title: Antihuman immunoglobulin affinity immunoadsorption strongly decreases proteinuria in patients with relapsing nephrotic syndrome.
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) reduces proteinuria in relapsing patients. To investigate whether the factor(s) that give rise to albuminuria are bound directly to protein A in the immunoadsorption procedure or are part of a complex with Ig, four patients with relapse of focal glomerulosclerosis presenting as nephrotic syndrome after transplantation were treated, sequentially, using a (non-protein A) anti-Ig affinity column and a protein A column. This study reports that the effect on proteinuria of immunoadsorption using 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' plasma of a factor capable of altering the albumin permselectivity of isolated glomeruli in vitro. This study demonstrates for the first time that immunoglobulins have a role in the nephrotic syndrome. In addition, the fact that the two different immunoadsorption procedures both resulted in the removal of the same putative albuminuric factor in these patients and that no autoreactivity of eluted immunoglobulins was observed on human tissues strongly suggests that the factor or factors that may be responsible for immediate nephrotic syndrome after transplantation are bound to an immunoglobulin. However, no firm evidence can be yet provided against a direct role of immunoglobulins.
authors.affiliation: Institut de Transplantation et de Recherche en Transplantation and Institut National de la Santé et de la Recherche Médicale, Unit 437, Nantes, France.
authors.forename: J
authors.initials: J
authors.lastname: Dantal
authors.forename: Y
authors.initials: Y
authors.lastname: Godfrin
authors.forename: R
authors.initials: R
authors.lastname: Koll
authors.forename: S
authors.initials: S
authors.lastname: Perretto
authors.forename: J
authors.initials: J
authors.lastname: Naulet
authors.forename: J F
authors.initials: JF
authors.lastname: Bouhours
authors.forename: J P
authors.initials: JP
authors.lastname: Soulillou
mesh_terms: D000328:Adult; D000419:Albuminuria / Q000378:metabolism / Q000517:prevention & control; D000961:Antilymphocyte Serum / Q000627:therapeutic use*; D002463:Cell Membrane Permeability / Q000276:immunology / Q000502:physiology; D005260:Female; D005500:Follow-Up Studies; D005923:Glomerulosclerosis, Focal Segmental / Q000473:pathology / Q000628:therapy; D006084:Graft Rejection / Q000378:metabolism / Q000517:prevention & control*; D006085:Graft Survival; D006801:Humans; D007163:Immunosorbent Techniques; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D007678:Kidney Glomerulus / Q000187:drug effects / Q000378:metabolism; D016030:Kidney Transplantation / Q000009:adverse effects / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000473:pathology / Q000628:therapy*; D011507:Proteinuria / Q000378:metabolism / Q000517:prevention & control*; D012008:Recurrence; D006435:Renal Dialysis; D013205:Staphylococcal Protein A / Q000378:metabolism*; D016896:Treatment Outcome
chemical_list: D000961:Antilymphocyte Serum; D007166:Immunosuppressive Agents; D013205:Staphylococcal Protein A