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Oxalate: From physiology to pathology

Par : Contributeur(s) : Type de matériel : TexteTexteLangue : français Détails de publication : 2023. Sujet(s) : Ressources en ligne : Abrégé : Hyperoxaluria is defined by an increase of urinary oxalate, leading to kidney stones, nephrocalcinosis, and/or chronic kidney disease. There are numerous diseases related to hyperoxaluria. The first is kidney stones, 50% of them being explained by intermittent hyperoxaluria, secondary to dietary mistakes such as low hydration, excess of oxalate consumption, and/or low calcium consumption. Second is primary hyperoxaluria, an orphan genetic disease responsible for large-scale production of oxalate by the liver, leading to tissue deposits that appear early (from childhood) and are severe (leading to end-stage kidney failure and thesaurismosis with multivisceral damage). The management of this disease is today being dramatically modified by the onset of new therapeutic tools such as RNA interference. Third is enteric hyperoxaluria, resulting from increased intestinal oxalate absorption because of intestinal malabsorption (short bowel syndrome, bariatric surgery, exocrine pancreatic insufficiency, etc.). The diagnosis and therapeutic management of these diseases require a full understanding of oxalate physiology, which we detail in this review.
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Hyperoxaluria is defined by an increase of urinary oxalate, leading to kidney stones, nephrocalcinosis, and/or chronic kidney disease. There are numerous diseases related to hyperoxaluria. The first is kidney stones, 50% of them being explained by intermittent hyperoxaluria, secondary to dietary mistakes such as low hydration, excess of oxalate consumption, and/or low calcium consumption. Second is primary hyperoxaluria, an orphan genetic disease responsible for large-scale production of oxalate by the liver, leading to tissue deposits that appear early (from childhood) and are severe (leading to end-stage kidney failure and thesaurismosis with multivisceral damage). The management of this disease is today being dramatically modified by the onset of new therapeutic tools such as RNA interference. Third is enteric hyperoxaluria, resulting from increased intestinal oxalate absorption because of intestinal malabsorption (short bowel syndrome, bariatric surgery, exocrine pancreatic insufficiency, etc.). The diagnosis and therapeutic management of these diseases require a full understanding of oxalate physiology, which we detail in this review.

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