What is glomerulonephritis?

Glomerulonephritis is inflammation and damage of the glomeruli — the million tiny filters in each kidney that separate waste from blood. When they are damaged, two things leak through that should not: blood and protein. Depending on the pattern of injury, the result is either a nephritic picture (blood in the urine, high blood pressure, swelling and falling kidney function) or a nephrotic picture (heavy protein loss, low blood albumin, marked swelling and high cholesterol). There are many distinct diseases within this umbrella — IgA nephropathy, membranous nephropathy, minimal change disease, lupus nephritis, ANCA-associated vasculitis and others — and they differ completely in cause, treatment and outlook, which is why a kidney biopsy is usually needed.

Why does blood plus protein in the urine matter so much?

Because it changes both the diagnosis and the specialty. Blood alone in an adult's urine usually prompts investigation of the bladder and kidneys for cancer, which is appropriate. But blood together with protein — or with high blood pressure, swelling, or a rising creatinine — points to the filters themselves being inflamed, and that requires urgent nephrology assessment rather than urological investigation. Under the microscope, the red cells from a glomerular source are distorted in shape and may be accompanied by red cell casts, which are effectively diagnostic. The reason this matters urgently is that some forms of glomerulonephritis destroy kidney tissue within weeks, and the damage is not recoverable once scarring is established.

When is glomerulonephritis an emergency?

When kidney function is falling rapidly. Rapidly progressive glomerulonephritis causes creatinine to rise over days to weeks, with blood and protein in the urine, and corresponds to crescent formation in the glomeruli — an aggressive, destructive process. Left untreated for even a few weeks, it converts recoverable inflammation into permanent scarring and dialysis dependence. Warning features: rapidly worsening kidney function; coughing blood, which suggests anti-GBM disease or ANCA-associated vasculitis affecting the lungs; a rash, joint pains, sinus symptoms or nerve involvement suggesting systemic vasculitis. This situation requires same-day blood tests for the relevant antibodies, urgent kidney biopsy, and treatment started immediately — often before the biopsy result is available, because waiting costs nephrons.

Is IgA nephropathy serious?

It can be, and it was underestimated for many years. IgA nephropathy is the most common primary glomerular disease worldwide, and often presents mildly — visible blood in the urine during a throat infection, or blood and protein found incidentally. But up to thirty to forty per cent of patients eventually develop kidney failure over the following decades, particularly those with persistent proteinuria, high blood pressure or scarring on biopsy. The encouraging change is that after decades in which only blood pressure control and protein reduction could be offered, there are now genuine treatment options: maximal blockade of the renin-angiotensin system and SGLT2 inhibitors as the foundation, plus newer targeted therapies including a gut-targeted steroid that acts where the abnormal IgA is produced, endothelin receptor antagonists, and complement pathway inhibitors.

What treatments are used?

Two layers. The first is supportive therapy, which applies to almost every patient and does more to determine long-term kidney survival than is usually appreciated: an ACE inhibitor or ARB pushed to the maximum tolerated dose to reduce protein leakage; an SGLT2 inhibitor, which now has strong evidence in non-diabetic proteinuric kidney disease; tight blood pressure control; a low-salt diet, without which the other drugs work far less well; statins; stopping smoking; and avoiding nephrotoxic drugs such as NSAIDs. The second layer is disease-specific immunosuppression, used only when the diagnosis warrants it — corticosteroids, mycophenolate, cyclophosphamide, rituximab, calcineurin inhibitors, or newer targeted agents — because immunosuppression in the wrong diagnosis, such as secondary FSGS or diabetic kidney disease, causes harm without benefit.

How does GMJ News cover glomerulonephritis?

GMJ News covers the haematuria-plus-proteinuria referral rule, the nephritic and nephrotic frameworks, rapidly progressive glomerulonephritis as an emergency with its three immunological patterns, IgA nephropathy and the new targeted therapies, membranous nephropathy and anti-PLA2R serology, lupus nephritis classification and newer agents, post-infectious glomerulonephritis and its different course in adults, complement patterns as a diagnostic shortcut, Alport syndrome and thin basement membrane disease, kidney biopsy indications and prognostic value, nephrotic syndrome complications including thromboembolism, and supportive therapy including SGLT2 inhibitors. Relevant to PHIG's kidney health and rheumatology programmes.

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Glomerulonephritis

GMJ News knowledge hub · last reviewed August 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Glomerulonephritis — immune-mediated inflammation of the glomeruli — encompasses a heterogeneous group of diseases that together represent a leading cause of end-stage kidney disease worldwide, and is conventionally approached through two clinical syndromes: nephritic (haematuria with dysmorphic red cells and red cell casts, hypertension, oedema and declining function) and nephrotic (proteinuria above 3.5g per day, hypoalbuminaemia, oedema and hyperlipidaemia), with the practical corollary that dipstick haematuria plus proteinuria in the same patient should always prompt urgent nephrology referral rather than urological investigation alone (WHO). The field has been transformed by molecular diagnosis and targeted therapy: the discovery that most primary membranous nephropathy is caused by antibodies against the phospholipase A2 receptor (PLA2R) made a serological diagnosis possible for the first time, while IgA nephropathy — the commonest primary glomerulonephritis globally — now has multiple newly approved targeted therapies after decades in which supportive care was all that could be offered.

