Diabetic Nephropathy (Diabetic Glomerulosclerosis): Understanding Your Pathology Report

by Cathryn Lapedis MD, MPH
July 20, 2026

Diabetic nephropathy, also called diabetic glomerulosclerosis or diabetic kidney disease, is kidney damage caused by diabetes. Over many years, high blood sugar injures the tiny filters of the kidney, called glomeruli, so that they gradually scar and leak protein into the urine. It is the most common cause of kidney failure worldwide. The two names mean the same thing: diabetic nephropathy refers to the disease, and diabetic glomerulosclerosis refers to the scarring of the glomeruli that a pathologist sees under the microscope.

Unlike most conditions described on this site, diabetic nephropathy is usually diagnosed without a biopsy, from the combination of long-standing diabetes and protein in the urine. When a kidney biopsy is done, it is often to check whether something other than diabetes is affecting the kidney. This article will help you understand the findings in your pathology report for diabetic nephropathy, what each term means, and why it matters for your care. The section on how the disease is classified explains the class I-IV system you are most likely to see on a biopsy 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, a supporting tissue called the mesangium holds the tiny vessels in place, and specialized cells called podocytes wrap around the filter and help control what stays in the blood. Diabetic nephropathy damages all of these parts, which is why terms like glomerulus, mesangium, and podocyte appear throughout the report.

What causes diabetic nephropathy?

Diabetic nephropathy, the most common cause of kidney failure worldwide, develops slowly over years in people with diabetes. Persistently high blood sugar injures the cells of the glomerulus, including the podocytes and the mesangium, and thickens and scars the filter over time. The longer a person has had diabetes and the higher their blood sugar has run, the greater the risk, although the two do not track perfectly, because inherited factors also make some people more susceptible regardless of how well their sugar is controlled. Other conditions that commonly travel with diabetes add to the risk, including high blood pressure, obesity, high blood fats, and smoking. High blood pressure in particular both results from kidney damage and worsens it, which is one reason controlling it is central to treatment.

What are the symptoms of diabetic nephropathy?

Most people with diabetic nephropathy have no symptoms until the disease is advanced, which is why people with diabetes are screened regularly with urine and blood tests to catch it early. When the disease is more advanced, protein loss and declining kidney function can cause swelling of the feet, ankles, and around the eyes, fatigue, and, eventually, the many effects of kidney failure. Because symptoms come so late, the numbers on screening and blood tests matter more here than how a person feels.

What the urine and blood tests show

Several tests are used to detect and follow diabetic nephropathy, and they often appear alongside the pathology findings:

Albumin in the urine — Albumin is a protein normally kept in the blood. When the glomeruli are damaged, it begins to leak into the urine. Small amounts (once called microalbuminuria) are often the earliest detectable sign, and larger amounts (proteinuria) appear as damage progresses. The amount of albumin in the urine is one of the most important indicators of disease activity and likelihood of progression.
HbA1c — A blood test that reflects the average blood sugar over the previous two to three months. It shows how well diabetes has been controlled, which is directly tied to the risk of kidney damage.
Creatinine and estimated GFR — Creatinine is a waste product the kidneys clear from the blood at a steady rate; a rising level signals reduced kidney function. From the creatinine level, laboratories calculate the estimated glomerular filtration rate (eGFR), a single number that summarizes how well the kidneys are filtering.
Cystatin C — Another blood marker of kidney function, sometimes used alongside creatinine to estimate filtration more accurately. As with creatinine, a higher blood level indicates reduced kidney function.

How is the diagnosis made?

In most people, diabetic nephropathy is diagnosed without a kidney biopsy. A person who has had diabetes for many years, has protein in the urine, and has diabetic damage in the eyes (diabetic retinopathy, which tends to appear alongside kidney damage) is generally diagnosed on that clinical picture alone, and treatment begins without examining kidney tissue. This is different from most diagnoses on this site, which require a tissue sample.

When a kidney biopsy is performed in a person with diabetes, it is often for a specific reason: to find out whether a kidney disease other than diabetes is present. Features that raise this question include sudden, rather than gradual, onset of protein or blood in the urine, rapid decline in kidney function, short duration of diabetes, or the absence of diabetic eye damage. In these situations, a biopsy can reveal a second, treatable condition, and studies find that a large share of diabetic patients who are biopsied for such reasons turn out to have a non-diabetic kidney disease, either instead of or in addition to diabetic nephropathy. If you have diabetes and a biopsy was recommended, this is usually why. A pathologist examines the tissue with an ordinary light microscope, and often with immunofluorescence and electron microscopy as well, both to confirm diabetic changes and to look for anything else.

What the pathologist sees under the microscope

Diabetic nephropathy produces characteristic changes, and your report may describe several of them. Understanding the main terms makes the report far easier to follow.

