IgA nephropathy is a long-term kidney condition in which clumps of an antibody called immunoglobulin A build up in the kidney’s tiny filters, causing inflammation and, over time, loss of kidney function [1].
This page provides general information. It does not replace advice from a doctor or another qualified healthcare professional.
Each kidney holds about a million tiny filtering units, each built around a knot of very small blood vessels, called a glomerulus, that separates waste from the blood [1].
Immunoglobulin A, or IgA, is an antibody, a protein the immune system makes to recognize germs [1]. In IgA nephropathy the body makes a faulty version, treats it as foreign, and makes antibodies against it, and the two form clumps that lodge in the glomeruli [4]. The kidney responds with inflammation, and over years the filters scar, leaking blood and protein into the urine and clearing waste less well [1].
The condition is autoimmune, meaning the immune system harms the person’s own tissue, and is also called Berger’s disease [1]. It differs from IgA vasculitis, which involves the same antibody but also affects skin, joints and gut, and from IgA that collects in the kidney because of another illness [2,3].
IgA nephropathy is the most common primary glomerulonephritis in the world, though beyond that, honest figures are harder to give than most sources suggest [7,5].
About 1 in 10 kidney biopsies in the United States show IgA nephropathy [1]. In the United Kingdom it is estimated to affect around 1 in 50,000 people, counting those diagnosed [3]. Reported incidence, meaning new cases each year, ranges from 0.06 per 100,000 people in South Africa to 4.2 per 100,000 in Japan [6].
Rates are higher in East Asia and lower in Africa, rising from west to east and south to north across Eurasia, partly because of how genetic risk variants are spread among people of European and East Asian ancestry [5,6].
Part of it is a measurement problem. Most of what is known comes from kidney biopsy records, which reflect how often biopsies are done, and that varies enormously between countries because of screening programs, referral patterns and access to health care [5]. Mild disease that never reaches a biopsy never enters the figures [5]. The gap between regions is therefore part real biology, part unequal detection, and nobody can say how the two divide.
The cause is not known. Research points to a combination of genes, the instructions inside cells, and environment [1]. No single gene change causes it, and no genetic test can diagnose it [3]. The immune clumps that form around the altered IgA settle in the kidney filters [4,17] and switch on part of the immune system called the complement pathway, adding to the inflammation [16].
A relative with IgA nephropathy or IgA vasculitis makes it somewhat more likely, though most people have no affected relative and no inherited pattern has been established [1,3]. It is more common between ages 10 and 40, in men, and in people of East Asian or white European ancestry, and is linked with celiac disease, hepatitis, cirrhosis and HIV infection [1]. Nothing a person did caused it, and it cannot be prevented [1].
Many people have no symptoms for years, and the condition is often found by chance on a routine urine test [1,3]. Common symptoms are [1,3,4]:
Over time the condition can lead to long-term kidney disease, heavy protein loss with swelling, and eventually kidney failure [1,17].
When to seek urgent help. In a few people kidney function falls quickly, and a fall of half or more within three months is urgent [2]. Contact a doctor or kidney team without delay if the urine passed drops suddenly, swelling worsens over days, breathing becomes difficult, or visible blood in the urine comes with feeling unwell [2].
First come urine tests for blood and protein, a blood test estimating kidney filtering, and a blood pressure check [1,4]. Care then passes to a nephrologist, a kidney specialist.
A kidney biopsy is needed next. That means taking one or more very small pieces of kidney with a needle, under local anesthetic, to examine under a microscope. It is the only way to confirm IgA nephropathy, and guidance updated in 2025 suggests biopsy at 0.5 grams of protein a day or more so treatment can start earlier [2].
The biopsy is scored with the MEST-C system, grading five features of damage in and around the filters: extra cells in two places, two kinds of scarring, and crescent-shaped patches of inflammation [2]. Results feed into the International IgAN Prediction Tool, which estimates the risk of kidney function halving or failing and was developed and tested in nearly 4,000 people [7]. Guidelines advise using it to support shared conversations about risk, not to choose a medicine [2]. Diagnosis is often delayed, since blood and protein in the urine can go unnoticed for years [3].
There is no cure. Treatment now has two halves: calming the immune process that makes the faulty IgA, and limiting the damage already done [2].
The foundation. Guidelines set a blood pressure target of 120/70 mmHg or below, and advise not smoking or vaping, salt below 2 grams a day, weight management and exercise [2]. The first medicines are an ACE inhibitor or an angiotensin receptor blocker at the highest tolerated dose, used even when blood pressure is normal because they also cut protein loss, often alongside a statin to protect the heart [1,2,3]. The aim is protein loss below 0.5 grams a day, ideally below 0.3 [2].
Added kidney protection. An SGLT2 inhibitor, a tablet first developed for diabetes, is suggested for people at risk of losing kidney function [2,3]. Sparsentan blocks two pathways involved in kidney damage and replaces the ACE inhibitor or blocker; it has full United States approval and European authorization [2,13,14]. Atrasentan, a related tablet, is added to standard care under accelerated United States approval [15].