Key messages

Haematuria plus proteinuria together means nephrology, not urology

The single most useful practical rule. Isolated visible haematuria in an adult warrants urological investigation for malignancy. But haematuria accompanied by proteinuria, hypertension, oedema or declining kidney function points to glomerular disease and requires urgent NEPHROLOGY referral. Dysmorphic red cells and red cell casts on urine microscopy confirm a glomerular source. Missing this pattern — investigating the urinary tract while glomerular inflammation progresses — is a recurrent cause of avoidable irreversible kidney damage.

Nephritic versus nephrotic — the organising framework

Nephritic syndrome: haematuria with dysmorphic red cells and red cell casts, variable proteinuria, hypertension, oedema and reduced GFR — reflecting inflammatory, proliferative glomerular injury. Causes: IgA nephropathy, post-infectious glomerulonephritis, ANCA-associated vasculitis, anti-GBM disease, lupus nephritis, membranoproliferative GN. Nephrotic syndrome: proteinuria above 3.5g/day, hypoalbuminaemia, oedema and hyperlipidaemia — reflecting podocyte injury without prominent inflammation. Causes: minimal change disease, FSGS, membranous nephropathy, diabetic nephropathy, amyloidosis. Many diseases produce mixed pictures, and the distinction guides urgency and investigation rather than replacing biopsy.

Rapidly progressive glomerulonephritis is a medical emergency

RPGN — a rise in creatinine over days to weeks with an active urinary sediment, corresponding to crescentic glomerulonephritis on biopsy — destroys nephrons irreversibly within weeks. The three immunological patterns: anti-GBM (Goodpasture) disease with linear IgG deposition, often with pulmonary haemorrhage; pauci-immune ANCA-associated vasculitis; and immune complex disease (lupus, IgA, post-infectious). Investigation must be same-day: ANCA, anti-GBM antibodies, ANA and anti-dsDNA, complement C3 and C4, hepatitis B and C, HIV, serum free light chains, plus urgent biopsy. Treatment cannot wait for the biopsy result in fulminant disease — delay of even days changes the outcome from recovery to dialysis dependence.

IgA nephropathy — the commonest primary GN worldwide, and now treatable

IgA nephropathy classically presents with visible haematuria occurring WITH an upper respiratory infection (synpharyngitic — distinguishing it from post-streptococcal GN, which follows 1-3 weeks later), or is found as asymptomatic haematuria and proteinuria. Long dismissed as benign, up to 30-40% reach kidney failure over decades. After decades in which supportive care was all that could be offered, the field has changed rapidly: maximal renin-angiotensin blockade and SGLT2 inhibitors as foundational therapy, plus targeted agents including a gut-targeted budesonide formulation acting on Peyer's patch IgA production, endothelin and dual endothelin-angiotensin receptor antagonists, and complement pathway inhibitors.

Membranous nephropathy — a serological diagnosis since PLA2R

The discovery that around 70-80% of primary membranous nephropathy is caused by autoantibodies against the M-type phospholipase A2 receptor on podocytes transformed the disease. Anti-PLA2R antibody testing allows diagnosis without biopsy in appropriate cases, monitors disease activity, predicts spontaneous remission and relapse, and guides immunosuppression duration — an unusual example of a true serological biomarker in nephrology. THSD7A accounts for a small further proportion. Secondary causes must still be excluded: malignancy (particularly in older patients — membranous nephropathy can be paraneoplastic), hepatitis B, lupus, and drugs including NSAIDs and penicillamine. Rituximab has largely replaced cyclophosphamide-based regimens as first-line immunosuppression.

Supportive therapy is not second-best — it is the foundation

Whatever the specific diagnosis, the therapy that determines long-term kidney survival is often supportive: maximally tolerated ACE inhibitor or ARB to reduce proteinuria (the single strongest modifiable predictor of progression); SGLT2 inhibitors, which now have proven benefit in non-diabetic proteinuric kidney disease and represent one of the most significant advances in nephrology in decades; strict blood pressure control; dietary sodium restriction, without which RAS blockade is far less effective; statins; smoking cessation; and avoidance of nephrotoxins including NSAIDs. In nephrotic syndrome, add attention to thromboembolic risk, which is substantially elevated, particularly with membranous nephropathy and serum albumin below 20-25 g/L.

Key statistics

Haematuria + proteinuria

together indicate glomerular disease — urgent nephrology, not urology, referral

KDIGO/ISN

RPGN

creatinine rising over days to weeks with active sediment — same-day serology and biopsy

KDIGO

30-40%

of IgA nephropathy patients reach kidney failure over decades — it is not benign

KDIGO/ISN

70-80%

of primary membranous nephropathy is anti-PLA2R positive — a serological diagnosis

NEJM/KDIGO

Proteinuria

the single strongest modifiable predictor of progression — reduction is the therapeutic target

KDIGO

SGLT2i

now proven in non-diabetic proteinuric kidney disease — foundational supportive therapy

NEJM/KDIGO

Primary glomerular disease — approximate relative frequency of biopsy diagnoses

Source: Registry data varies substantially by region, ethnicity and biopsy policy — IgA nephropathy predominates in East Asia.