Glomerulosclerosis — Scarring of the glomeruli, the kidney’s filters. A small amount is normal with age, but more extensive scarring reflects kidney injury. When a large proportion of glomeruli are scarred, the kidney is less able to recover.
Mesangial sclerosis — Scarring and expansion of the mesangium, the supporting tissue between the small vessels of the glomerulus. This is one of the earliest visible changes of diabetic nephropathy.
Nodular sclerosis (Kimmelstiel-Wilson lesions) — As mesangial scarring advances, it can form rounded balls, or nodules, within the glomerulus. These nodules, called Kimmelstiel-Wilson lesions, are the classic and most specific sign of diabetic nephropathy, and they indicate more advanced disease.
Hyaline arteriolosclerosis — A buildup of protein-rich material in the walls of the smallest arteries (arterioles), which stiffens them and reduces their ability to regulate blood flow into the glomeruli. It is very common in diabetic nephropathy.
Arterial sclerosis — Thickening and hardening of the larger arteries that supply the kidney, reducing blood flow and contributing to damage over time.
Tubular atrophy — Shrinkage and scarring of the tubules, the small tubes that turn filtered fluid into urine, 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. Together with tubular atrophy, it is one of the strongest predictors of long-term kidney function.

Words used to describe how much tissue is involved

Kidney reports use four terms to describe the extent of a change: 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 “diffuse mesangial sclerosis” means mesangial scarring is present throughout.

How diabetic nephropathy is classified

When a biopsy is examined, pathologists grade the glomerular changes using a system that runs from class I (earliest) to class IV (most advanced). The class summarizes how far the glomerular damage has progressed and appears prominently on the report.

Class I — The glomeruli look normal or nearly normal under an ordinary microscope, and the only sign of damage, thickening of the filter wall, is visible only with an electron microscope. This is the earliest change.
Class II — Scarring of the mesangium is visible under an ordinary microscope, without nodules. It is divided into class IIa (mild) and class IIb (moderate to severe), depending on the extent of mesangial scarring.
Class III — At least one Kimmelstiel-Wilson nodule is present, marking nodular sclerosis and more advanced disease.
Class IV — More than half of the glomeruli are completely (globally) scarred. This is advanced diabetic nephropathy, typically accompanied by the other changes listed above.

The report also grades the amount of scarring outside the glomeruli, the tubular atrophy and interstitial fibrosis, and the blood vessel changes, because these strongly influence how the kidney is likely to function over time. Taken together, the glomerular class and the degree of scarring give a fuller picture than either alone.

What is the outlook?

Diabetic nephropathy tends to progress slowly over years, and its course depends heavily on how well the underlying diabetes, blood pressure, and protein loss are controlled. With good control and modern treatment, progression can be slowed substantially, and many people maintain adequate kidney function for a long time. Without it, the disease can advance to kidney failure requiring dialysis or a transplant; diabetic nephropathy is the single most common cause of kidney failure worldwide.

On the biopsy, the findings most strongly linked with a poorer long-term outlook are a higher class (especially class IV), extensive global glomerulosclerosis, and a high degree of tubular atrophy and interstitial fibrosis. Clinically, a large and rising amount of protein in the urine and a falling filtration rate are the measures that matter most. Importantly, when a biopsy shows a treatable non-diabetic kidney disease in addition to or instead of diabetic changes, treating that condition can meaningfully change the course, which is part of why the biopsy is done.

What happens after the diagnosis?

Diabetic nephropathy is managed jointly by the family doctor, an endocrinologist or diabetes specialist, and often a kidney specialist (a nephrologist). Its treatment has advanced considerably in recent years, moving well beyond blood sugar control alone. The biopsy findings, the amount of protein in the urine, and the kidney function guide which of the approaches below the treatment team considers. This is a general overview; the specific plan is individual, and this article does not recommend any particular treatment.

Controlling blood sugar and blood pressure — Keeping blood sugar and blood pressure in target ranges remains the foundation, because both drive the damage. This usually involves diabetes medications and lifestyle measures, along with attention to blood fats and stopping smoking.
Protecting the kidney with targeted drugs — Several classes of medication now slow the progression of diabetic kidney disease, and current guidelines recommend using more than one together in many patients. A drug that blocks the renin-angiotensin system (an ACE inhibitor or an ARB) reduces protein in the urine and protects the filter. SGLT2 inhibitors, originally developed to lower blood sugar, have been shown to slow kidney decline substantially and are now a cornerstone of treatment. Finerenone, a newer drug that reduces inflammation and scarring in the kidney, adds further protection. GLP-1 receptor agonists, another class of diabetes drug, also improve kidney and heart outcomes. Which combination is appropriate depends on kidney function, protein levels, and other health factors.
Treating any non-diabetic kidney disease found — If the biopsy revealed a second condition, such as one of the immune-related kidney diseases, that condition is treated on its own terms, which may open options that would not apply to diabetic nephropathy alone.
Monitoring and planning ahead — Follow-up tracks kidney function, urinary protein, and blood sugar over time. If kidney function declines significantly over years, planning for dialysis or a kidney transplant becomes part of the conversation, ideally well before it is needed.

Questions to ask your doctor

Was my diabetic nephropathy diagnosed clinically, or from a biopsy?
If I had a biopsy, did it show diabetic nephropathy alone, or another kidney disease as well?
What class (I to IV) was my diabetic nephropathy, and what does that mean?
How much scarring (tubular atrophy and interstitial fibrosis) did the biopsy show?
How much protein is in my urine, and what are we aiming for?
What is my current kidney function (eGFR), and how will it be monitored?
Am I on the recommended kidney-protecting medications, such as an ACE inhibitor or ARB, an SGLT2 inhibitor, and finerenone?
What are my targets for blood sugar (HbA1c) and blood pressure?
What lifestyle changes would most help protect my kidneys?
How quickly is my kidney disease likely to progress?
At what point should we discuss dialysis or a transplant?
What signs should prompt me to contact you between visits?