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NDT Advance Access originally published online on July 4, 2006
Nephrology Dialysis Transplantation 2006 21(8):2063-2064; doi:10.1093/ndt/gfl305
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Editorial Comment

Is liver analysis still required for the diagnosis of primary hyperoxaluria type 2?

Gill Rumsby

Clinical Biochemistry, UCL Hospitals, London, UK

Correspondence and offprint requests to: Gill Rumsby, PhD, FRCPath, Clinical Biochemistry, UCL Hospitals, 60 Whitfield St, London W1T 4EU, UK. Email: gill.rumsby@uclh.nhs.uk

Keywords: glyoxylate reductase; GRPHR; primary hyperoxaluria type 2 (PH2)

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The primary hyperoxalurias (PH) are inherited disorders of glyoxylate metabolism, leading to endogenous oxalate overproduction and the inevitable precipitation of calcium oxalate, leading to renal stones and/or nephrocalcinosis and renal failure. Type 1 PH (PH1) is caused by deficiency of alanine: glyoxylate aminotransferase (AGT), while the type 2 disease (PH2) is due to lack of glyoxylate reductase/hydroxypyruvate reductase (GRHPR). While AGT is liver-specific, GRHPR is ubiquitously expressed although predominantly in the liver [1,. . . [Full Text of this Article]


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