Anti-PLA2R autoantobodies can provide important information on the clinical activity of MN. Different studies have shown that disease course and therapy success in patients with pMN can be assessed by monitoring of the anti-PLA2R antibody titer.
For example, patients with acute nephrotic syndrome (high protenuria) showed high anti-PLA2R titers; with spontaneous remission or remission due to treatment (low protenuria), however, the titers decreased to below the detection limit. In patients with initially high titers, spontaneous remission occurred much less frequently than in patients with low titers. Moreover, a relapse of the pMN was associated with an increase in the antibody level. From these observations, the authors concluded that the antibody level also reflects the severity of the pMN.1,2
The anti-PLA2R titer is also useful for therapy monitoring. In patients who respond well to immunosuppressive treatment, it decreases. With a relapse of the disease, the antibody titer increases again.3,4 Moreover, a high anti-PLA2R titer was identified as a risk factor for patients not achieving a remission of proteinuria by the treatment.
As is shown clearly by the study of Beck et al., the immediate immunological responde to therapy is much stronger than the clinical reaction. For example, titers of anti-PLA2R autontibodies in patients responding to immunosuppresive treatment decreased months prior to a decrease in proteinuria.3 Hoxha et al. found the same in the investigated patients: a reduction of the anti-PLA2R titers by 81% within 3 months after the start of immunosuppressive treatment. At the same time, the proteinuria decreased by around 39%.4
Despite the obvious link, the anti-PLA2R titer as an immunological marker should be observed apart from the proteinuria which acts as a clinical marker. Based on the chronological order of these events in the pMN pathogenesis known so far, it must be assumed that the markers react similarly over the disease course, but with a time lag.
In around 40% of pMN patients, the disease reappears after kidney transplantation.6 The risk of recurrence is especially high if anti-PLA2R autoantibodies persist over a time period of six months after the organ transplant.7 As part of the risk assessment the titer can help to determined the necessity and intensity of immunosuppressive treatment after kidney transplantion in order to prevent a relapse.
1Hofstra et al., Clin J Am Soc Nephrol 6, 1286-1291 (2011)
2Hofstra et al., Clin J Am Soc Nephrol 23, 1735-1743 (2012)
3Beck et al., J Am Soc Nephrol 22, 1543-1550 (2011)
4Hoxha et al., J Am Soc Nephrol 25, 1357-1366 (2014)
5Beck et Salant, Kidney Int 77, 765-770 (2010)
6El-Zoghby et al., Am J Transplant 9, 2800-2807 (2009)
7Seitz-Polski et al., Nephrol Dial Tranplant 0, 1-9 (2014)
8Hofstra et al., Nat Rev Nephrol 9, 443-458 (2013)