Glomerulonephritis for NEET PG — Complete Guide 2026 | NEETPGAI
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Glomerulonephritis for NEET PG — Complete Guide 2026
Master glomerulonephritis for NEET PG 2026: nephrotic vs nephritic syndromes, minimal change, FSGS, membranous, IgA, PSGN, MPGN, RPGN, lupus nephritis, Alport syndrome, and biopsy-directed management.
NEETPGAI EditorialPublished 26 Jan 202620 min read
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This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
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Membranous — anti-PLA2R (70–80% primary); spikes on silver stain; rule out malignancy, HBV, SLE; modified Ponticelli or rituximab for high-risk
IgA nephropathy — commonest primary GN globally; synpharyngitic haematuria (within 1–3 d of URI); RAAS blockade + steroids in high-risk (KDIGO 2021)
PSGN — 1–3 wk post-pharyngitis / 3–6 wk post-pyoderma; low C3 (recovers <8 wk); subepithelial humps on EM; supportive care
MPGN — tram-track GBM; split into C3 glomerulopathy (alternative complement dysregulation) and immune-complex (HCV cryo, SLE)
RPGN — crescents >50% of glomeruli; type I anti-GBM, type II immune-complex, type III pauci-immune ANCA (GPA/MPA/EGPA); pulse steroids + cyclophosphamide/rituximab ± plasmapheresis
Lupus nephritis — ISN/RPS 2003: I minimal, II mesangial, III focal, IV diffuse, V membranous, VI advanced sclerosis; III/IV = immunosuppress
Alport — X-linked COL4A5 (85%); GN + sensorineural deafness + lenticonus; basket-weave GBM; thin basement membrane disease is the benign familial haematuria mimic
Glomerulonephritis vignettes pepper NEET PG — the child with periorbital oedema and frothy urine, the man with cola-coloured urine 2 weeks after sore throat, the young woman with malar rash and proteinuria, the smoker with haemoptysis and acute renal failure. Getting the nephrotic-vs-nephritic decision right, reading the complement pattern, and recognising the named antibodies (anti-PLA2R, ANCA, anti-GBM) separates marks. This guide covers syndromes, biopsy patterns, lupus classes, Alport, and management. Pair with the medicine subject hub, the AKI and CKD guide, and the autoimmune and connective tissue disease guide for integrated revision.
Nephrotic vs nephritic syndromes
Nephrotic and nephritic syndromes are the two clinical phenotypes of glomerular disease — defined by urinary features, mechanism of injury, and renal function — and separating them frames all further work-up.
Minimal change disease and focal segmental glomerulosclerosis sit at the primary-podocytopathy end of the nephrotic spectrum — both cause foot-process effacement, but light microscopy and prognosis differ.
Minimal change disease (MCD):
Commonest cause of nephrotic syndrome in children (~80–90%, peak 2–6 years)
10–15% of adult nephrotic syndrome
Light microscopy — normal glomeruli
Immunofluorescence — negative
Electron microscopy — diffuse podocyte foot-process effacement (pathognomonic)
Secondary / genetic — RAAS blockade and treat cause; steroids NOT indicated
HIV-associated nephropathy (HIVAN) — ART dramatically improves outcomes
Membranous nephropathy and IgA nephropathy
Membranous nephropathy (MN) and IgA nephropathy represent two classic primary glomerulonephritides — one nephrotic and subepithelial, one nephritic and mesangial.
