Glomerulonephritis is one of the leading causes of kidney failure worldwide, yet many people have never heard the term until they receive the diagnosis. Glomerulonephritis refers to inflammation of the glomeruli – the tiny filtering units within the kidneys responsible for removing waste and excess fluid from the blood. When these structures become inflamed, they lose their ability to filter properly, allowing protein and blood to leak into the urine while waste products accumulate in the bloodstream. The condition can develop suddenly or progress over years, and identifying the underlying cause is critical for guiding treatment. According to the NIDDK, glomerular diseases account for a substantial share of end-stage kidney disease in the United States. For additional kidney and other conditions, see our medical conditions guide.
When to Seek Urgent or Emergency Care
Glomerulonephritis can occasionally progress rapidly and threaten your kidneys within days. Seek urgent medical care or go to the emergency room if you have:
- Significantly reduced urine output or passing little to no urine
- Severe or rapidly worsening swelling (legs, face, or abdomen) or shortness of breath, which can signal dangerous fluid overload
- Signs of a hypertensive emergency – severe headache, chest pain, vision changes, or confusion with very high blood pressure
- Symptoms of acute kidney injury – nausea and vomiting, confusion, extreme fatigue, or difficulty breathing
- Coughing up blood together with these symptoms (can occur in certain aggressive forms)
Rapidly progressive glomerulonephritis can cause permanent kidney damage quickly, so do not wait if these signs appear.
The short version: Glomerulonephritis is a group of diseases that inflame the kidney’s filters. It can be mild and self-limited or a fast-moving emergency, so any blood or protein in the urine, unexplained swelling, or new high blood pressure deserves prompt evaluation. Diagnosis often needs a kidney biopsy, and treatment – which may include immune-suppressing medicines and kidney-protective drugs – depends entirely on the specific type. This is a condition for nephrology, not self-management.
This article is general health information, not medical advice. Diagnosis and treatment must be individualized by a qualified clinician – never start, stop, or change immunosuppressant or blood-pressure medication on your own.
Understanding the Glomeruli
Each kidney contains approximately one million nephrons, the functional units that filter blood and produce urine. At the beginning of each nephron sits a glomerulus – a ball-shaped cluster of tiny capillaries surrounded by a specialized capsule (Bowman’s capsule). Blood enters the glomerulus under pressure, and the capillary walls act as a filter, allowing water, electrolytes, and small waste molecules to pass through while retaining large molecules like proteins and blood cells.
The glomerular filtration barrier has three layers: the capillary endothelium, the glomerular basement membrane (GBM), and the podocytes – specialized cells with foot-like projections that interdigitate to form the final filtration slit. When any component of this barrier is damaged by inflammation, immune attack, or other mechanisms, the filter becomes “leaky.” Protein (particularly albumin) spills into the urine (proteinuria), red blood cells pass through (hematuria), and the kidney’s filtration capacity declines.
Glomerulonephritis is not a single disease but rather a group of diseases with diverse causes that share a common target – the glomerulus. The classification of these diseases is based on their clinical presentation, their histological pattern on kidney biopsy, and their underlying cause. Getting that classification right matters enormously, because two people with “glomerulonephritis” can need completely different treatments and face very different outlooks.
Acute vs. Chronic Glomerulonephritis
Acute Glomerulonephritis
Acute glomerulonephritis develops suddenly, often over days to weeks. The classic example is post-infectious (often post-streptococcal) glomerulonephritis, which occurs one to several weeks after a streptococcal throat or skin infection. Immune complexes formed in response to the infection deposit in the glomeruli, triggering inflammation. This form is most common in children and typically resolves completely, though it can cause significant acute kidney injury during the active phase.
Other causes of acute glomerulonephritis include IgA nephropathy (Berger’s disease), rapidly progressive glomerulonephritis (RPGN), lupus nephritis, ANCA-associated vasculitis, anti-GBM disease (Goodpasture’s syndrome), and various infections including endocarditis, hepatitis B, and hepatitis C. RPGN is a medical emergency – if untreated, it can destroy kidney function within weeks to months. It is characterized by crescent formation on kidney biopsy and requires urgent immunosuppressive therapy.
