IgA Nephropathy (Berger’s Disease): Understanding Your Pathology Report

by Jason Wasserman MD PhD FRCPC and Md Shahrier Amin, M.B.B.S., Ph.D.
July 19, 2026

IgA nephropathy, also known as Berger’s disease, is a kidney condition in which an antibody called immunoglobulin A (IgA) builds up in the kidney’s filtering units and causes inflammation. Antibodies are proteins the immune system normally makes to fight infection. In IgA nephropathy, an abnormal form of IgA accumulates in the kidneys, triggers inflammation, and, over time, can damage the filters. It is the most common disease of the kidney’s filters worldwide, and it ranges widely in severity, from a mild condition found only on a urine test to a cause of kidney failure.

The diagnosis of IgA nephropathy is made from a kidney biopsy, and the report that follows contains a set of terms and scores that can be hard to interpret. This article will help you understand the findings in your pathology report for IgA nephropathy, what each term means, and why it matters for your care. The section on the Oxford (MEST-C) classification explains the string of letters and numbers you are most likely to see on the report.

What do the kidneys do?

The kidneys are two bean-shaped organs that filter the blood, removing waste and extra water as urine while keeping the body’s salts and fluids in balance. The filtering happens in millions of tiny units called nephrons. At the start of each nephron is a cluster of small blood vessels called a glomerulus (the plural is glomeruli), which works like a sieve. Within each glomerulus, supporting cells called mesangial cells hold the tiny vessels in place. Understanding these two words, glomerulus and mesangial cell, makes the rest of the report easier to follow, because IgA nephropathy is fundamentally a disease of the glomerulus, and it begins in the mesangial cells.

What causes IgA nephropathy?

IgA nephropathy, the most common disease of the kidney’s filters, is now understood to be an autoimmune condition, meaning the immune system mistakenly acts against the body’s own tissue. Doctors describe the process as a series of steps, sometimes referred to as the multi-hit process. First, the body makes an abnormal form of IgA in which a sugar called galactose is missing from part of the antibody; this is called galactose-deficient IgA1. Second, the immune system treats this abnormal IgA as foreign and makes other antibodies against it. Third, the two stick together to form clumps called immune complexes. Fourth, these clumps settle on the mesangial cells of the glomerulus, trigger inflammation, and damage the filter. This sequence explains why several of the newer treatments work the way they do, by reducing the abnormal IgA or by calming the inflammation that follows.

A tendency to make the abnormal IgA runs in families and is partly genetic, which is why IgA nephropathy is sometimes seen in more than one relative. Flares often follow an infection of the throat or gut, and it is common for the first sign, visible blood in the urine, to appear within a day or two of a sore throat. IgA nephropathy also has a close relative, called IgA vasculitis (previously Henoch-Schönlein purpura), in which the same kind of IgA clumps affect the skin, joints, and gut as well as the kidney. Occasionally, IgA builds up in the kidney because of another condition, such as long-standing liver disease; this is called secondary IgA nephropathy, and your report or your doctor may mention it if it applies.

What are the symptoms of IgA nephropathy?

Many people with IgA nephropathy have mild or no symptoms at first, and the condition is often first suspected when a routine urine test shows blood or protein. When symptoms do occur, they may include:

Blood in the urine, either visible (making the urine pink, red, or brown) or detected only on a urine test.
Foamy or bubbly urine, caused by protein leaking into the urine.
Swelling of the hands, feet, or face.
High blood pressure.
Fatigue and, in more advanced disease, reduced kidney function.

A characteristic pattern is visible blood in the urine appearing during or just after a throat or gut infection. Two words used for these findings appear throughout kidney reports and are worth knowing: hematuria means blood in the urine, and proteinuria means protein in the urine. The amount of proteinuria is one of the most important measures of disease activity and likelihood of progression, and it is the main target of treatment.

How is the diagnosis made?

