Abstract
Primary focal segmental glomerulosclerosis (FSGS) accounts for nearly 10 % of patients who require renal replacement therapy. Elevated circulating levels of soluble urokinase receptor (suPAR) have been identified as a biomarker to discriminate primary FSGS from other glomerulopathies. Subsequent reports have questioned the diagnostic utility of this test. In a study in BMC Medicine, Huang et al. demonstrate that urinary soluble urokinase receptor (suPAR) excretion assists in distinguishing primary FSGS from other glomerular diseases, and that high plasma suPAR concentrations are not directly linked to a decline in glomerular filtration rate (GFR). This observation suggests that further investigation of suPAR is warranted in patients with FSGS. It should be interpreted in light of a recent report that B7-1 is expressed in the podocytes of a subset of patients with FSGS, and that blocking this molecule may represent the first successful targeted intervention for this disease. These advances highlight the rapid pace of scientific progress in the field of nephrology. Nephrologists should work together, share resources, and expedite the design of protocols to evaluate these novel biomarkers in a comprehensive and scientifically valid manner.Please see related article http://www.biomedcentral.com/1741-7015/12/81.
Highlights
There appears to be a basic drive in human beings to try to become members of teams
focal segmental glomerulosclerosis (FSGS) is an important cause of glomerular disease in children and adults, and accounts for nearly 10% of patients who develop end stage kidney disease
The current position of suPAR in the setting of glomerular disease has been succinctly summarized in a recent, balanced editorial commentary [24]
Summary
There appears to be a basic drive in human beings to try to become members of teams. It is part of our nature as social animals to define ourselves based on our self-perception of who we are and how we differ from those outside our group [1]. The molecule appeared to be more than an epiphenomenon in FSGS, because in vitro studies indicated that suPAR binds to β3 integrin in the podocyte membrane, activates intracellular signaling, promotes foot process effacement, and disrupts glomerular barrier function, leading to proteinuria [7]. This exciting observation was followed by several supportive reports [9,10,11]. The community is splitting up into teams: those who consider suPAR, B7-1, or other favorite candidates to be the main causal factor for FSGS
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