Glomerulonephritis: Kidney Inflammation Causes & Treatment

What Is Glomerulonephritis?

Glomerulonephritis is inflammation affecting the glomeruli, the microscopic filtering units in the kidneys. Each kidney contains approximately one million glomeruli that filter blood and remove waste while retaining essential proteins and blood cells. When inflamed, these filters become damaged, allowing blood and protein to leak into urine while impairing the kidney's ability to remove waste.

The term glomerulonephritis literally means inflammation (-itis) of the glomeruli, which are clusters of tiny blood vessels within the kidneys. These delicate structures perform the vital function of filtering blood approximately 50 times per day, producing about 180 liters of filtrate that gets concentrated into roughly 1.5 liters of urine. When the glomeruli become inflamed, this efficient filtration system breaks down, leading to a cascade of problems that can affect the entire body.

Glomerulonephritis represents a group of diseases rather than a single condition. Each type has different causes, progression rates, and treatment approaches. Some forms develop suddenly after infections and may resolve completely, while others progress slowly over years, potentially leading to permanent kidney damage. Understanding the specific type through proper diagnosis is crucial for effective treatment planning.

The kidneys play a central role in maintaining overall health beyond just filtering waste. They regulate blood pressure, stimulate red blood cell production, maintain electrolyte balance, and activate vitamin D for bone health. When glomerulonephritis impairs kidney function, these processes can be disrupted, explaining why the condition can cause symptoms throughout the body, not just in the urinary system.

How the Glomeruli Work

Each glomerulus consists of a tuft of specialized capillaries surrounded by a cup-shaped structure called Bowman's capsule. Blood enters under pressure, and the capillary walls act as a sophisticated filter. The filter has three layers: the capillary endothelium (inner lining), the basement membrane (middle layer), and podocytes (specialized cells with foot-like projections). This structure normally allows water, small molecules, and waste products to pass through while retaining larger molecules like proteins and all blood cells.

In glomerulonephritis, various mechanisms can damage this filtering apparatus. The immune system may attack the glomerular structures directly, or immune complexes (antibody-antigen combinations) may deposit in the glomeruli and trigger inflammation. This inflammation causes the filter to become leaky, allowing proteins and red blood cells to escape into the urine. Simultaneously, the swelling and scarring can reduce the filter's permeability to waste products, causing them to accumulate in the blood.

Primary vs. Secondary Glomerulonephritis

Glomerulonephritis is classified as primary when the kidneys are the main organs affected, or secondary when it occurs as part of a systemic disease affecting multiple organs. Primary forms include IgA nephropathy, membranous nephropathy, and minimal change disease. Secondary forms occur in conditions like lupus, diabetes, and various infections. This distinction is important because treatment may need to address the underlying systemic condition in secondary forms.

What Causes Glomerulonephritis?

Glomerulonephritis can be caused by infections (particularly streptococcal), autoimmune diseases (like lupus), genetic conditions, certain medications, or may develop without a known cause. The common thread is that the immune system damages the glomeruli, either by attacking them directly or through the deposition of immune complexes.

Understanding the underlying cause of glomerulonephritis is essential for effective treatment. While some causes can be addressed directly, leading to potential cure, others require ongoing management to control the immune response and protect kidney function. The diverse causes reflect the complex interplay between the immune system and kidney structures.

Post-infectious glomerulonephritis remains one of the most common and well-understood forms, particularly in children. It typically develops one to three weeks after a streptococcal infection of the throat or skin. The immune system produces antibodies against the bacterial proteins, and these antibody-antigen complexes deposit in the glomeruli, triggering inflammation. This form usually resolves completely, though full recovery may take months.

Autoimmune diseases represent another major category of causes. In systemic lupus erythematosus (SLE), the immune system attacks various body tissues, including the kidneys, causing lupus nephritis in approximately 50% of patients. Other autoimmune causes include ANCA-associated vasculitis, where antibodies target specific proteins in blood vessel walls, causing severe inflammation that can rapidly destroy kidney function if untreated.