Chronic Glomerulonephritis
Chronic glomerulonephritis develops gradually over months to years, often without an identifiable acute trigger. It may be discovered incidentally through routine blood work or urinalysis showing persistent proteinuria or elevated creatinine. By the time symptoms develop, significant and often irreversible kidney damage has occurred. Many cases of chronic glomerulonephritis represent the smoldering progression of a disease that began acutely but was never diagnosed or fully resolved. This is why persistent findings on a routine urine test – even without symptoms – should never be ignored.
Common Causes and Types of Glomerulonephritis
Glomerulonephritis has many underlying causes: infections (post-streptococcal and other post-infectious forms, hepatitis B and C, HIV, endocarditis), autoimmune diseases (lupus, IgA nephropathy, IgA vasculitis), small-vessel vasculitis (ANCA-associated), antibody-mediated disease (anti-GBM), and inherited or metabolic conditions. The major types include the following.
IgA Nephropathy: The most common form of glomerulonephritis globally, IgA nephropathy is caused by deposits of immunoglobulin A in the glomeruli. It often presents as recurrent episodes of visible blood in the urine coinciding with upper respiratory infections. A substantial share of patients progress toward kidney failure over the following decades. The last few years have brought several newer, targeted options for IgA nephropathy in appropriate patients – including a gut-directed budesonide formulation (Tarpeyo), the dual endothelin/angiotensin receptor antagonist sparsentan (Filspari), and the complement inhibitor iptacopan (Fabhalta) – and additional therapies continue to move through late-stage trials. Which, if any, is appropriate is a decision for a nephrologist based on your biopsy and risk of progression. Research published in the New England Journal of Medicine has driven much of this shift toward earlier, more aggressive protection of kidney function.
Membranous Nephropathy: Characterized by thickening of the glomerular basement membrane due to immune complex deposits, membranous nephropathy is a leading cause of nephrotic syndrome in adults. Most primary cases are caused by antibodies against the PLA2R (phospholipase A2 receptor) on podocytes, and measuring anti-PLA2R antibody levels now helps guide both diagnosis and treatment decisions. Roughly speaking, about one-third of patients remit spontaneously, one-third have persistent proteinuria with stable kidney function, and one-third progress toward kidney failure.
Focal Segmental Glomerulosclerosis (FSGS): FSGS involves scarring of some (focal) glomeruli in some (segmental) portions. It is a common cause of nephrotic syndrome and is increasingly prevalent. Causes include genetic mutations in podocyte proteins, viral infections such as HIV, obesity, and adaptive changes from reduced nephron mass. Primary FSGS is often resistant to treatment and has a high rate of progression to kidney failure.
Lupus Nephritis: Kidney involvement occurs in roughly half of patients with systemic lupus erythematosus (SLE) and is one of the most serious complications of lupus. It is classified into six classes (I-VI) based on kidney biopsy findings, with classes III and IV (proliferative lupus nephritis) requiring aggressive immunosuppressive therapy. In recent years, add-on agents such as belimumab and voclosporin have been approved to improve kidney responses alongside standard immunosuppression. According to the National Kidney Foundation, lupus nephritis is a leading cause of kidney failure in young women.
ANCA-Associated and Anti-GBM Disease: ANCA-associated glomerulonephritis is a form of small-vessel vasculitis that can progress rapidly and often affects the lungs as well as the kidneys. Anti-GBM (Goodpasture’s) disease is driven by antibodies against the glomerular basement membrane. Both are among the most urgent forms of glomerulonephritis and require prompt specialist treatment.
Symptoms
The symptoms of glomerulonephritis depend on whether the presentation is nephritic (inflammatory) or nephrotic (protein-losing), and how rapidly the disease is progressing. The nephritic syndrome is characterized by blood in the urine (which may be visible as cola- or tea-colored urine or detected only on dipstick testing), mild to moderate proteinuria, high blood pressure, reduced urine output, and fluid retention with edema.
The nephrotic syndrome involves heavy proteinuria (more than about 3.5 grams per day), low serum albumin, severe edema (particularly around the eyes, ankles, and abdomen), high cholesterol, and increased risk of blood clots. Some patients present with features of both syndromes.
