Challenges in IgA Nephropathy Management: An Era of Complement Inhibition

Tesař, Vladimı́r; Charu, Vivek; Barratt, Jonathan

doi:10.1016/j.ekir.2023.06.010

Cited by 5 publications

(2 citation statements)

References 81 publications

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“… 24 Finally, because numerous therapies aiming to inhibit the different complement pathways are in the pipeline, complement inhibition might be valuable in patients with an aggressive MPGN pattern. 25 …”

Section: Discussionmentioning

confidence: 99%

Clinical Presentation, Pathological Spectrum, and Outcomes of Alcoholic Cirrhosis-Related Immunoglobulin A Nephropathy

Ronsin,

Braud,

Kandel-Aznar

et al. 2024

Kidney International Reports

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Section: Discussionmentioning

confidence: 99%

Clinical Presentation, Pathological Spectrum, and Outcomes of Alcoholic Cirrhosis-Related Immunoglobulin A Nephropathy

Ronsin,

Braud,

Kandel-Aznar

et al. 2024

Kidney International Reports

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“…Moreover, it should be mentioned that pegcetacoplan (APL-2), which is a PEGylated, lab-made peptide derivative of compstatin that prevents the cleavage and activation of C3 (NCT03453619) [58,59] and vemircopan (ALXN2050), is an oral factor D inhibitor that inhibits the alternative pathway in a near-complete and sustained manner (NCT05047458 and NCT05047484) [60,61].…”

Section: Inhibitors Of Complement Cascadesmentioning

confidence: 99%

Refractory IgA Nephropathy: A Challenge for Future Nephrologists

Di Leo,

Annese,

Papadia

et al. 2024

Medicina

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IgA nephropathy (IgAN) represents the most prevalent form of primary glomerulonephritis, and, on a global scale, it ranks among the leading culprits behind end-stage kidney disease (ESKD). Presently, the primary strategy for managing IgAN revolves around optimizing blood pressure and mitigating proteinuria. This is achieved through the utilization of renin–angiotensin system (RAS) inhibitors, namely, angiotensin-converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARBs). As outlined by the KDIGO guidelines, individuals who continue to show a persistent high risk of progressive ESKD, even with comprehensive supportive care, are candidates for glucocorticoid therapy. Despite these therapies, some patients have a disease refractory to treatment, defined as individuals that present a 24 h urinary protein persistently >1 g after at least two rounds of regular steroids (methylprednisolone or prednisone) and/or immunosuppressant therapy (e.g., mycophenolate mofetil), or who do not tolerate regular steroids and/or immunosuppressant therapy. The aim of this Systematic Review is to revise the current literature, using the biomedical database PubMed, to investigate possible therapeutic strategies, including SGLT2 inhibitors, endothelin receptor blockers, targeted-release budesonide, B cell proliferation and differentiation inhibitors, fecal microbiota transplantation, as well as blockade of complement components.

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