Infectious Causes

Beyond streptococcal infections, various pathogens can trigger glomerulonephritis. Viral infections including hepatitis B, hepatitis C, and HIV can cause glomerular disease through different mechanisms. Bacterial endocarditis (infection of heart valves) can release immune complexes that deposit in the kidneys. Parasitic infections like malaria remain significant causes in endemic regions. The treatment approach varies significantly depending on the infectious agent involved.

Autoimmune and Inflammatory Causes

IgA nephropathy, the most common primary glomerulonephritis worldwide, involves abnormal IgA antibody production that deposits in the glomeruli. Its exact trigger remains unclear, but upper respiratory infections often precede flares. Anti-glomerular basement membrane (anti-GBM) disease, also known as Goodpasture's syndrome when lungs are also affected, involves antibodies directly attacking the glomerular basement membrane, causing rapidly progressive kidney failure without prompt treatment.

Genetic and Hereditary Factors

Alport syndrome is a hereditary condition affecting the collagen in the glomerular basement membrane, leading to progressive kidney disease along with hearing loss and eye abnormalities. Fabry disease, caused by enzyme deficiency, leads to abnormal fat accumulation in various organs including the kidneys. Identifying these genetic causes has implications for family screening and genetic counseling.

What Are the Symptoms of Glomerulonephritis?

Glomerulonephritis symptoms include blood in urine (pink, red, or cola-colored), foamy urine from protein loss, swelling in the face, hands, feet and ankles, high blood pressure, fatigue, and reduced urine output. Some people have no symptoms initially, making routine health screenings important for early detection.

The symptoms of glomerulonephritis reflect the disruption of normal kidney function. When the glomerular filter is damaged, substances normally retained in the blood escape into urine, while waste products normally filtered out accumulate in the blood. The presentation can range from dramatic symptoms requiring immediate medical attention to subtle changes detected only through laboratory testing.

Hematuria, or blood in the urine, is one of the hallmark symptoms. The urine may appear pink, red, or cola-colored depending on the amount of blood present. Sometimes the blood is microscopic and only detected on urinalysis. The presence of blood indicates that red blood cells are escaping through the damaged glomerular filter, which normally would not allow cells of that size to pass.

Proteinuria, or protein in the urine, causes the characteristic foamy or bubbly appearance when urinating. Normally, proteins are too large to pass through the glomerular filter, but inflammation makes it leaky. Significant protein loss leads to decreased blood protein levels, particularly albumin, which normally keeps fluid in blood vessels. Without adequate albumin, fluid leaks into tissues, causing the characteristic swelling of glomerulonephritis.

Edema and Swelling

Swelling (edema) typically appears in areas where tissue is loose and gravity pulls fluid downward. Many patients first notice puffiness around the eyes in the morning, as fluid accumulates overnight in the facial tissues. As the day progresses and they remain upright, swelling often shifts to the ankles and feet. Severe protein loss can cause generalized edema affecting the entire body, including fluid accumulation in the abdomen (ascites) and around the lungs (pleural effusion).

High Blood Pressure

Hypertension develops in glomerulonephritis through multiple mechanisms. The kidneys normally regulate blood pressure by adjusting fluid and sodium excretion. When this function is impaired, fluid and sodium retention increases blood volume and pressure. Additionally, the damaged kidneys may produce excessive amounts of renin, a hormone that raises blood pressure. Controlling blood pressure is crucial not only for cardiovascular health but also because high blood pressure accelerates kidney damage.

Urinary Changes

Beyond color changes from blood, patients may notice decreased urine output (oliguria) as kidney function declines. Some patients experience urgency or frequency, though these symptoms are more typical of bladder or prostate conditions. Complete cessation of urine production (anuria) indicates severe kidney failure requiring emergency treatment.

Systemic Symptoms

As kidney function declines, waste products accumulate in the blood, causing fatigue, weakness, and difficulty concentrating. Nausea, loss of appetite, and a metallic taste in the mouth may develop. Sleep disturbances and restless legs are common. These symptoms often develop gradually in chronic glomerulonephritis and may be attributed to other causes before kidney disease is diagnosed.

What Are the Different Types of Glomerulonephritis?