Nonspecific symptoms may include fatigue, decreased appetite, nausea, and foamy urine (a sign of protein in the urine). In rapidly progressive forms, kidney function can deteriorate so quickly that patients develop symptoms of acute kidney failure – dramatically reduced urine output, severe fluid overload, and dangerously elevated potassium levels. Any of the warning signs in the red-flag box above should prompt urgent evaluation.
Diagnosis
The diagnostic workup for suspected glomerulonephritis begins with urine analysis – looking for proteinuria, hematuria, and red blood cell casts (which strongly point to glomerular disease). Quantifying proteinuria with a spot urine protein-to-creatinine ratio (or albumin-to-creatinine ratio) helps determine severity and guides treatment. Blood tests include serum creatinine and eGFR (to assess kidney function), serum albumin, cholesterol, and complement levels (which are low in certain types).
Serologic testing helps narrow the differential diagnosis. Anti-nuclear antibodies (ANA) and anti-dsDNA antibodies suggest lupus. Anti-neutrophil cytoplasmic antibodies (ANCA) point toward vasculitis-associated glomerulonephritis. Anti-GBM antibodies indicate Goodpasture’s disease. Anti-PLA2R antibodies suggest membranous nephropathy. Serum complement levels, hepatitis B and C serologies, HIV testing, and serum protein electrophoresis complete the standard workup.
Kidney biopsy is the definitive diagnostic procedure for most forms of glomerulonephritis. A needle is guided (usually by ultrasound) into the kidney to obtain a small tissue sample, which is examined under light microscopy, immunofluorescence, and electron microscopy. The biopsy identifies the specific type of glomerulonephritis, determines the degree of active inflammation versus chronic scarring, and guides treatment decisions. According to the American Society of Nephrology, kidney biopsy remains indispensable for accurate diagnosis and prognosis in glomerular disease.
Treatment
Treatment of glomerulonephritis has two components: general measures to protect kidney function and specific therapy targeting the underlying disease. All treatment is clinician-directed and individualized; the descriptions below are general and do not include dosing.
General measures apply to nearly all patients. ACE inhibitors or ARBs reduce proteinuria (by lowering intraglomerular pressure) and slow the progression of kidney disease – they are cornerstone therapy regardless of the specific diagnosis. Blood pressure control is essential, with targets set by your clinician. Dietary sodium restriction helps control blood pressure and edema, and diuretics manage fluid overload. Statins treat the hyperlipidemia associated with nephrotic syndrome. SGLT2 inhibitors (such as dapagliflozin and empagliflozin), once used mainly for diabetes, are now an established kidney-protective therapy for many people with chronic kidney disease and proteinuria, including certain glomerular diseases, and have become part of standard supportive care.
Specific therapy varies by diagnosis. Post-infectious glomerulonephritis is treated supportively, as it usually resolves on its own. IgA nephropathy is managed first with RAAS blockade and SGLT2 inhibition, with corticosteroids or the newer targeted therapies mentioned above added for patients at high risk of progression. Membranous nephropathy with severe nephrotic syndrome may be treated with rituximab, cyclophosphamide, or calcineurin inhibitors. Lupus nephritis typically requires induction therapy followed by maintenance immunosuppression, increasingly with an add-on agent. ANCA-associated glomerulonephritis is treated with corticosteroids, rituximab or cyclophosphamide, and sometimes plasma exchange.
Anti-GBM disease (Goodpasture’s) requires plasma exchange (plasmapheresis) to remove the pathogenic antibodies, combined with immunosuppression. This is a true emergency – delays in treatment can result in permanent kidney failure and life-threatening pulmonary hemorrhage. Understanding the costs of immunosuppressive therapies and specialty care is important for patients facing these complex treatment regimens. Because immunosuppressants raise infection risk and require careful monitoring, they must always be managed by your care team – never adjusted or stopped on your own.
