Activation of complement in crescentic IgA nephropathy

Abstract

IgA nephropathy (IgAN) has become the most prevalent form of glomerulonephritis affecting almost 1.3% of the total population worldwide. It is an autoimmune disorder where the host autoantibody forms an immune complex with the defective galactose-deficient IgA1 and gets deposited at the mesangium and endocapillary region of glomeruli. IgA has the capability to activate alternative and lectin complement cascades which even aggravates the condition. Properdin is directly associated with IgAN by activating and stabilising the alternative complement pathway at the mesangium, thereby causing progressive renal damage.The present review mainly focuses on correlating the influence of properdin in activating the complement cascade at glomeruli which is the major cause of disease exacerbation. Secondly, we have described the probable therapies and new targets that are under trials to check their efficacy in IgAN.An in-depth research was carried out from different peer-reviewed articles till December 2020 from several renowned databases like PubMed, Frontier, and MEDLINE, and the information was analysed and written in a simplified manner.Co-deposition of properdin is observed along with IgA and C3 in 75%–100% of the patients. It is not yet fully understood whether properdin inhibition can attenuate IgAN, as many conflicting reports have revealed worsening of IgAN after impeding properdin.With no specific cure still available, the treatment strategies are of great concern to find a better target to restrict the disease progression. More research and clinical trials are required to find out a prominent target to combat IgAN.