The main types include IgA nephropathy (most common worldwide), membranous nephropathy, minimal change disease, focal segmental glomerulosclerosis (FSGS), and rapidly progressive glomerulonephritis. Each type has different causes, progression patterns, and treatment approaches, making accurate diagnosis through kidney biopsy essential.

Classification of glomerulonephritis is based on the pattern of damage seen on kidney biopsy. The histological appearance, combined with clinical features and laboratory findings, determines the specific diagnosis. This precision is important because different types respond to different treatments and have varying prognoses. Understanding your specific type helps predict disease course and guide treatment decisions.

Glomerulonephritis can also be categorized by clinical presentation into nephrotic syndrome, nephritic syndrome, or a combination of both. Nephrotic syndrome features heavy proteinuria (greater than 3.5 grams per day), low blood albumin, high cholesterol, and significant edema. Nephritic syndrome presents with blood in urine, variable protein loss, elevated blood pressure, and impaired kidney function. These clinical patterns help guide initial management while awaiting biopsy results.

IgA Nephropathy (Berger's Disease)

IgA nephropathy is the most common form of primary glomerulonephritis worldwide, particularly in Asian populations. It typically presents in young adults with episodes of visible blood in urine, often occurring during or shortly after upper respiratory infections. The disease involves deposition of IgA antibodies in the glomeruli. While many patients have a benign course, approximately 30-40% progress to end-stage kidney disease over 20-25 years. Treatment focuses on blood pressure control and reducing proteinuria, with immunosuppression reserved for progressive cases.

Membranous Nephropathy

Membranous nephropathy is a leading cause of nephrotic syndrome in adults. It involves thickening of the glomerular basement membrane due to immune complex deposition. About 80% of cases are primary (idiopathic), while secondary causes include hepatitis B, lupus, certain medications, and malignancies. The course is variable: about one-third remit spontaneously, one-third have persistent proteinuria with stable function, and one-third progress to kidney failure. Treatment decisions depend on kidney function, degree of proteinuria, and presence of secondary causes.

Minimal Change Disease

Minimal change disease is the most common cause of nephrotic syndrome in children, accounting for approximately 90% of cases in those under 10 years. The name reflects that kidney biopsy appears nearly normal under standard microscopy; electron microscopy reveals characteristic changes in the podocyte foot processes. It responds well to corticosteroid treatment, with most patients achieving remission, though relapses are common. The prognosis is generally excellent with preserved long-term kidney function.

Focal Segmental Glomerulosclerosis (FSGS)

FSGS is characterized by scarring affecting some (focal) but not all glomeruli, and only segments of those affected glomeruli. It can be primary (unknown cause) or secondary to obesity, HIV, heroin use, or as an adaptation to reduced kidney mass. FSGS is a common cause of end-stage kidney disease, particularly in Black populations. Treatment typically involves immunosuppression for primary forms, though response rates are variable. Addressing secondary causes is essential when identified.

Rapidly Progressive Glomerulonephritis (RPGN)

RPGN represents a medical emergency characterized by rapid loss of kidney function over days to weeks. On biopsy, it shows crescents - proliferations of cells in Bowman's space. Causes include anti-GBM disease, ANCA-associated vasculitis, and severe forms of other glomerulonephritis types. Without prompt treatment with immunosuppression and often plasmapheresis, kidney function can be permanently lost. Early recognition and aggressive treatment are essential for kidney survival.

How Is Glomerulonephritis Diagnosed?

Diagnosis involves urinalysis to detect blood and protein, blood tests for kidney function (creatinine, eGFR) and immunological markers, imaging studies, and often a kidney biopsy. The biopsy examines tissue under light, immunofluorescence, and electron microscopy to determine the specific type and guide treatment.

The diagnostic process for glomerulonephritis typically begins when abnormalities are found on routine urinalysis or when symptoms prompt investigation. A systematic approach combines clinical history, physical examination, laboratory tests, imaging studies, and often kidney biopsy to establish the diagnosis and determine the underlying cause. This comprehensive evaluation ensures appropriate treatment selection.