Long-Term Management and Prognosis
The prognosis of glomerulonephritis varies enormously by type and severity. Post-infectious glomerulonephritis in children has an excellent prognosis, with most children recovering kidney function. IgA nephropathy has a more variable course – some patients have benign disease, while others progress slowly to kidney failure, though newer therapies aim to change that trajectory. Membranous nephropathy follows a rough “rule of thirds.” RPGN, FSGS, and aggressive vasculitis generally carry a more guarded prognosis, especially when treatment is delayed.
Long-term monitoring includes regular measurement of kidney function (eGFR), proteinuria, blood pressure, and disease-specific biomarkers such as anti-PLA2R antibodies. Patients on immunosuppressive therapy require monitoring for medication side effects, including infection risk, bone density loss, elevated blood sugar, and (with certain agents) bladder toxicity and effects on fertility. Vaccinations and infection precautions are an important part of care while on these medicines.
If kidney function declines to end-stage kidney disease, renal replacement therapy – dialysis or kidney transplantation – becomes necessary. Transplantation is generally the preferred option when feasible, though some types of glomerulonephritis (particularly FSGS) can recur in the transplanted kidney. Patients should begin discussions about transplant options well before reaching end-stage disease, allowing time for evaluation and planning.
Frequently Asked Questions
Is glomerulonephritis an autoimmune disease?
Many forms of glomerulonephritis have an autoimmune component – the immune system attacks the kidney’s own tissue or deposits immune complexes in the glomeruli. Lupus nephritis, anti-GBM disease, and ANCA-associated glomerulonephritis are clearly autoimmune. IgA nephropathy and membranous nephropathy involve abnormal immune responses. However, some forms are triggered by infections or other non-autoimmune mechanisms, so glomerulonephritis as a whole is not exclusively autoimmune.
Can glomerulonephritis be cured?
Some forms can be cured or achieve lasting remission. Post-infectious glomerulonephritis typically resolves completely. Some cases of membranous nephropathy remit spontaneously or with treatment. However, chronic forms like IgA nephropathy and FSGS are generally not curable – the goal is to slow or halt progression and maintain kidney function as long as possible. Early diagnosis and modern, aggressive treatment improve outcomes significantly.
What does foamy urine mean?
Persistently foamy urine can be a sign of protein in the urine (proteinuria), which is a hallmark of glomerular disease. Occasional foamy urine from concentrated or fast-flowing urine is normal. If you consistently notice excessive foam that does not dissipate quickly, you should have your urine tested for protein. Even a simple urine dipstick can detect significant proteinuria.
Can diet help manage glomerulonephritis?
Diet plays a supportive role. Sodium restriction helps control blood pressure and edema. In nephrotic syndrome, a moderate-protein diet (avoiding both excess and deficiency) is generally recommended. As kidney function declines, dietary restrictions on potassium, phosphorus, and protein may become necessary. A renal dietitian can provide personalized guidance based on your specific condition and kidney function level. Diet supports, but does not replace, medical treatment.
How common is glomerulonephritis in children?
Glomerulonephritis is more common in children than many realize, with post-infectious glomerulonephritis being a frequent cause of acute kidney disease in children worldwide. Minimal change disease (a related glomerular condition) is the most common cause of nephrotic syndrome in children. Most pediatric glomerular diseases respond well to treatment, and the overall prognosis in children is generally better than in adults.
Partnering With Your Nephrologist
Glomerulonephritis management requires a close, ongoing relationship with a nephrologist. If you have been diagnosed, make sure you understand your specific type – the name matters because different types have vastly different treatment approaches and prognoses. Take all medications as prescribed, attend every monitoring appointment, and report new symptoms like increased swelling, decreased urine output, or worsening fatigue promptly.
Be proactive about kidney-protective measures: control your blood pressure, take your ACE inhibitor or ARB and any SGLT2 inhibitor as prescribed, limit sodium, and avoid nephrotoxic medications (especially NSAIDs) unless your kidney doctor approves them. If immunosuppressive therapy is recommended, understand the rationale, the expected benefits, and the potential side effects – and never stop it on your own, even if you feel better. Glomerulonephritis is a serious diagnosis, but with accurate diagnosis, targeted treatment, and consistent monitoring, many patients maintain kidney function for decades.