The diagnosis of IgA nephropathy can only be confirmed with a kidney biopsy, in which a thin needle is used to extract one or more small cores of kidney tissue, which a pathologist examines under the microscope. Blood and urine tests point toward the diagnosis by showing blood and protein in the urine and by measuring kidney function, but they cannot confirm it on their own. The biopsy is examined in three complementary ways, and understanding what each one contributes explains why all three appear in the report.

The first is light microscopy, in which thin tissue slices are stained with dyes such as hematoxylin and eosin and viewed under an ordinary microscope. This shows the overall structure of the glomeruli and the surrounding kidney, including any increases in cell number, inflammation, or scarring, and it forms the basis of the Oxford score described below. The second, and the one that actually confirms the diagnosis, is immunofluorescence. In this test, the tissue is treated with antibodies tagged with a glowing dye that stick to specific proteins. In IgA nephropathy, IgA is the dominant or codominant protein deposited in the mesangial areas of the glomeruli, usually alongside the complement protein C3. This finding, dominant mesangial IgA, is what defines the disease, and no other single test replaces it. The third is electron microscopy, which magnifies the tissue sufficiently to show the IgA clumps directly as dense deposits within the mesangium, confirming what immunofluorescence indicated. A diagnosis of IgA nephropathy rests on all three together, with the mesangial IgA on immunofluorescence as the essential ingredient.

The Oxford (MEST-C) classification

Once IgA nephropathy is confirmed, pathologists score the biopsy using the Oxford classification, also called the MEST-C score. This is the part of the report most patients find puzzling, because it appears as a short row of letters and numbers, such as “M1 E0 S1 T1 C0.” Each letter represents one feature of the biopsy, and the number after it indicates how much of that feature is present. The score matters because it summarizes how active and advanced the disease is and helps predict whether kidney function is likely to worsen. The five letters are:

M — Mesangial hypercellularity — Whether there are too many cells in the mesangial areas that support the glomerular filter. M0 means not increased; M1 means increased.
E — Endocapillary hypercellularity — Whether there are too many cells inside the small blood vessels of the glomerulus, a sign of active inflammation. E0 means absent; E1 means present.
S — Segmental glomerulosclerosis — Whether part of any glomerulus has become scarred. S0 means absent; S1 means present.
T — Tubular atrophy and interstitial fibrosis — How much of the kidney tissue around the filters has become scarred and shrunken. This reflects long-standing damage and is one of the strongest predictors of the outlook. T0 means little or none (25% or less of the tissue); T1 means moderate (26 to 50%); T2 means severe (more than 50%).
C — Crescents — Whether crescent-shaped clusters of cells have formed inside glomeruli, a sign of severe, active injury. C0 means none; C1 means crescents in less than one quarter of the glomeruli; C2 means crescents in one quarter or more.

A useful way to read the score is that the M, E, and C features reflect active disease, the kind that inflammation-calming treatment can improve, while the S and T features reflect chronic scarring that has already occurred and cannot be reversed. A biopsy with high activity scores but little scarring points toward treatable disease; a biopsy dominated by scarring reflects damage that has already accumulated. Your doctor uses the total score, along with your kidney function and the amount of protein in your urine, to assess how the disease is progressing.

Other findings that may be described in your report

Beyond the MEST-C score, the report usually describes several additional features that help gauge the extent of damage and how long it has been developing.

Number of glomeruli examined — The report states how many glomeruli were in the biopsy. A larger number makes the assessment more reliable, because the features above are judged from how many glomeruli are affected.
Global glomerulosclerosis — Glomeruli that have become entirely scarred and no longer work. A higher proportion indicates more permanent, long-standing damage.
Segmental sclerosis — Scarring of only part of a glomerulus, which reflects ongoing injury and may progress to complete scarring over time. This is the same feature captured by the “S” of the MEST-C score.
Interstitial fibrosis and tubular atrophy — Scarring and shrinkage of the tissue around the tubules, the small tubes that process fluid and waste. This is the same feature captured by the “T” score and is a key measure of long-standing damage.
Arteriosclerosis — Thickening and hardening of the kidney’s small arteries, which reduces blood flow and usually reflects long-term injury, often related to high blood pressure.
Arteriolar hyalinosis — A buildup of protein-rich material in the walls of the smallest arteries, associated with long-standing high blood pressure or diabetes.