Initial laboratory evaluation includes urinalysis with microscopy, which can reveal red blood cells, red cell casts (cylindrical structures formed in kidney tubules), and protein. Quantifying proteinuria through a 24-hour urine collection or spot urine protein-to-creatinine ratio helps assess severity. Blood tests measure kidney function (creatinine, blood urea nitrogen, and estimated glomerular filtration rate) and may reveal anemia, electrolyte abnormalities, and changes in blood proteins.

Immunological Testing

Serological tests help identify specific causes of glomerulonephritis. Antinuclear antibodies (ANA) and anti-double-stranded DNA suggest lupus. Anti-neutrophil cytoplasmic antibodies (ANCA) indicate ANCA-associated vasculitis. Anti-glomerular basement membrane (anti-GBM) antibodies diagnose Goodpasture's syndrome. Complement levels (C3, C4) may be low in post-infectious glomerulonephritis and lupus. Hepatitis B and C testing identifies infection-related cases.

Imaging Studies

Kidney ultrasound is typically the first imaging study, assessing kidney size, shape, and appearance. In acute glomerulonephritis, kidneys may appear enlarged and echogenic. Chronic disease often shows small, scarred kidneys. Ultrasound also helps guide kidney biopsy and rules out obstruction or other structural abnormalities. CT or MRI scans may be used in specific circumstances but are not routinely required.

Kidney Biopsy

Kidney biopsy remains the gold standard for diagnosing and classifying glomerulonephritis. The procedure involves inserting a needle through the skin into the kidney under ultrasound guidance to obtain small tissue samples. These are examined using three techniques: light microscopy shows overall structure and patterns of damage; immunofluorescence reveals immune complex deposits using antibodies that glow under special light; electron microscopy provides detailed views of glomerular structures at high magnification.

Biopsy is particularly important when the diagnosis is uncertain, treatment would involve significant medications (like immunosuppressants), or the clinical course is unusual. It provides essential information about disease activity versus scarring, helping predict prognosis and guide treatment intensity. While biopsy carries small risks of bleeding and pain, the information gained usually outweighs these risks in appropriate candidates.

How Is Glomerulonephritis Treated?

Treatment depends on the type and severity but typically includes ACE inhibitors or ARBs to reduce blood pressure and proteinuria, immunosuppressive medications (corticosteroids, cyclophosphamide, mycophenolate) for inflammatory types, dietary modifications, and management of complications. Severe cases may require dialysis or kidney transplantation.

The treatment approach for glomerulonephritis aims to address the underlying cause when possible, control symptoms, reduce proteinuria, manage blood pressure, and slow disease progression. Treatment intensity varies from supportive care alone for mild cases to aggressive immunosuppression for rapidly progressive disease. All patients benefit from measures that protect kidney function and prevent complications.

Blood pressure control is fundamental in managing glomerulonephritis. The target blood pressure is typically below 130/80 mmHg, and even lower (below 125/75) may be recommended for those with significant proteinuria. ACE inhibitors (such as lisinopril, ramipril) and angiotensin receptor blockers (ARBs such as losartan, valsartan) are preferred because they provide additional kidney protection beyond blood pressure lowering. These medications reduce pressure within the glomeruli and decrease proteinuria by 30-50%, slowing disease progression.

Immunosuppressive Therapy

Many forms of glomerulonephritis involve immune-mediated damage, making immunosuppression a cornerstone of treatment. Corticosteroids (prednisone, methylprednisolone) are often first-line agents, reducing inflammation and immune activity. For severe or steroid-resistant cases, additional immunosuppressants may be added. Cyclophosphamide is used for lupus nephritis and ANCA-associated vasculitis. Mycophenolate mofetil offers an alternative with potentially fewer side effects. Rituximab, a monoclonal antibody, is increasingly used for various forms including membranous nephropathy.

The choice and duration of immunosuppressive therapy depend on the specific type of glomerulonephritis, disease severity, response to treatment, and individual patient factors. Treatment courses may last months to years. Close monitoring for medication side effects, including infection risk, bone loss, and diabetes, is essential. The goal is to use the minimum effective immunosuppression to control disease while minimizing adverse effects.