Membranous nephropathy:
Commonest primary cause of adult nephrotic syndrome in many series
Primary (idiopathic) — ~75%; anti-PLA2R antibody in 70–80% (phospholipase A2 receptor on podocytes); anti-THSD7A in ~5%; anti-NELL1 etc. are newer antigens
Risk stratification (KDIGO 2021): low / moderate / high / very-high risk by GFR, proteinuria, anti-PLA2R titre
Low risk — RAAS blockade, diuretics, statin, anticoagulation if albumin <2 g/dL
Moderate–high risk — immunosuppression: rituximab (first-line alternative) or modified Ponticelli (alternating monthly IV methylprednisolone + oral cyclophosphamide × 6 months)
Very-high risk / rituximab-resistant — cyclophosphamide-based or calcineurin inhibitors
Exclude and treat secondary cause first
IgA nephropathy (Berger disease):
Commonest primary GN globally; high prevalence in East Asia
Classic — synpharyngitic haematuria (episodic visible haematuria within 1–3 days of URI or mucosal infection) — distinguish from PSGN (10–21 day latency)
Also — isolated microscopic haematuria, proteinuria, hypertension, nephrotic range in advanced disease
Light microscopy — mesangial proliferation
IF — dominant IgA deposits in the mesangium, often with C3
RAAS blockade (ACEi/ARB) for proteinuria >0.5 g/day, target BP <120/80
Glucocorticoids (or enteric-coded budesonide targeting Peyer's patches) for persistently high-risk (proteinuria >1 g/day after 3–6 months of optimal supportive care)
Cyclophosphamide + steroids for RPGN / crescentic IgA
SGLT2 inhibitors (dapagliflozin, empagliflozin) reduce proteinuria and slow progression
Henoch-Schönlein purpura (IgA vasculitis) is the systemic form — purpura, arthritis, abdominal pain, nephritis; same renal treatment principles
Post-streptococcal GN and MPGN
Post-streptococcal glomerulonephritis and membranoproliferative glomerulonephritis both cause nephritic syndrome with hypocomplementaemia — but temporal pattern, pathology, and prognosis separate them.
Post-streptococcal glomerulonephritis (PSGN):
Classic paediatric nephritic syndrome, ages 3–12 years
Trigger — group A beta-haemolytic streptococcus (certain "nephritogenic" M serotypes — 1, 4, 12, 49, 55)
Rapidly progressive glomerulonephritis (RPGN) is the nephrology emergency — a nephritic syndrome with rapid decline in renal function over days to weeks, defined pathologically by crescents in >50% of glomeruli.
Crescent formation — inflammatory cells (macrophages, T cells), fibrin, and Bowman capsule epithelial cells fill the urinary space; represents severe GBM injury with rupture.
Induction for class III/IV (and V with nephrotic-range):
High-dose steroids + MMF (2–3 g/day) or IV cyclophosphamide (NIH or Euro-Lupus low-dose)
Belimumab or voclosporin as add-on per 2024 guidelines
Rituximab in refractory disease
Maintenance — MMF or azathioprine, low-dose steroid; usually >3 years before attempting taper.
Adjuncts — hydroxychloroquine in all SLE, statin, RAAS blockade, BP <130/80, sun protection.
Alport syndrome and thin basement membrane disease
Alport syndrome is a hereditary type IV collagen disorder causing progressive glomerulonephritis, sensorineural deafness, and ocular anomalies — and it must be distinguished from the benign thin basement membrane disease.
Alport syndrome:
Inheritance
Gene
Frequency
Notes
X-linked
COL4A5
~85% (classical)
Severe in males, milder in heterozygous females
Autosomal recessive
COL4A3 or COL4A4
~10%
Severe in both sexes
Autosomal dominant
COL4A3/4
~5%
Milder
Type IV collagen α3/α4/α5 trimer — GBM, cochlea, lens, retina
Clinical triad:
Progressive GN — microscopic haematuria from early childhood, proteinuria, hypertension, ESRD by 20s–30s in X-linked males
Bilateral sensorineural hearing loss — high-frequency; develops in late childhood/adolescence
Biopsy — electron microscopy shows diffuse GBM thickening with basket-weave splitting (lamellation of lamina densa); IF may show absence of α3/α4/α5 on monoclonal staining
Dialysis and transplant for ESRD — post-transplant anti-GBM disease possible (in the ~3–5% who make anti-α5 antibodies against the normal donor kidney)
Treat cause (HCV DAA, autoimmune) ± immunosuppression
C3 glomerulopathy
RAAS; eculizumab / complement-targeted in selected
RPGN anti-GBM
Plasmapheresis + steroids + cyclophosphamide
RPGN ANCA
Steroids + cyclophosphamide or rituximab ± plasmapheresis (severe)
LN III/IV (A)
Steroids + MMF or IV cyclophosphamide; add belimumab / voclosporin
LN V (nephrotic)
MMF + steroids (or CNI)
LN VI
Transplant; immunosuppression futile
Alport
RAAS blockade ± SGLT2i; transplant in ESRD
Sources and references
Harrison's Principles of Internal Medicine, 21st Edition (Loscalzo, Fauci, Kasper, Hauser, Longo, Jameson, Eds., 2022) — Chapters on glomerular diseases and lupus nephritis.
