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Current approaches to the management of primary hyperoxaluria
Pierre Cochata, Odile Basmaisonb
a Département
de Pédiatrie, Hôpital Edouard Herriot and Université Claude
Bernard, Lyon, France, b Centre
d'Etude des Maladies Métaboliques, Hôpital Debrousse, Lyon, France
Correspondence to: Professor Cochat, Département de Pédiatrie, Hôpital Edouard Herriot, 69437 Lyon cedex 03, France email: cochat@univ-lyon1.fr
Accepted 22 March 2000
| The first 150 words of the full text of this article appear below. |
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Introduction |
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Primary hyperoxalurias (PH) are very rare diseases characterised by overproduction and accumulation of oxalate in the body. The main target organ is the kidney, as oxalate cannot be metabolised and is excreted in the urine, leading to nephrocalcinosis, recurrent urolithiasis, and subsequent renal impairment. During the last decade, major advances in enzymology, molecular genetics, and cell biology have generated excellent reviews on both pathophysiology and management1 2; however, specific questions remain unanswered.
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Urinary oxalate |
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Basically, hyperoxaluria (normal urinary oxalate < 0.5 mmol/1.73 m2 per day; normal urinary oxalate to creatinine ratio
< 0.10 mmol/mmol) and calcium oxalate crystallisation are the
hallmarks of any kind of PH.1 The presence of monohydrated
calcium oxalate crystals in the urine or tissues can be assessed by
infrared spectrometry or polarised light microscopy.3
Hyperoxaluria may be associated with increased urinary excretion of
either glycolate in PH1 or L-glycerate in PH2, but urinary
metabolites are no longer adequate for accurate
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