Supportive Care

Diuretics help manage fluid retention and edema. Statins are often prescribed for high cholesterol associated with nephrotic syndrome. Anticoagulation may be considered for severe nephrotic syndrome due to increased clotting risk. Dietary protein restriction may slow progression in some cases, though recommendations vary. Vaccination against pneumococcus, influenza, and hepatitis B is important, especially before starting immunosuppression.

Treatment of Underlying Causes

When glomerulonephritis is secondary to another condition, treating that condition is essential. Antiviral therapy for hepatitis B or C may lead to remission of associated kidney disease. Antibiotics treat active infections. Stopping culprit medications allows drug-induced cases to improve. Cancer treatment addresses malignancy-associated forms. Successful treatment of the underlying cause can lead to significant improvement or resolution of kidney disease.

Dialysis and Transplantation

When kidney function declines severely (end-stage renal disease), renal replacement therapy becomes necessary. Dialysis mechanically filters blood either through a machine (hemodialysis) or using the abdominal lining (peritoneal dialysis). Kidney transplantation offers the best outcomes for eligible patients, providing near-normal kidney function and better quality of life than dialysis. However, some forms of glomerulonephritis can recur in transplanted kidneys, requiring ongoing monitoring and sometimes preventive treatment.

What Lifestyle Changes Help Manage Glomerulonephritis?

Lifestyle modifications include reducing sodium intake to less than 2,300 mg daily, maintaining healthy body weight, avoiding nephrotoxic medications like NSAIDs, limiting alcohol, stopping smoking, staying physically active as tolerated, and working with a renal dietitian for individualized nutrition guidance based on kidney function.

While medications form the foundation of glomerulonephritis treatment, lifestyle modifications provide important supportive benefits. These changes help control blood pressure, reduce strain on the kidneys, prevent complications, and may slow disease progression. Making sustainable lifestyle changes requires understanding their importance and receiving proper guidance.

Sodium (salt) restriction is one of the most impactful dietary changes. Excess sodium causes fluid retention, increases blood pressure, and may worsen proteinuria. Most people consume far more sodium than needed, primarily from processed and restaurant foods rather than the salt shaker. Reading food labels, cooking at home, and choosing fresh over processed foods helps reduce intake. The goal is typically less than 2,300 mg daily, with some patients benefiting from stricter limits.

Dietary Protein Considerations

Protein restriction was historically recommended to reduce kidney workload, but current guidelines are more nuanced. Moderate protein intake (0.8 g/kg body weight daily) may benefit some patients, while excessively restricting protein can lead to malnutrition. Patients with nephrotic syndrome losing large amounts of protein may need higher intake to maintain nutrition. A renal dietitian can provide individualized recommendations based on kidney function, proteinuria levels, and nutritional status.

Fluid and Potassium Management

Fluid restriction may be necessary when kidneys cannot adequately eliminate fluid, leading to swelling and high blood pressure. The degree of restriction depends on urine output and edema severity. As kidney function declines, potassium excretion may be impaired, requiring dietary potassium restriction to prevent dangerous accumulation. High-potassium foods include bananas, oranges, potatoes, tomatoes, and many vegetables. Again, individualized guidance from a dietitian is valuable.

Medications to Avoid

Nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and naproxen can worsen kidney function and should generally be avoided. Some herbal supplements and over-the-counter products can harm kidneys or interact with medications. Always consult your healthcare team before taking new medications or supplements. Contrast dye used in some imaging studies can be harmful; if such procedures are necessary, protective measures should be taken.

Physical Activity and Weight Management

Regular physical activity benefits cardiovascular health, helps control blood pressure and weight, and improves overall well-being. Most patients can and should remain physically active, though the intensity may need adjustment during disease flares. Maintaining a healthy weight reduces cardiovascular risk and may help control blood pressure. Obesity can independently contribute to kidney damage and may reduce the effectiveness of some treatments.

When Should You See a Doctor?

See a doctor promptly if you notice blood in your urine, persistent foamy urine, unexplained swelling (especially of face, hands, or feet), or symptoms like severe fatigue or decreased urine output. Seek emergency care for sudden severe symptoms including severe headache with vision changes, difficulty breathing, or rapid significant swelling.