Brenner and Rector's The Kidney, 11th Edition (Yu, Chertow, Luyckx, Marsden, Skorecki, Taal, Eds., 2020) — Detailed chapters on MCD, FSGS, membranous, IgA, MPGN, RPGN, and lupus nephritis.
KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Int 2021; 100(4S):S1-S276.
Rovin BH et al. KDIGO 2024 Clinical Practice Guideline for the Management of Lupus Nephritis. Kidney Int 2024; 105(6S):S1-S69.
Appel GB and Jayne D. Rapidly progressive glomerulonephritis. NEJM 2021; 384:1038-1048.
Lafayette RA and Kelepouris E. Immunoglobulin A Nephropathy: Advances in Understanding of Pathogenesis and Treatment. Am J Nephrol 2022; 53:712-726.
Frequently asked questions
How many glomerulonephritis questions appear in NEET PG?
Glomerulonephritis contributes 3-4 direct questions per NEET PG paper across medicine, pathology, and paediatrics. Recurring themes include distinguishing nephrotic from nephritic syndrome, minimal change disease as the commonest nephrotic syndrome in children, IgA nephropathy as the commonest primary glomerulonephritis globally, membranous nephropathy and anti-PLA2R antibody, rapidly progressive GN pathology (crescents), and ISN/RPS lupus nephritis classes III and IV mandating immunosuppression.
What is the difference between nephrotic and nephritic syndrome?
Nephrotic syndrome is defined by heavy proteinuria (greater than 3.5 g/24 h in adults), hypoalbuminaemia (less than 3 g/dL), oedema, hyperlipidaemia, and lipiduria with bland urinary sediment. Nephritic syndrome is characterised by haematuria (dysmorphic RBCs, RBC casts), variable proteinuria (usually less than 3.5 g/24 h), hypertension, oedema, and renal dysfunction (rising creatinine). Pathologically, nephrotic syndromes have podocyte/basement-membrane injury with minimal inflammation, while nephritic syndromes are inflammatory with endothelial and mesangial proliferation.
What is the commonest cause of nephrotic syndrome in children?
Minimal change disease (MCD) accounts for about 80-90 percent of nephrotic syndrome in children aged 1-10 years. Light microscopy is normal; electron microscopy shows diffuse podocyte foot-process effacement. Most children respond to oral prednisolone 60 mg/m^2/day for 4-6 weeks, with response defining steroid-sensitive nephrotic syndrome. About 25 percent are frequent relapsers. Biopsy is NOT routinely needed in a typical 1-10 year old — empirical steroids are given; biopsy is reserved for steroid resistance, atypical features (hypertension, haematuria, raised creatinine), or age outside the typical window.
What is FSGS and how is it treated?
Focal segmental glomerulosclerosis is a histological pattern of focal (some glomeruli) segmental (part of glomerulus) sclerosis. Variants include tip, perihilar, cellular, collapsing (classic HIV-associated, most aggressive), and NOS. Secondary causes include HIV, heroin, obesity, reflux nephropathy, reduced nephron mass, and APOL1 risk alleles (African ancestry). Primary/idiopathic FSGS is treated with prolonged corticosteroids; calcineurin inhibitors (ciclosporin, tacrolimus) or rituximab in steroid-resistant. Secondary FSGS is treated by addressing the underlying cause plus RAAS blockade; steroids are not indicated.
What is the antibody associated with membranous nephropathy?
