Albuminuria associated with CD2AP knockout mice is primarily due to dysfunction of the renal degradation pathway processing of filtered albumin

Leileata M. Russo, Subhashini Srivatsan, Matthew Seaman, Hani Suleiman, Andrey S. Shaw, Wayne D. Comper

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

Here we address the assumption that the massive intact albuminuria accompanying mutations of structural components of the slit diaphragm is due to changes in glomerular permeability. The increase in intact albumin excretion rate in Cd2ap knockout mice by >100-fold was not accompanied by equivalent changes in urine flow rate, glomerular filtration rate or increases in dextran plasma clearance rate, which demonstrates that changes in glomerular permeability alone could not account for the increase in intact albumin excretion. The albuminuria could be accounted for by inhibition of the tubule degradation pathway associated with degrading filtered albumin. There are remarkable similarities between these results and all types of podocytopathies in acquired and toxin-induced renal disease, and nephrotic states seen in mice with podocyte mutations.

Original languageEnglish
Pages (from-to)3738-3741
Number of pages4
JournalFEBS Letters
Volume587
Issue number22
DOIs
StatePublished - Nov 15 2013

Keywords

  • Albumin degradation
  • Albuminuria
  • Glomerular permeability
  • Transgenic mice

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