoxaluria, or with hyperoxaluria secondary to bariatric surgery or cystic fibrosis.
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Appreciation is expressed to SE Brown for editorial assistance.Funding information
This work was supported by NIH Grants DK073730 (to SR Marengo) and HL18708 (to AMP Romani) and by the American Urological Association Foundation (SR Marengo).
Susan R Marengo, Case Western Reserve University School of Medicine, Department of Physiology and Biophysics, 10900 Euclid Avenue, Cleveland, OH 44106-4970, USA; Email email@example.com
Nat Clin Pract Nephrol. 2008;4(7):368-377. © 2008
Nature Publishing Group
Cite this: Oxalate in Renal Stone Disease: The Terminal Metabolite That Just Won't Go Away - Medscape - Jul 01, 2008.