ANTIHUMAN IMMUNOGLOBULIN AFFINITY IMMUNOADSORPTION STRONGLY DECREASESPROTEINURIA IN PATIENTS WITH RELAPSING NEPHROTIC SYNDROME

Citation
J. Dantal et al., ANTIHUMAN IMMUNOGLOBULIN AFFINITY IMMUNOADSORPTION STRONGLY DECREASESPROTEINURIA IN PATIENTS WITH RELAPSING NEPHROTIC SYNDROME, Journal of the American Society of Nephrology, 9(9), 1998, pp. 1709-1715
Citations number
27
Categorie Soggetti
Urology & Nephrology
ISSN journal
10466673
Volume
9
Issue
9
Year of publication
1998
Pages
1709 - 1715
Database
ISI
SICI code
1046-6673(1998)9:9<1709:AIAISD>2.0.ZU;2-V
Abstract
Approximately 20 to 30% of patients with idiopathic nephrotic syndrome and focal glomerulosclerosis experience a relapse of their nephrotic syndrome after transplantation. Previously, it has been shown that ex vivo immunoadsorption on protein A strongly (although transiently) red uces proteinuria in relapsing patients. To investigate whether the fac tor(s) that give rise to albuminuria are bound directly to protein A i n the immunoadsorption procedure or are part of a complex with Ig, fou r patients with relapse of focal glomerulosclerosis presenting as neph rotic syndrome after transplantation were treated, sequentially, using a (non-protein A) anti-Ig affinity column and a protein A column. Thi s study reports that the effect on proteinuria of immunoadsorption usi ng an anti-Ig immunoaffinity column is comparable in its magnitude and kinetics to that of immunoadsorption on protein A. The two procedures were also equally effective in depleting the relapsing patients' plas ma of a factor capable of altering the albumin permselectivity of isol ated glomeruli in vitro. This study demonstrates for the first time th at immunoglobulins have a role in the nephrotic syndrome. In addition, the fact that the two different immunoadsorption procedures both resu lted in the removal of the same putative albuminuric factor in these p atients and that no autoreactivity of eluted immunoglobulins was obser ved on human tissues strongly suggests that the factor or factors that may be responsible for immediate nephrotic syndrome after transplanta tion are bound to an immunoglobulin. However, no firm evidence can be yet provided against a direct role of immunoglobulins.