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Potential mechanisms of marked hyperoxaluria not due to primary hyperoxaluria I or II.

Authors
  • Monico, Carla G1
  • Persson, Mai
  • Ford, G Charles
  • Rumsby, Gill
  • Milliner, Dawn S
  • 1 Division of Nephrology, General Clinical Research Center, Mayo Clinic Rochester, Minnesota 55905, USA. [email protected]
Type
Published Article
Journal
Kidney international
Publication Date
August 2002
Volume
62
Issue
2
Pages
392–400
Identifiers
PMID: 12110000
Source
Medline
License
Unknown

Abstract

These patients illustrate a novel form of hyperoxaluria and urolithiasis, without excess Diet(ox), enteric hyper-absorption, or hepatic AGT, GR/HPR deficiency. Alterations in pathways of oxalate synthesis, in liver or kidney, or in renal tubular oxalate handling are possible explanations. The affected sibling pair suggests an inherited basis.

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