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Néphrologie & Thérapeutique

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Oxalate : de la physiologie à la pathologie Volume 19, issue 3, June 2023

Figures


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Tables

Authors
1 Centre hospitalier Fleyriat, service de néphrologie-dialyse, 900, route de Paris, 01012 Bourg-en-Bresse, France
2 Hôpital Édouard Herriot, Hospices civils de Lyon, service de néphrologie, dialyse, hypertension et exploration fonctionnelle rénale, 5, place d’Arsonval, 69003 Lyon, France
3 Centre de référence des maladies rénales rares et phosphocalciques – Néphrogones, Hôpital Femme-Mère-Enfant, 32, avenue du Doyen Jean Lépine, 69500 Bron, France
4 Faculté de médecine Lyon Est, Université Claude Bernard, Lyon 1, 43, bd du 11 novembre 1918, 69100 Villeurbanne, France
5 Laboratoire de biologie tissulaire et ingénierie thérapeutique, CNRS UMR 5305, 7, passage du Vercors, 69367 Lyon Cedex 7, France
6 Inserm U1060 CarMeN, Groupement hospitalier Est, 59, bd Pinel, 69500 Bron, France
7 Groupement hospitalier Est, Hospices civils de Lyon, service de biochimie et biologie moléculaire, Unité des maladies héréditaires du métabolisme, 59, bd Pinel, 69677 Bron, France
8 Hôpital Édouard Herriot, Hospices civils de Lyon, service d’urologie et de chirurgie de la transplantation, 5, place d’Arsonval, 69003 Lyon, France
9 Hôpital Femme-Mère-Enfant, Hospices civils de Lyon, service de néphrologie-rhumatologie-dermatologie pédiatriques, 59, bd Pinel, 69500 Bron, France
10 Inserm U1033, Prévention des maladies osseuses, 7, rue Guillaume Paradin 69372 Lyon Cedex 08, France
11 Hôpital Lyon Sud, Hospices civils de Lyon, service de nutrition clinique intensive, 165, chemin du Grand Revoyet, 69495 Pierre-Bénite, France
Correspondance : C. Grocholski
christophe.grocholski@gmail.com

Hyperoxaluria is defined by an increase of urinary oxalate, leading to kidney stones, nephrocalcinosis and/or chronic kidney disease. There are different diseases related to hyperoxaluria: (1) 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; (2) primary hyperoxaluria, a genetic orphan disease inducing a massive production of oxalate by the liver, leading to increased plasma oxalate increase and saturation, and further systemic oxalosis with oxalate deposition, nephrocalcinosis and ultimately kidney failure, the management of this disease being currently dramatically modified by the onset of new therapeutic tools such as RNA interference; and (3) enteric hyperoxaluria, resulting from increased intestinal oxalate absorption because of intestinal malabsorption (short bowel syndrome, bariatric surgery, exocrine pancreatic insufficiency, etc.). Diagnosis and therapeutic management of these diseases require a full understanding of oxalate physiology that we detail in this review.