Sizing up sialic acid in glomerular disease

Susan E. Quaggin*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

20 Scopus citations


A new study by Galeano and colleagues in this issue of the JCI reports the first glomerular disease caused by a genetic defect in sialic acid biosynthesis (see the related article beginning on page 1585). Mice that harbor mutations in the Gne/Mnk gene produce lower amounts of sialic acid, suffer from hematuria, proteinuria, and structural defects in the glomerulus and die within days after birth. Remarkably, the lesion can be reversed through dietary addition of N-acetylmannosamine, a sialic acid precursor, raising the intriguing possibility that this approach might have therapeutic benefit in patients with glomerular disease.

Original languageEnglish (US)
Pages (from-to)1480-1483
Number of pages4
JournalJournal of Clinical Investigation
Issue number6
StatePublished - Jun 1 2007

ASJC Scopus subject areas

  • General Medicine


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