Autoimmune Glomerular Diseases

IgA Nephropathy (IgAN), also known as Berger’s disease, damages the glomeruli (tiny filters) within the kidneys. In individuals with IgAN, modified IgA proteins and others accumulate, forming clumps that harm the glomeruli and, consequently, the kidneys. Regulating these proteins may reduce kidney damage. A medication is being explored for its potential to regulate the immune system by inhibiting plasma cells and B-cells from producing IgA.

Similarly, IgA Vasculitis with Nephritis (IgAVN), formerly known as Henoch Schonlein Purpura (HSP), is a disease affecting both blood vessels and kidneys. Like IgAN, IgA proteins damage the glomeruli, but IgAVN also causes widespread inflammation, potentially leading to skin rashes (purpura), impaired intestinal blood flow, or joint inflammation.

Primary Membranous Nephropathy (pMN) causes the kidney’s glomeruli to become permeable, leading to significant protein leakage into the urine. This extensive protein loss results in low blood albumin and bodily swelling. Antibodies, proteins produced by the immune system to combat infections, can in some cases mistakenly target parts of the body, causing autoimmune diseases like pMN.

Minimal Change Disease (MCD) and Focal Segmental Glomerulosclerosis (FSGS) are a group of diseases characterized by leaky glomeruli, resulting in high levels of protein in the urine, leading to low albumin and swelling (nephrotic syndrome). This protein leakage and swelling can fluctuate even with treatment. The immune system is believed to be the cause of the leaky filter in some cases. The purpose of this study is to investigate the effects of a study drug on mitigating kidney damage in individuals with IgAN/IgAVN, pMN, or MCD/FSGS.