Anti-phospholipase A2 receptor (anti-PLA2R) antibody is positive in about 70-80 percent of primary (idiopathic) membranous nephropathy and is useful both for diagnosis and treatment monitoring. Anti-THSD7A (5 percent) is another primary marker. Secondary causes include malignancy (especially solid tumours in the elderly), hepatitis B, SLE, drugs (penicillamine, NSAIDs, gold), and autoimmune disease. Light microscopy shows thickened GBM with spikes on silver stain; electron microscopy shows subepithelial deposits. Treatment uses the modified Ponticelli regimen or rituximab for high-risk primary MN; treat the cause in secondary.
What is IgA nephropathy?
IgA nephropathy (Berger disease) is the commonest primary glomerulonephritis globally. Classic presentation is recurrent synpharyngitic haematuria — episodic visible haematuria within 1-3 days of an upper respiratory infection (note — post-streptococcal GN is 10-14 days after, with a latent period). Renal biopsy shows IgA-dominant mesangial deposits on immunofluorescence, mesangial proliferation on light microscopy. Management is RAAS blockade for proteinuria greater than 1 g/day, blood-pressure control, and glucocorticoids (or targeted budesonide) for persistently high-risk patients per KDIGO 2021 guidelines.
How does post-streptococcal glomerulonephritis present?
Post-streptococcal GN (PSGN) is a nephritic syndrome 1-3 weeks after a group A streptococcal pharyngitis (or 3-6 weeks after pyoderma) in children aged 3-12 years. Features include haematuria (often cola-coloured), hypertension, oedema (especially periorbital), and oliguria. Investigations show elevated ASO titre or anti-DNase B, low C3 complement (lasts less than 8 weeks — a longer drop suggests MPGN or lupus), and subepithelial humps on electron microscopy. Management is supportive — fluid and salt restriction, loop diuretics for volume overload, antihypertensives. Most children recover fully; prognosis is worse in adults.
What is rapidly progressive glomerulonephritis?
Rapidly progressive glomerulonephritis (RPGN) is a nephritic syndrome with rapid loss of renal function over days to weeks, pathologically defined by crescents in greater than 50 percent of glomeruli. Three types by immunofluorescence — type I (linear) anti-GBM / Goodpasture, type II (granular) immune-complex (lupus, post-infectious, IgA, cryoglobulinaemia, HSP), type III (pauci-immune) ANCA-associated (GPA, MPA, EGPA). Management is urgent — pulse methylprednisolone plus cyclophosphamide or rituximab, plus plasmapheresis for anti-GBM disease and for ANCA-associated RPGN with alveolar haemorrhage or dialysis-dependent creatinine.
What are the ISN/RPS classes of lupus nephritis?
The ISN/RPS 2003 (updated 2018) classification has six classes. Class I — minimal mesangial; Class II — mesangial proliferative. Class III — focal (less than 50 percent glomeruli); Class IV — diffuse (greater than or equal to 50 percent); each subdivided into active (A), chronic (C), or mixed. Class V — membranous (subepithelial deposits). Class VI — advanced sclerosis (greater than or equal to 90 percent globally sclerosed). Classes III and IV require immunosuppression (steroids + mycophenolate mofetil or cyclophosphamide); class V with nephrotic-range proteinuria is treated; class VI is not reversible with immunosuppression.
What is Alport syndrome?
Alport syndrome is a hereditary collagen IV disorder caused by mutations in COL4A3, COL4A4 (autosomal), or COL4A5 (X-linked — commonest, about 85 percent). The triad is progressive glomerulonephritis (haematuria progressing to proteinuria and renal failure), bilateral sensorineural hearing loss (high-frequency), and ocular anomalies (anterior lenticonus, dot-and-fleck retinopathy). Electron microscopy shows basket-weave splitting of the GBM. Thin basement membrane disease (benign familial haematuria) is heterozygous COL4A3/4 and causes isolated microscopic haematuria with a uniformly thin GBM. Management is RAAS blockade to delay progression; dialysis or transplant in ESRD.
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This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
Written by: NEETPGAI Editorial Team
Reviewed by: Pending SME Review
Last reviewed: January 2026
This article is reviewed by qualified medical professionals for clinical accuracy and exam relevance. For corrections or updates, contact the editorial team.
