1 Ploug Group, BRIC Research Groups, BRIC, Københavns Universitet2 Sorbonne Universités, UPMC Univ Paris 06, UMR_S 1155 - "Rare and common kidney diseases, matrix remodeling and tissue repair," Paris, France;3 unknown4 Ploug Group, BRIC, Faculty of Health and Medical Sciences, Københavns Universitet5 Ploug Group, BRIC, Faculty of Health and Medical Sciences, Københavns Universitet
Circulating levels of soluble forms of urokinase-type plasminogen activator receptor (suPAR) are generally elevated in sera from children and adults with FSGS compared with levels in healthy persons or those with other types of kidney disease. In mice lacking the gene encoding uPAR, forced increases in suPAR concentration result in FSGS-like glomerular lesions and proteinuria. However, whether overexpression of suPAR, per se, contributes to the pathogenesis of FSGS in humans remains controversial. We conducted an independent set of animal experiments in which two different and well characterized forms of recombinant suPAR produced by eukaryotic cells were administered over the short or long term to wild-type (WT) mice. In accordance with the previous study, the delivered suPARs are deposited in the glomeruli. However, such deposition of either form of suPAR in the kidney did not result in increased glomerular proteinuria or altered podocyte architecture. Our findings suggest that glomerular deposits of suPAR caused by elevated plasma levels are not sufficient to engender albuminuria.
Journal of the American Society of Nephrology : Jasn, 2014, Vol 25, Issue 8, p. 1662-1668