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DGKE Variants Cause a Glomerular Microangiopathy That Mimics Membranoproliferative GN
Journal article   Open access   Peer reviewed

DGKE Variants Cause a Glomerular Microangiopathy That Mimics Membranoproliferative GN

Fatih Ozaltin, Binghua Li, Alysha Rauhauser, Sung-Wan An, Oguz Soylemezoglu, Ipek Isik Gonul, Ekim Z. Taskiran, Tulin Ibsirlioglu, Emine Korkmaz, Yelda Bilginer, …
Journal of the American Society of Nephrology, Vol.24(3), pp.377-384
12/28/2012
DOI: 10.1681/ASN.2012090903
PMCID: PMC3582208
PMID: 23274426
url
https://doi.org/10.1681/ASN.2012090903View
Published (Version of record) Open Access

Abstract

Renal microangiopathies and membranoproliferative GN (MPGN) can manifest similar clinical presentations and histology, suggesting the possibility of a common underlying mechanism in some cases. Here, we performed homozygosity mapping and whole exome sequencing in a Turkish consanguineous family and identified DGKE gene variants as the cause of a membranoproliferative-like glomerular microangiopathy. Furthermore, we identified two additional DGKE variants in a cohort of 142 unrelated patients diagnosed with membranoproliferative GN. This gene encodes the diacylglycerol kinase DGKε, which is an intracellular lipid kinase that phosphorylates diacylglycerol to phosphatidic acid. Immunofluorescence confocal microscopy demonstrated that mouse and rat Dgkε colocalizes with the podocyte marker WT1 but not with the endothelial marker CD31. Patch-clamp experiments in human embryonic kidney (HEK293) cells showed that DGKε variants affect the intracellular concentration of diacylglycerol. Taken together, these results not only identify a genetic cause of a glomerular microangiopathy but also suggest that the phosphatidylinositol cycle, which requires DGKE , is critical to the normal function of podocytes.
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