Updated on November 11, 2026.
Immunoglobulin A nephropathy (IgAN) is a disorder that damages the kidneys, a pair of fist-sized organs that act as filters for the blood. Here are five things to know about IgAN, including the potential causes and potential complications.
How does IgAN damage the kidneys?
IgAN does not damage the kidneys directly. IgAN begins with a problem with the immune system and the formation of abnormal immunoglobulin A proteins. These proteins normally help fight off infections in the respiratory system and digestive tract.
When a person has IgAN, the body produces abnormal immunoglobulin A, the immune system produces antibodies to try to get rid of the defective immunoglobulin A, and these proteins clump together. These clumps of proteins circulate in the blood, become stuck in the tiny blood vessels inside the kidneys, and form clogs.
The immune system responds to these clogs by releasing inflammatory chemicals and activating various immune pathways. It’s this immune response that causes inflammation, damage, and sometimes scarring in the kidneys.
Why does IgAN cause urine to change color?
Some of the most common symptoms of IgAN are hematuria (blood in the urine) and proteinuria (protein in the urine). These symptoms occur as blood and protein leak through damaged filtering units inside the kidneys and end up in urine.
In the early stages of IgAN, hematuria and proteinuria may be invisible, and only detectable with a urinalysis test. As the disease progresses, urine may be foamy or change color, appearing pink, reddish, dark brown, cola-colored, or tea-colored.
What causes IgAN?
The majority of IgAN cases have no identifiable cause. This is referred to as sporadic, idiopathic, or primary IgAN.
Primary IgAN is thought to occur due to a combination of genetics and environmental factors. In this scenario, genetics would predispose an individual to having IgAN, while an environmental factor, such as an infection, triggers a response from the immune system that leads to the production of abnormal IgAN.
While genetics appear to predispose some people to having IgAN, only a small percentage of overall cases involve specific gene variations that have been identified.
Can IgAN be caused by another condition?
Secondary IgAN occurs as a result of another health condition or as a side effect from certain drugs. Liver disease, Celiac disease, inflammatory bowel disease (IBD), psoriasis, certain autoimmune disorders, and upper respiratory infections have all been associated with secondary IgAN.
The use of blood thinners and medications that act on the immune system—including some drugs that treat inflammatory disorders like psoriasis and IBD—have also been associated with secondary IgAN.
What complications can IgAN cause?
The severity of IgAN varies from person to person. Some people only experience mild symptoms. Others progress to end-stage renal disease. As IgAN progresses, potential complications can include:
- Hypertension, or chronically high blood pressure
- Edema, swelling due to fluid buildup, often affecting the lower limbs and/or face
- Anemia, or low red blood cell counts
- Heart failure, where the heart cannot pump enough blood
- Pulmonary edema, a buildup of fluid in the lungs that is often caused by heart failure
- End-stage renal disease (kidney failure), where the kidneys no longer work well enough to keep a person alive
Preventing complications is an important goal of treatment. There is no cure for IgAN, and treatment focuses on managing symptoms and protecting kidney function.
Treatment plans typically include medications to control blood pressure and proteinuria, as well as reducing salt intake (which helps with blood pressure), quitting smoking (for anyone who smokes), and other lifestyle changes that benefit kidney health.
Distinguishing between primary and secondary IgAN is a critical step in diagnosis and treatment. Treatment for primary IgAN can include medications to control inflammation and immune system activity, while treatment for secondary IgAN focuses on addressing the underlying cause.