Reducing faulty IgA. Targeted-release budesonide is a nine-month course of capsules releasing a steroid in the gut where much of the faulty IgA is made, limiting effects elsewhere. It has full United States approval and European authorization as Kinpeygo [11,12].
Where steroids sit. This is genuinely contested. STOP-IgAN found that adding immunosuppression to well-optimized supportive care did not slow kidney function loss and caused more severe infections, weight gain and blood sugar problems [10]. TESTING did show fewer people losing kidney function, yet serious side effects at the original dose forced a switch midway to a lower dose with antibiotic cover [9]. Guidelines therefore use the reduced dose only, as a fallback where budesonide is unavailable [2].
Newer targeted medicines. Iptacopan, a tablet blocking the complement pathway, gained full United States approval in 2026 after showing slower kidney function decline over two years [16]. Sibeprenlimab and atacicept are injections blocking APRIL, a signal driving faulty IgA production, and in atacicept’s case BAFF as well; both have accelerated approval, cleared on protein in the urine with proof of kidney protection still to come [17,18]. Availability differs greatly between countries, and new medicines rarely reach lower-resource settings [2].
Most people are followed for years by a kidney team, with regular blood pressure checks and urine and blood tests tracking protein loss and filtering [2]. Daily habits count more here than in many conditions: not smoking or vaping, keeping salt down, staying a healthy weight and exercising all protect the kidneys [2].
Family planning needs a conversation in advance. Several of the usual medicines must be stopped before trying to conceive, and endothelin-blocking medicines can seriously harm a developing baby, so reliable contraception and monthly pregnancy tests are required while taking them [2]. Ask early, so blood pressure can be controlled on pregnancy-safe medicines first. A diagnosis this young is a lot to carry, which is why guidelines recommend pointing people toward patient organizations for peer support [2].
Clinical trials test whether a treatment works and is safe. IgA nephropathy is a very active research area, so studies come up reasonably often. Deciding whether to look into one is personal, and it helps to take it in steps.
It is worth being clear on what a study involves:
Every trial has rules about who can take part, called eligibility criteria. Some describe who can join, others who cannot. For an IgA nephropathy study, they might include a diagnosis confirmed by kidney biopsy, a certain amount of protein in the urine, a kidney filtering rate within a set range, a stable dose of an ACE inhibitor or blocker beforehand, blood pressure within limits, and reliable contraception for some medicines.
trialport’s medifit helps people consider information related to possible medical suitability. It does not diagnose a condition, confirm eligibility or replace formal screening by the study team.
Explore IgA nephropathy clinical trials through trialport
Medical suitability is only part of the picture. A study can look right on paper and still be hard in practice. Worth thinking through:
trialport’s readifit helps people reflect on their understanding, motivation, time, routines, support, emotions and practical arrangements.
Useful questions to put to a research team:
Taking part is voluntary. A person can ask questions, speak with people they trust and choose not to participate.
Search for clinical trials at app.trialport.com.
Research has moved faster in the past five years than in the previous fifty:
Study status checked: 3 August 2026. Research moves quickly and what is studied changes, so this list will date. For current information, search at app.trialport.com.
In the United States, the IgA Nephropathy Foundation is the main condition-specific organization, run largely by people affected by IgAN, with education, a provider finder and an ambassador program [19]. The National Kidney Foundation has a plain-language IgAN section [4], and the NIDDK a short overview in English and Spanish [1].
In the United Kingdom, Kidney Care UK has quality-marked information, a free support line, counseling, grants and patient stories from people with IgAN [3].
Coverage elsewhere is uneven. Many countries have a general kidney charity rather than an IgAN-specific one, and material in other languages is limited. Where no local group exists, a national kidney association or the treating kidney unit is the best starting point [2].
Donald Jones, a wide receiver for the Buffalo Bills and later the New England Patriots, was diagnosed with IgA nephropathy at college and retired from professional football in 2013, aged 25, because of it. He received a kidney from his father, wrote a book about the experience, and is a board member and national spokesperson for the IgA Nephropathy Foundation [20].
Kidney failure has many causes and assumptions about someone’s diagnosis are often wrong, so this page names only people who have described this condition publicly themselves.
Is IgA nephropathy serious?
About 1 in 5 people diagnosed develop kidney failure within 10 years, and most are at risk over a lifetime unless kidney function loss is kept very slow [1,8]. Treatment changes that path [2].
Why does blood appear in my urine after a cold?
IgA works in the linings of the nose and throat, so an infection there raises IgA production, which flares inflammation in the kidney filters for a few days [1,4].
Can it be inherited?
Usually not in a simple way. A relative with IgA nephropathy or IgA vasculitis raises the chance somewhat, though most people have no affected relative [1,3].
Do I really need a biopsy?
Yes. No blood or urine test can diagnose it [2].
Will I need dialysis or a transplant?
Not necessarily. Some people keep stable kidney function for decades. Where the kidneys do fail, dialysis or a transplant is needed [1].
Does diet matter?
No evidence links food to causing it, though less salt helps blood pressure and swelling [1,2].
Written by: trialport editorial team
Reviewed by: Keith Berelowitz, Founder and CEO, trialport
Reviewed on: 3 August 2026
Next review due: 3 August 2027
References last checked: 3 August 2026