What is the outlook?

IgA nephropathy varies more than almost any other kidney disease. In some people it stays mild for life and causes no lasting harm; in others it slowly damages the kidneys over years or decades, and a proportion eventually progresses to kidney failure requiring dialysis or a transplant. Because the range is so wide, no single figure describes the outlook for everyone, and the point of the biopsy and blood and urine tests is to place each person along that range.

The findings most strongly linked with a higher risk of kidney function worsening over time are a large amount of protein in the urine, reduced kidney function at the time of diagnosis, high blood pressure, and, on the biopsy, a high “T” score for scarring and the presence of crescents. Lowering the amount of protein in the urine has become the central goal of treatment because it is associated with long-term protection of kidney function. Many people with IgA nephropathy live full lives with the condition controlled by treatment and monitoring, which is why staying engaged with follow-up matters so much.

What happens after the diagnosis?

IgA nephropathy is managed by a kidney specialist (a nephrologist), and its treatment has changed substantially in recent years, shifting from a few general measures to several disease-specific drugs. The pathology findings, particularly the amount of active inflammation versus chronic scarring, along with the amount of protein in the urine and the kidney function, guide which of these the treatment team considers. This is a general overview; the specific plan is individual, and this article does not recommend any particular treatment.

Supportive care, the foundation for everyone — Good blood pressure control, a lower-salt diet, and a drug that blocks the renin-angiotensin system (an ACE inhibitor or an ARB) are the starting point for nearly all patients, because they reduce protein in the urine and protect kidney function. A second class of drug, the SGLT2 inhibitors, is now widely added for its kidney-protective effect.
Disease-specific drugs for higher-risk disease — For people who continue to have significant protein in the urine despite supportive care, several newer treatments are now available. Targeted-release budesonide (Nefecon or Tarpeyo) is a steroid designed to act on the gut tissue where the abnormal IgA is made. Sparsentan (Filspari) blocks two signals that drive protein loss and is taken in place of an ACE inhibitor or ARB. Complement inhibitors, such as iptacopan (Fabhalta), block the inflammatory pathway that IgA clumps activate. Additional drugs in the same families have been approved recently and others are in trials, so the available options are expanding.
Treatment for severe, active disease — When the biopsy shows crescents and rapidly worsening kidney function, stronger medicines that suppress the immune system may be considered, a decision weighed carefully against their side effects.
Monitoring and follow-up — Because IgA nephropathy is usually a long-term condition, follow-up includes regular checks of blood pressure, kidney function, and the amount of protein in the urine. These numbers, rather than repeat biopsies, are what the team uses to judge whether treatment is working. If kidney function declines significantly over many years, planning for dialysis or a kidney transplant becomes part of the conversation; IgA nephropathy can return in a transplanted kidney, and your team will discuss what that means.

Questions to ask your doctor

What did my biopsy show, and how severe is my IgA nephropathy?
What is my MEST-C score, and what does each letter mean for me?
Does my biopsy show mostly active inflammation, mostly scarring, or both?
How much protein is in my urine, and what is the target we are aiming for?
Is my kidney function normal now, and how will it be monitored?
Do I need disease-specific treatment, or is supportive care enough for now?
Would a newer treatment such as targeted-release budesonide, sparsentan, or a complement inhibitor be appropriate for me?
How will we know whether treatment is working?
Are there lifestyle changes, such as salt reduction, that would help protect my kidneys?
Should my blood pressure or other conditions be managed differently because of this diagnosis?
Could this condition run in my family, and should relatives be checked?
What signs should prompt me to contact you between visits?