Glossary of key terms

Kidney biopsy
NephrologyThe definitive investigation in glomerular disease, providing light microscopy, immunofluorescence and electron microscopy — all three are necessary, since the pattern of immune deposits on immunofluorescence and podocyte changes on electron microscopy frequently determine the diagnosis when light microscopy is non-specific. Indications: nephrotic syndrome in adults (children with typical minimal change presentation are usually treated empirically first); unexplained acute kidney injury with active sediment; suspected RPGN; systemic disease with renal involvement; and progressive proteinuric CKD of unclear cause. Risks: bleeding requiring transfusion in around 1%, and intervention in a smaller proportion; managed by correcting coagulopathy, controlling blood pressure and stopping antiplatelet agents beforehand. Biopsy also provides essential prognostic information — the degree of interstitial fibrosis and tubular atrophy predicts outcome better than the glomerular lesion itself.

Complement in glomerular disease
Immunology/NephrologyComplement levels are cheap, fast and highly informative in narrowing the differential. LOW C3 with low or normal C4: post-infectious glomerulonephritis (C3 recovers within 8-12 weeks — persistent low C3 should prompt reconsideration), C3 glomerulopathy, membranoproliferative GN. LOW C3 AND LOW C4: lupus nephritis, cryoglobulinaemia, endocarditis-associated GN. NORMAL complement: IgA nephropathy, ANCA-associated vasculitis, anti-GBM disease, minimal change, FSGS, membranous nephropathy. C3 glomerulopathy specifically results from dysregulation of the alternative complement pathway, often with C3 nephritic factor or genetic complement abnormalities, and is a target for the complement inhibitor drugs now entering nephrology.

Post-infectious glomerulonephritis
Infectious/NephrologyClassically follows group A streptococcal pharyngitis or skin infection after a latent period of 1-3 weeks (contrast with the synpharyngitic haematuria of IgA nephropathy, which occurs during the infection). Presents with nephritic syndrome: cola-coloured urine, oedema, hypertension, reduced urine output. Investigations: low C3 with normal or low C4, recovering by 8-12 weeks; ASO or anti-DNase B titres. Prognosis in children is excellent with supportive management alone — antibiotics do not alter the renal course, since it is immune complex mediated. In adults, particularly those with diabetes, alcohol dependence or immunosuppression, the picture is different: staphylococcus-associated glomerulonephritis carries a substantially worse prognosis, and endocarditis and deep-seated infection must be excluded before immunosuppression is considered.

Lupus nephritis
Rheumatology/NephrologyAffects a substantial proportion of patients with systemic lupus erythematosus, and is a major determinant of morbidity and mortality. Classified by the ISN/RPS system into classes I-VI, with class III (focal proliferative), class IV (diffuse proliferative — the most severe) and class V (membranous) determining treatment. Monitoring: urine protein-creatinine ratio, sediment, complement and anti-dsDNA. Because clinically silent nephritis is common, urinalysis at every lupus review is essential. Treatment has advanced considerably: mycophenolate mofetil or low-dose cyclophosphamide with corticosteroids as induction, and newer additions — belimumab and voclosporin — improving renal response rates when added to standard therapy. Hydroxychloroquine should be continued in all patients unless contraindicated, as it improves renal and overall outcomes.

Alport syndrome and thin basement membrane disease
Genetics/NephrologyImportant causes of persistent non-visible haematuria that are frequently mislabelled. Alport syndrome: mutations in type IV collagen genes (COL4A3, COL4A4, COL4A5), most commonly X-linked, causing progressive haematuric nephropathy with sensorineural hearing loss and ocular abnormalities including anterior lenticonus. Male X-linked patients typically progress to kidney failure; heterozygous females were historically considered carriers but are now recognised to have meaningful lifetime risk. Thin basement membrane nephropathy (benign familial haematuria) reflects heterozygous COL4A3/COL4A4 variants and is usually non-progressive — but the two conditions form a spectrum, and genetic testing has largely replaced the older assumption of benignity. RAS blockade started early slows progression in Alport syndrome, making early diagnosis genuinely consequential.

Nephrotic syndrome complications
ClinicalBeyond the oedema, nephrotic syndrome carries specific and serious complications that must be actively managed. Thromboembolism: urinary loss of antithrombin III and other regulatory proteins produces a hypercoagulable state — deep vein thrombosis, pulmonary embolism and renal vein thrombosis (classically in membranous nephropathy, presenting with flank pain, haematuria and deteriorating function); prophylactic anticoagulation is considered when albumin falls below approximately 20-25 g/L, particularly in membranous disease. Infection: loss of immunoglobulins and complement factors increases susceptibility to encapsulated organisms — pneumococcal vaccination is indicated, and spontaneous bacterial peritonitis occurs particularly in children. Also: acute kidney injury from intravascular depletion or interstitial oedema, hyperlipidaemia, vitamin D deficiency, and protein malnutrition.