Membranous Nephropathy: Understanding Your Pathology Report

by Cathryn Lapedis MD, MPH
July 19, 2026

Membranous nephropathy, also called membranous glomerulonephritis or membranous glomerulopathy, is a kidney disease in which the immune system damages the tiny filters of the kidney, called glomeruli, causing large amounts of protein to leak into the urine. It is one of the most common causes of a condition called nephrotic syndrome in adults, described below. It is an autoimmune disease, meaning the immune system mistakenly attacks the body’s own tissues.

The diagnosis of membranous nephropathy is made from a kidney biopsy, and the report that follows contains a set of terms and findings that can be difficult to interpret. This article will help you understand the findings in your pathology report for membranous nephropathy, what each term means, and why it matters for your care. Two ideas run through the whole report and are worth watching for as you read: whether the disease is primary or secondary, and whether a protein called PLA2R is involved, both explained below.

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. The wall of this sieve, called the glomerular basement membrane, lets water and waste pass into the urine while holding back useful large molecules such as proteins. Sitting on the urine side of this wall are specialized cells called podocytes, which wrap around the filter and help control what stays in the blood. Membranous nephropathy is fundamentally a disease of the podocytes and the filtration barrier they sit on, which is why these two structures recur throughout the report.

What causes membranous nephropathy?

Membranous nephropathy is caused by antibodies that attack the podocytes of the glomerulus. Antibodies (also called immunoglobulins) are proteins made by immune cells called plasma cells, and they normally stick to foreign targets such as viruses and bacteria. In an autoimmune disease, the body makes abnormal antibodies, called autoantibodies, that stick to its own tissue instead. In membranous nephropathy, these autoantibodies stick to proteins on the surface of the podocytes.

When an autoantibody binds its target protein, the two form a clump called an immune complex. In membranous nephropathy, these immune complexes build up on the outer side of the filter wall, in a space between the podocyte and the basement membrane. Over time, the deposits injure the podocytes and thicken the filter wall, and because the podocytes can no longer hold back large molecules, protein leaks from the blood into the urine. The location of the deposits on the outer surface of the filter wall is what gives membranous nephropathy its characteristic appearance under the microscope, as described below.

Primary versus secondary membranous nephropathy

One of the most important questions in this disease is whether it is primary or secondary, because the answer shapes the entire evaluation and much of the treatment.

Primary membranous nephropathy — The disease arises in the kidney on its own, with no other condition driving it. This accounts for most cases. In the large majority of primary cases, the target the autoantibody attacks is a podocyte protein called the M-type phospholipase A2 receptor, almost always shortened to PLA2R. A second target, called THSD7A, is involved in a small number of cases.
Secondary membranous nephropathy — The same kind of kidney injury is triggered by another condition elsewhere in the body. Recognized causes include certain cancers, autoimmune diseases such as lupus, some infections such as hepatitis B, and certain medications. When the disease is secondary, treating or removing the underlying cause is central to treating the kidney.

Because a secondary cause changes the plan, finding membranous nephropathy usually prompts a search for one, particularly in older adults, in whom an underlying cancer is looked for. The pathology findings, especially the PLA2R result described below, help indicate whether the disease is primary or secondary.

What are the symptoms of membranous nephropathy?

The symptoms of membranous nephropathy come from protein leaking into the urine. People may notice:

Foamy or bubbly urine, caused by the protein.
Swelling (edema) around the eyes, ankles, and feet, caused by low protein levels in the blood.
Weight gain from fluid retention, and fatigue.

When blood and urine tests are done, they typically show large amounts of protein in the urine, low levels of a blood protein called albumin, and often elevated blood fats (lipids). This particular combination has a name.

What is nephrotic syndrome?

Nephrotic syndrome is the term for the combination of heavy protein loss in the urine, low albumin in the blood, and swelling, often with high blood lipids. It is not a disease in itself but a pattern that results when the glomerular filter leaks badly. Membranous nephropathy is one of the most common causes of nephrotic syndrome in adults, and many people with membranous nephropathy have it. People with nephrotic syndrome also have a higher risk of blood clots, which is why this pattern is taken seriously and monitored.

How is the diagnosis made?

The diagnosis of membranous nephropathy is confirmed with a kidney biopsy, in which a thin needle is used to take one or more small cores of kidney tissue that a pathologist examines under the microscope. The biopsy is studied in three complementary ways, and each contributes something the others cannot, which is why all three appear in the report.

The first is light microscopy, in which thin slices of tissue are stained with dyes and viewed under an ordinary microscope. A silver stain highlights the filter wall, which in membranous nephropathy appears thickened, with tiny projections and pits often described as “spikes and craters” or as a fuzzy appearance. These spikes form as the filter wall grows up around the immune deposits. The second is immunofluorescence, in which the tissue is treated with antibodies tagged with a glowing dye that stick to specific proteins. In membranous nephropathy this shows the antibody immunoglobulin G (IgG) and a complement protein called C3 deposited evenly along the filter wall in a fine granular pattern. Critically, the tissue can also be stained for PLA2R: a positive result strongly supports primary membranous nephropathy and is one of the most useful findings on the whole report. The third is electron microscopy, which magnifies the tissue enough to show the immune deposits directly, sitting on the outer surface of the filter wall exactly where they are expected, confirming the diagnosis. Together these three methods establish both that the disease is membranous nephropathy and, through the PLA2R result, whether it is likely primary.

