Complement 3 glomerulopathy (C3G) and immunoglobulin A nephropathy (IgAN) kidney diseases are progressive glomerular conditions. Their treatments typically involve medications to control inflammation and reduce damage to the kidneys.

Complement 3 glomerulopathy (C3G) and immunoglobulin A nephropathy (IgAN) are rare conditions of chronic kidney disease (CKD). They’re glomerular disorders, meaning they stem from processes that affect your kidney’s filtration structures, the glomeruli.

In both C3G and IgAN, buildup inside the glomeruli cause inflammation and damage, limiting how well your kidneys can filter the blood stream.

Over time, the inflammation and damage results in CKD and related health challenges. C3G and IgAN can be treated, and receiving treatment as soon as possible can help preserve your kidney function.

C3G and IgAN are caused by different types of buildup in the glomeruli of the kidneys.

C3G is caused by a build-up of the protein C3, a protein produced by your body’s complement system, also known as the “complement cascade response.”

The complement system supports your immune system function in a number of ways. When it becomes dysregulated (impaired), as in C3G, C3 protein builds up in the glomeruli and leads to kidney damage.

Immune system dysfunction also causes IgAN. In IgAN, the buildup in the glomeruli is IgA, immunoglobulin A, an antibody produced by your white blood cells. In some, but not all cases, IgA may activate the complement cascade, also creating C3 deposits.

C3G and IgAN are different diagnoses, but as glomerular disorders they share common treatment approaches.

ACE inhibitors, angiotensin-converting enzyme inhibitors, are medications that help control your blood pressure by blocking enzymes that constrict blood vessels.

Angiotensin II receptor blockers (ARBs) also help reduce blood pressure. They work by promoting blood vessel relaxation and improving how well the heart pumps blood.

In C3G and IgAN, ACE inhibitors and ARBs help improve blood vessel capacity in the glomeruli and reduce the strain high blood pressure can put on the kidneys. These medications can also decrease proteinuria, or the amount of protein lost in the urine.

There are two main ways to manage inflammatory processes that lead to kidney damage in C3G and IgAN:

  • reducing the immune response leading to kidney deposits
  • calming inflammation caused by glomeruli buildup

Steroids are medications known for their ability to reduce inflammation. While prolonged use is no longer recommended for C3G and IgAN, short-term courses of steroids are sometimes paired with immunosuppressant medications.

C3G and IGAN are immune-mediated diseases. Their underlying causes stem from immune system dysfunction. Doctors use immunosuppressants to help manage atypical immune reactions in the body.

There are many different immunosuppressants that may be used depending on your diagnosis of C3G or IgAN.

According to a 2022 review on C3G, the effectiveness of immunosuppressant therapy is mixed in research, and some people living with C3G may see more benefit than others.

Since your complement system is a major component in C3G pathology, drugs that target complement cascade activation are an area of growing therapy interest.

Anti-complement drugs, such as eculizumab and ravulizumab, work by blocking certain phases of complement system activity, controlling the production of the protein C3.

The efficacy of anti-complement medications can vary between people and may not be applicable for all cases of glomerular kidney disease.

Not all diagnoses of IgAN, for example, will require complement inhibitor use, but if you’re experiencing C3 buildup, these medications may be a part of your treatment plan.

Plasma therapy, also known as plasmapheresis, is a treatment that uses a machine to filter your blood, separating out plasma from other types of cells. You’re then given a plasma substitute to replace what was removed.

The complement proteins responsible for C3G are contained in the plasma that was removed from your body. In addition to eliminating C3, plasma therapy can also remove immune complexes like IgA and autoantibodies, the antibodies that attack healthy cells.

Plasma therapy may not work for everyone. According to a 2019 review, no treatment is universally effective or considered a cure, and more detailed research into plasma therapy is lacking.

As kidney function deteriorates, your doctor may recommend more advanced treatments like dialysis.

Dialysis, like plasma therapy, involves machine-assisted blood filtration. In dialysis, the focus is on removing excess fluids and waste products, not plasma, from the blood.

Dialysis does not treat C3G or IgAN directly. It helps assist your body in waste removal when the kidneys are no longer functioning well enough.

In rare cases, kidney transplant may be an option. Because C3G and IgAN have underlying immunological causes and are not caused by the kidneys themselves, the use of transplantation in treatment is debatable.

For example, almost half of all kidney transplants for C3G fail.

The National Kidney Foundation notes that both C3G and IgAN might benefit from a reduction of dietary salt and protein to help ease the amount of waste your kidneys need to filter from the blood stream.

Although research is limited on the role of dietary supplements in treatment for these conditions, some evidence suggests omega 3-fatty acids in the form of fish oil supplements may offer anti-inflammatory benefits for IgAN.

As of 2021, budesonide (Tarpeyo), a corticosteroid, has been approved by the Food and Drug Adnministration (FDA) for the management of IgAN. By lowering the amount of protein in the urine, budesonide may lower the risk of end stage kidney disease.

More recently, sparsentan (Filspari) was approved by the FDA in 2023 and it also lowers protein in the urine.

Sodium-glucose cotransporter inhibitors, or SGLT-2 inhibitors, commonly used to manage diabetes may also benefit those with IgAN. In one analysis, dapagliflozin reduced the risk of end stage kidney disease and increased survival in people both with and without type 2 diabetes and IgAN.

According to, there are 20 clinical trials in various stages for CG3, including several that are currently recruiting.

If you’re interested in participating in clinical trials for C3G and IgAN, you can learn more by visiting:

There’s currently no cure for C3G or IgAN kidney disease. Both conditions are progressive, though treatment can slow or delay kidney damage.

According to a 2022 long-term outcome study, by 30 years after diagnosis, 20% to 50% of participants living with IgAN developed end stage kidney disease.

In C3G, progressive kidney damage is typically seen after 10 years, with up to half of patients experiencing end stage kidney disease by that time.

Because C3G and IgAN are rare and understudied conditions, it’s not yet possible to know how significantly treatment can improve overall prognosis.

As glomerular disorders, C3G and IgAN kidney diseases share a number of treatment approaches with the overall goal to control inflammatory processes and slow kidney damage.

Blood pressure drugs, immunosuppressants, and complement inhibitors may all be a part of your treatment plan.

Currently, there’s no universally effective treatment or cure for C3G or IgAN. Each therapy option may have varying effectiveness depending on the person being treated.