What is IgA nephropathy?
IgA nephropathy (IgAN, pronounced “I-Gan”) is a rare kidney condition that occurs when a protein called Immunoglobulin A (IgA) gets ‘trapped’ in the filters of the kidneys and causes inflammation and damage. This affects the kidneys’ ability to clear waste from the body.
IgAN affects around 1 in 50,000 people in the UK. It is one of the most common causes of chronic kidney disease and kidney failure. Men are more likely to be affected than women.
IgAN is also known as Berger’s disease.
What are the signs and symptoms of IgAN?
Some people with IgAN do not have any symptoms. For those who do, the common symptoms are:
- Blood in the urine (haematuria) – the urine may look red or dark brown (like a cola drink). This is more likely to occur after an infection such as a cold or sore throat and usually fades after a few days. The haematuria may also be invisible to the naked eye but seen under a microscope when the urine is tested (microscopic haematuria).
- Protein in the urine (proteinuria) – this is likely to only be seen under a microscope but if there a lot of protein, the urine may look frothy
- Swelling or puffiness (oedema) in different parts of the body, especially around the eyes, legs and feet
- High blood pressure – this can damage the structure of the kidney if it is not treated.
What causes IgAN?
IgAN is caused by increased production of the Immunoglobulin A protein, which is produced by the immune system to fight infections in the body. In people with IgAN, this protein gets stuck in the microscopic blood vessels of the kidney (glomeruli). Over time the protein builds up and damages the glomeruli. This stops the kidneys from working properly.
How is IgAN diagnosed?
IgAN is often diagnosed after a routine urine test shows signs of blood and/or protein. A kidney biopsy may then be conducted. This can confirm the diagnosis by showing IgA deposits in the glomeruli when they are examined under a microscope.
IgAN is usually diagnosed in young adults, although it often goes unrecognised for long periods of time before diagnosis.
Does IgAN affect other parts of the body?
IgAN only affects the kidneys, but it is related to another condition called IgA vasculitis, (previously known as Henoch Schonlein Purpura or HSP) that can affect the skin, gut and joints, as well as the kidneys.
Does IgAN run in families?
IgAN can occasionally run in families, although no genetic basis has yet been found. It is likely that a range of genetic and environmental factors contribute to the development of the condition. However, the exact factors involved have not yet been identified.
How is IgAN treated?
Some people with IgAN do not need any treatment and the condition remain stable over time.
If treatment is needed, the initial aim is to protect kidney function by lowering blood pressure via lifestyle measures such as losing weight, stopping smoking and reducing salt in the diet.
Blood pressure medication may also be prescribed, such as angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs).
If you have protein in the urine, you may be prescribed blood pressure medication, even if you do not have high blood pressure.
SGLT2 (sodium-glucose co-transporter 2) inhibitors, are also often prescribed to slow the progression of IgAN.
If such supportive treatment methods do not help, immunosuppressants such as steroids may be prescribed, to dampen the immune system.
Targeted-release budesonide can help to slow the decline of kidney function by reducing the amount of the IgA protein that builds up in the kidneys.
In most people, kidney function deteriorates slowly. Around 1 in 3 people with IgAN will require dialysis and/or transplant within around 20 years.
Where can I get more information or support about IgAN?
For more information on IgAN, including its diagnosis, symptoms and treatment, visit the Leicester IgAN Research Group.
There are currently a number of clinical trials taking place to research further treatment options for IgAN. Talk to your kidney team for more information.
Publication date: 1/2025
Review date: 1/2028
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