Innovative Treatments for ANCA-Associated Vasculitis

ANCA-associated vasculitis is a group of autoimmune diseases that cause inflammation in small blood vessels. Its two varieties are granulomatosis with polyangiitis and microscopic polyangiitis. Untreated, these conditions may lead to deadly complications such as kidney failure and lung damage. For years, the use of glucocorticoids and immunosuppressive drugs such as cyclophosphamide and rituximab was predominant in the management of AAV. Though these therapies have become life-saving, their severe side effects, particularly the long-term administration of glucocorticoids, have driven research into developing more effective and less toxic therapies. Recently, new therapies have emerged that not only reduce disease burden but also minimize treatment-related complications. Some of these emerging therapies are discussed below in the context of ANCA-associated vasculitis.

ANCA-Associated Vasculitis: Challenges in Treatment

The current therapy for AAV is high-dose glucocorticoids combined with either cyclophosphamide or rituximab. While these treatments have been helpful for most patients who went into remission, they are certainly also accompanied by severe limitations. Glucocorticoids are toxic on their own, even at low doses, with a long list of adverse effects, including infections, osteoporosis, hypertension, and diabetes. Long-term usage leads to the massive impairment of the quality of life and considerable morbidity.

Remission induction stays of old include cyclophosphamide and rituximab; however, each comes with its own complications. Cyclophosphamide is very effective but does carry with it risks to fertility, cancer, and bladder toxicity. Rituximab, the anti-CD20 monoclonal antibody, has successfully replaced cyclophosphamide for patients with relapsing disease, although with some risks too, including infections and infusion reactions. Considering these limitations, glucocorticoid-sparing treatments that provide as little use of glucocorticoids as possible coupled with more targeted and less toxic treatment alternatives are badly needed .

Avacopan: The Glucocorticoid-Sparing Agent

The most significant advancement in the AAV arena lately has been the selective avacopan, which is a C5a receptor inhibitor. C5a represents one of the most potent pro-inflammatory mediators involved with the activation of neutrophils and inflammation and destruction seen in AAV. This is manifested through the disruption of the inflammatory cascade responsible for the disease caused by decreased neutrophil activation and subsequent migration.

In a randomized controlled trial of patients with AAV, avacopan was compared with standard glucocorticoid therapy. The participants were assigned to receive either avacopan or oral prednisone in combination with standard immunosuppressive treatment with cyclophosphamide or rituximab. The two major endpoints were remission at 26 weeks and sustained remission at 52 weeks.

Remission at 26 weeks was comparable between the groups, with 72.3% of patients on avacopan achieving remission versus 70.1% on prednisone. But at 52 weeks of sustained remission, avacopan offers a very clear advantage, with 65.7% of patients on avacopan achieving sustained remission versus 54.9% on prednisone. This means avacopan spares the patients from glucocorticoid side effects and brings more sustained disease control.

The safety profile of avacopan was also favorable, with fewer serious AEs than in the prednisone group, making it a drug of choice for those intolerant to glucocorticoids or at high risk for steroid complications.

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Rituximab and Plasma Exchange: Next Step—A Revisit to Combination Therapy

Rituximab has been established as the backbone of the treatment of AAV, particularly in patients with relapsing disease. The drug depletes B cells, which are integral to the synthesis of ANCA; hence, it is an efficient agent for inducing and maintaining remission. Plasma exchange and other treatments other than corticosteroid therapy are of unknown benefit in patients with significant renal impairment, and their use remains within the domain of investigation.

Plasma exchange, also known as plasmapheresis, refers to the removal of plasma from blood and substituting it with a plasma substitute. This would theoretically remove circulating ANCA antibodies, immune complexes, and other inflammatory mediators from circulation, thus decreasing the burden on the kidneys and other organs.

A retrospective cohort study addressed the question of which patients with severe renal involvement were better treated with rituximab or cyclophosphamide, with or without plasma exchange. It was reported that the proportions achieving remission at six months were similar between rituximab and cyclophosphamide, while plasma exchange added to neither of these treatments in raising the rates of remission substantially, nor did it decrease the risk of ESKD or mortality at 18 months.

This finding brought into question the paradigm of requiring plasmapheresis as the therapeutic intervention for patients with severe renal involvement. Though this might still be deemed helpful for particular clinical settings, such as lethal pulmonary hemorrhage, routine utilization in all patients with renal involvement of such severe severity would perhaps be assessed differently in light of the current findings.

