Immunoadsorption in SLE: three different high affinity columns are adequately effective in removing autoantibodies and controlling disease activity.
BACKGROUND
Pathogenic autoantibodies (Abs) are a hallmark of SLE and their rapid removal is beneficial in active SLE. Immunoadsorption (IAS) is effective in removing serum levels of all classes of immunoglobulin (Ig), immune complexes (IC) and anti-dsDNA Abs and appears superior to plasmapheresis with respect to side effects. IAS can be performed with different columns, which use different ligands to bind their target. In particular, high affinity columns are in the focus of interest. Their ligands are either sheep IgG directed against human Ig (Ig-column, Ig-Therasorb®), or staphylococcal Protein A (ProtA-column, Immunosorba®), or the synthetic peptide Gam146 (GAM-column, Globaffin®). In our experience Ig-columns have been effective in treating active renal SLE. However, no analysis has so far been published on which column type should be preferred in treating SLE patients.


METHODS
Among our SLE patients maintained on prolonged IAS therapy, we identified those with stable renal SLE and low to moderate disease activity who were successfully treated by using Ig-columns. Six of these patients were switched to ProtA-columns, keeping the rest of the protocol and the medication constant. In addition, two patients were switched from Ig- to GAM-columns.


RESULTS
All types of columns significantly lowered the serum levels of IgG, IgM, and anti-dsDNA Abs. Disease activity was constantly low before and after the switch, as were parameters of renal function. In addition, patients with highly active disease were effectively treated when ProtA- (n=6) or GAM-columns (n=1) were used as first-line extracorporeal treatment.


CONCLUSIONS
Our data demonstrate that all columns are adequately effective in controlling key parameters of SLE. Thus, it is not the type of the ligand, but only the outcome, i.e. the successful removal of Ig, IC, and (auto-) Abs that is required for controlling SLE activity.
Division of Nephrology, Dept. of Internal Medicine III, Medical University of Vienna, Austria.
P
P
Biesenbach
S
S
Schmaldienst
J S
JS
Smolen
W H
WH
Hörl
K
K
Derfler
G H
GH
Stummvoll
D000328:Adult; D000704:Analysis of Variance; D000974:Antibodies, Antinuclear / Q000097:blood; D001317:Austria; D001323:Autoantibodies / Q000097:blood*; D001666:Binding Sites, Antibody; D015415:Biomarkers / Q000097:blood; D001781:Blood Component Removal / Q000009:adverse effects / Q000295:instrumentation*; D004867:Equipment Design; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D007163:Immunosorbent Techniques / Q000009:adverse effects / Q000295:instrumentation*; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000276:immunology / Q000628:therapy*; D008181:Lupus Nephritis / Q000097:blood / Q000276:immunology / Q000628:therapy*; D010455:Peptides / Q000378:metabolism; D011507:Proteinuria / Q000097:blood / Q000276:immunology / Q000628:therapy; D012189:Retrospective Studies; D013205:Staphylococcal Protein A / Q000378:metabolism; D013997:Time Factors; D016896:Treatment Outcome; D055815:Young Adult
D000974:Antibodies, Antinuclear; D001323:Autoantibodies; D015415:Biomarkers; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D010455:Peptides; D013205:Staphylococcal Protein A