The PLA2R antibody: on the biopsy and in the blood

The discovery that PLA2R is the main target in primary membranous nephropathy has been the single biggest advance in this disease, and it appears in the report in a way worth understanding. PLA2R can be detected in two places. On the biopsy, staining for PLA2R shows whether the protein is present in the deposits, as described above. In the blood, a test can measure the level of anti-PLA2R antibody, the autoantibody itself. This blood test is useful in three ways: it helps confirm primary membranous nephropathy without always needing a biopsy, its level tends to track how active the disease is, and following it over time helps show whether treatment is working. A falling antibody level often comes before the protein in the urine improves, giving an early sign that the disease is responding. If your report or your nephrologist mentions a PLA2R antibody titer or level, this is what it refers to. A small number of primary cases involve the THSD7A target instead, and other rarer targets have been identified, so a PLA2R-negative result does not rule out primary disease.

How the biopsy describes the stage and severity

Beyond confirming the diagnosis, the biopsy describes how far the disease has advanced. Several terms are used, and understanding them helps you read the report.

Ehrenreich and Churg stage

Pathologists often describe how far the filter-wall changes have progressed using a four-stage system called the Ehrenreich and Churg staging system. It reflects how much the filter wall has reacted to the immune deposits, from earliest to latest, and it describes the appearance rather than predicting the outcome on its own.

Stage I — Small immune deposits sit on the outer surface of the filter wall, with no thickening yet.
Stage II — The filter wall grows up around the deposits, forming the spike-like projections seen on the silver stain.
Stage III — The filter wall has expanded to surround the deposits.
Stage IV — The deposits are fully enclosed within the thickened wall and may later be reabsorbed and fade.

Scarring and long-term damage

The report also describes features that reflect how much permanent damage has accumulated, which matters more for the outlook than the stage above. These are the same kinds of chronic changes reported in other kidney diseases:

Glomerulosclerosis — Scarring of the glomeruli. A small amount is normal with age, but a higher proportion signals long-standing disease. When more than about half of the glomeruli are scarred, the kidney is less likely to recover fully.
Tubular atrophy — Shrinkage and scarring of the tubules, the small tubes that turn filtered fluid into urine. It is usually reported as a percentage of the tissue affected.
Interstitial fibrosis — Scarring of the supporting tissue that holds the nephrons together, also reported as a percentage. Along with tubular atrophy, it is one of the strongest predictors of long-term kidney function.
Arterial sclerosis — Thickening and hardening of the kidney’s arteries, which reduces blood flow and reflects long-term injury, often related to high blood pressure.

Words used to describe how much tissue is involved

Kidney reports use four words to describe the extent of a change, and they appear throughout: global means the whole glomerulus is involved; segmental means only part of a glomerulus is involved; focal means some but not all glomeruli are affected; and diffuse means the change is seen throughout the tissue. For example, “global glomerulosclerosis” means an entire glomerulus is scarred, while “segmental” scarring affects only part of one.

What is the outlook?

Membranous nephropathy varies widely from person to person, and its course is often described in thirds. About one third of people improve on their own, with the protein leak resolving without immunosuppressive treatment (a spontaneous remission). About one third have persistent protein in the urine but stable kidney function over the long term. The remaining third slowly lose kidney function over years and may eventually progress to kidney failure requiring dialysis or a transplant. Because of this variability, treatment is not the same for everyone, and part of the purpose of the biopsy and the blood tests is to judge which course is more likely.

The findings most strongly linked with a higher risk of kidney function worsening are a large and persistent amount of protein in the urine, reduced kidney function at diagnosis, a high level of anti-PLA2R antibody in the blood, and, on the biopsy, a high degree of scarring (tubular atrophy and interstitial fibrosis). These measures are combined to sort people into risk groups, which then guide how actively the disease is treated.

What happens after the diagnosis?

Membranous nephropathy is managed by a kidney specialist (a nephrologist), and treatment has become more targeted as the role of PLA2R has become understood. The pathology findings, the amount of protein in the urine, the kidney function, and the PLA2R antibody level guide which approach the treatment team considers. This is a general overview; the specific plan is individual, and this article does not recommend any particular treatment.

Searching for a secondary cause — Because secondary membranous nephropathy is treated by addressing its underlying cause, the first step is often to look for one, particularly an underlying cancer, infection, autoimmune disease, or medication, especially in older adults or when PLA2R is negative.
Supportive care for everyone — Good blood pressure control and a drug that blocks a hormone system called the renin-angiotensin system (an ACE inhibitor or an ARB) are used in nearly all patients, because they lower protein in the urine and protect kidney function. Because nephrotic syndrome raises the risk of blood clots, a blood thinner is sometimes considered.
Immunosuppressive treatment for higher-risk disease — For people at higher risk of losing kidney function, treatment aimed at the immune system may be considered. Rituximab, a drug that depletes the immune cells producing the harmful antibodies, has become a first-line option for primary membranous nephropathy. Other regimens combine a steroid with another immune-suppressing drug. Low-risk disease is often watched carefully first, because of the real chance of spontaneous remission.
Monitoring — Follow-up tracks the amount of protein in the urine, kidney function, and, in PLA2R-associated disease, the anti-PLA2R antibody level, which often signals a response before the urine improves. Repeat biopsies are usually not needed; these blood and urine measures guide treatment instead.

Questions to ask your doctor

Is my membranous nephropathy primary or secondary?
Was my biopsy positive for PLA2R, and was my blood tested for the PLA2R antibody?
If it may be secondary, what tests will look for an underlying cause?
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?
What did my biopsy show about scarring, and what does that mean for my outlook?
Am I in a low-, moderate-, or high-risk group, and what does that mean for treatment?
Should we watch and wait, or start immune-suppressing treatment now?
Would rituximab be appropriate for me?
Do I need treatment to prevent blood clots because of nephrotic syndrome?
How will we know whether treatment is working?
What signs should prompt me to contact you between visits?