C5 Convertase Blockade: The Therapeutic Targeting of Complement in ANCA Vasculitis

Another potential strategy that has emerged in the management of AAV is the blockade of the complement system, particularly C5 convertase. The complement pathway has a pivotal role in the immune response and has also been identified as a key driving force behind inflammation in AAV; consequently, disturbances in the complement pathway, particularly the alternative pathway, have been implicated in the pathogenesis of AAV.

The use of the monoclonal antibody eculizumab, directed against C5 convertase, was investigated in a clinical trial among patients with complement-mediated glomerulonephritis. disease that appears to share many characteristics with AAV. The drug resulted in a gross diminution of proteinuria and an improvement in renal function in some patients. On these grounds, blockade of the complement system may represent an interesting strategy for treatment in AAV, in particular among patients with evidence of complement-mediated renal involvement.

While primarily developed for atypical hemolytic uremic syndrome and paroxysmal nocturnal hemoglobinuria, the success of eculizumab in such complement-mediated diseases makes strong rationale for pursuing its role in AAV. Whether C5 blockade is similarly beneficial in AAV or specifically in patients with more severe renal or pulmonary disease remains an open question.

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Future Directions: Toward Personalized Treatment

Our understanding of AAV pathogenesis thus continuously evolves with new directions in terms of potentially more individualized treatments. The therapies, such as avacopan, are a far cry from the broad immunosuppressive strategies that had dominated treatment for decades.

Many such groups will be characterised with ambiguous comparison between symptomatic and asymptomatic infections, posing an interesting problem forward, which will be to identify the best patients for giving the new therapies and to decide whether certain patients may have genetic or molecular markers that make them more responsive to complement-targeted therapies versus others who are best approached by B cell depletion. The most important ongoing research into the molecular mechanism of AAV will aid in developing personalized treatment plans that maximize efficacy while minimizing toxicity.

In the future, research has to look beyond identifying predictors of response to treatment. Long-term safety and efficacy of the therapeutic agents have to be accessed. Whereas early data coming out on avacopan and other targeted therapies are promising, long follow-up studies would be needed to discern their impact on long-term outcomes such as relapse rates, kidney function, and overall survival.

Conclusion

With such new developments, avacopan opens a novel avenue of hope in the treatment of ANCA-associated vasculitis and provides an alternative option to patients who cannot tolerate traditional regimens or are at high risk for complications from steroid therapy. The therapeutic role of rituximab is still well established in relapsing disease; however, the place of plasma exchange in the seriously diseased patient needs to be reassessed in this new light of studies. This encompasses drugs aimed at complement components, including C5 convertase inhibitors, and is an exciting frontier for the treatment of AAV patients, predominantly those suffering from complement-mediated disease.

Thus, new pathways continue to be discovered in the pathogenesis of AAV, and any future research will produce a potential scope for even more personalized and targeted treatments. Indeed, these advances do not only enhance the control of the disease but they also minimize the burden of treatment-related side effects, thus improving the quality of life of patients and prognosis in the long term.

References

  1. Jayne, D.R., Merkel, P.A., Schall, T.J. and Bekker, P., 2021. Avacopan for the treatment of ANCA-associated vasculitis. New England Journal of Medicine384(7), pp.599-609.
  2. Moura, M.C., Irazabal, M.V., Eirin, A., Zand, L., Sethi, S., Borah, B.J., Winters, J.L., Moriarty, J.P., Cartin-Ceba, R., Berti, A. and Baqir, M., 2020. Efficacy of rituximab and plasma exchange in antineutrophil cytoplasmic antibody–associated vasculitis with severe kidney disease. Journal of the American Society of Nephrology31(11), pp.2688-2704.
  3. Smith, R.M., Jones, R.B., Specks, U., Bond, S., Nodale, M., Aljayyousi, R., Andrews, J., Bruchfeld, A., Camilleri, B., Carette, S. and Cheung, C.K., 2020. Rituximab as therapy to induce remission after relapse in ANCA-associated vasculitis. Annals of the rheumatic diseases79(9), pp.1243-1249.
  4. Ruggenenti, P., Daina, E., Gennarini, A., Carrara, C., Gamba, S., Noris, M., Rubis, N., Peraro, F., Gaspari, F., Pasini, A. and Rigotti, A., 2019. C5 convertase blockade in membranoproliferative glomerulonephritis: a single-arm clinical trialAmerican Journal of Kidney Diseases74(2), pp.224-238.
  5. Walsh, M., Merkel, P.A., Peh, C.A., Szpirt, W.M., Puéchal, X., Fujimoto, S., Hawley, C.M., Khalidi, N., Floßmann, O., Wald, R. and Girard, L.P., 2020. Plasma exchange and glucocorticoids in severe ANCA-associated vasculitis. New England Journal of Medicine382(7), pp.622-631.

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