Early detection and treatment of glomerulonephritis significantly improves outcomes. Many people are diagnosed through routine health screenings before symptoms develop, highlighting the importance of regular check-ups that include urinalysis. However, certain signs and symptoms warrant prompt medical evaluation.

Visible blood in urine should always be evaluated. While blood can come from various urinary tract sources, glomerular bleeding has a characteristic appearance - often described as smoky, tea-colored, or cola-colored due to the time blood spends in the urinary tract. Even if blood in urine resolves on its own, underlying kidney disease may still be present and require treatment.

Persistent or unexplained swelling, particularly of the face, hands, or lower extremities, suggests fluid retention that may indicate kidney problems. Morning facial puffiness that resolves as the day progresses is particularly characteristic of nephrotic syndrome. Rapid onset or progression of swelling warrants urgent evaluation.

Signs Requiring Emergency Care

Severe or rapidly worsening symptoms require immediate medical attention. A sudden severe headache with vision changes could indicate malignant hypertension (dangerously high blood pressure) that can damage the brain, heart, and kidneys. Difficulty breathing may result from fluid accumulation in the lungs. Significant decrease or absence of urine output suggests acute kidney injury requiring urgent intervention. Confusion or decreased alertness can indicate severe kidney failure with toxin accumulation.

Regular Monitoring for Those with Known Disease

Patients already diagnosed with glomerulonephritis need regular follow-up to monitor disease activity and treatment response. The frequency of visits and tests depends on disease severity and stability. Most patients need blood pressure monitoring, blood tests for kidney function, and urine tests for protein and blood at regular intervals. Any change in symptoms between scheduled appointments should prompt contact with the healthcare team.

What Is the Prognosis for Glomerulonephritis?

Prognosis varies widely depending on the type, cause, severity at diagnosis, and response to treatment. Some forms like post-infectious glomerulonephritis and minimal change disease often resolve completely. Others like IgA nephropathy and FSGS may progress slowly over years. Early diagnosis, effective blood pressure control, and proteinuria reduction significantly improve long-term outcomes.

The outlook for patients with glomerulonephritis has improved substantially with better understanding of disease mechanisms and more effective treatments. However, prognosis remains highly variable and depends on numerous factors. Having an honest discussion with your nephrologist about expected outcomes helps with planning and decision-making.

Acute post-infectious glomerulonephritis, particularly in children, has an excellent prognosis. Most patients recover completely within weeks to months, though microscopic abnormalities may persist longer. Adult cases and those with more severe initial presentations may have a less favorable course. Long-term follow-up ensures complete resolution and monitors for any late complications.

Minimal change disease also generally has an excellent prognosis, with most patients achieving remission with corticosteroid treatment. However, relapses are common and may require repeated treatment courses. Despite this, long-term kidney function is usually preserved, and the condition rarely progresses to kidney failure.

Factors Affecting Prognosis

Several factors influence the likely course of glomerulonephritis. The degree of proteinuria is one of the strongest predictors - higher protein excretion generally indicates more severe disease and greater risk of progression. Blood pressure control significantly impacts outcomes, with well-controlled pressure associated with slower decline in kidney function. Kidney function at diagnosis matters; those presenting with more preserved function generally do better. Response to treatment, particularly reduction in proteinuria, predicts better outcomes.

Histological findings on kidney biopsy provide prognostic information. The degree of scarring (fibrosis) in the glomeruli and tubules reflects irreversible damage and indicates poorer prognosis. The presence of crescents suggests aggressive disease requiring prompt treatment. Certain specific findings predict response to particular treatments, guiding therapy selection.

Living with Glomerulonephritis

Many patients with glomerulonephritis lead full, active lives with proper management. Regular medical care, adherence to treatment, and lifestyle modifications help maintain the best possible kidney function. Support from family, patient organizations, and mental health professionals can help address the emotional challenges of living with a chronic condition. Advances in treatment continue to improve outcomes, and research into new therapies offers hope for even better results in the future.