Quick Answer
Glomerular diseases deliver 2 to 3 NEET PG questions per paper across Pediatrics, Nephrology, and Pathology. The high-yield framework:
- Nephrotic — heavy proteinuria (above 3.5 g per day), hypoalbuminaemia, edema, hyperlipidaemia. Major causes: minimal change (children), FSGS (adults overall), membranous (older adults), diabetic nephropathy (most common secondary cause).
- Nephritic — haematuria with red cell casts, mild proteinuria, hypertension, oliguria. Major causes: PSGN, IgA nephropathy, MPGN, anti-GBM, lupus, ANCA-associated, RPGN.
- MCD in children — biopsy not needed before steroid trial; over 90 percent respond to steroids.
- Membranous — anti-PLA2R antibody is diagnostic in primary form; rule out malignancy and hepatitis B in adults above 50.
- PSGN — low C3, normalises in 6 to 8 weeks; supportive care.
- RPGN — emergency. Crescents on biopsy. Pulse steroids plus cyclophosphamide or rituximab; plasmapheresis for anti-GBM and severe ANCA disease.
Glomerular disease is one of the highest-yield Internal Medicine and Pediatrics topics on NEET PG because the pathology classification, the histology images, and the clinical-vignette pattern recognition all converge into a small number of testable archetypes. The 2021 KDIGO Glomerular Diseases guideline restructured therapy, and Indian paediatric protocols (ISPN 2021) align closely with international consensus while accounting for local infection profiles.
This NEETPGAI deep dive walks through the nephrotic and nephritic phenotypes, the histopathology patterns examiners ask repeatedly, the steroid-response algorithm, the second-line agents, and the high-yield traps that distinguish good answers from great ones. Pair it with the Pediatrics subject hub and the acute kidney injury and CKD guide.
Nephrotic vs nephritic — clinical distinction
The first NEET PG question in this topic is almost always to assign a stem to one of two camps.
| Feature | Nephrotic syndrome | Nephritic syndrome |
|---|
| Proteinuria | Above 3.5 g per day (massive) | Mild to moderate (under 3 g per day) |
| Haematuria | Microscopic if any | Macroscopic with red cell casts |
| Red cell casts | Absent | Present |
| Edema | Marked, periorbital and dependent | Mild, periorbital |
| Hypertension | Late or absent | Early and prominent |
| Oliguria/AKI | Late | Often early |
| Serum albumin | Below 3 g/dL | Usually preserved |
| Hyperlipidaemia | Marked | Absent |
| Biopsy hallmark | Podocyte / GBM disease | Inflammatory cell infiltrate, crescents in severe cases |
A "mixed" picture (nephritic-nephrotic overlap) is common in MPGN, lupus class IV, and severe IgA — a frequent stem variant.
Nephrotic syndrome — causes
Minimal change disease (MCD)
The most common nephrotic cause in children aged 1 to 10 years (above 80 percent of paediatric cases). Adults — about 10 to 15 percent of primary nephrotic syndrome.
- Pathology — light microscopy normal; electron microscopy shows diffuse podocyte foot-process effacement; immunofluorescence negative.
- Clinical pearls — abrupt onset, classic triphasic course (frequent relapser in some children).
- Secondary causes — Hodgkin lymphoma, NSAIDs, lithium.
- Treatment — empirical steroids in children: prednisolone 2 mg/kg/day (max 60 mg) for 4 to 6 weeks, then 1.5 mg/kg alternate-day for 4 to 6 weeks, then taper. About 90 percent respond.
Focal segmental glomerulosclerosis (FSGS)
The most common cause of primary nephrotic syndrome in adults overall, particularly in African and South Asian populations.
- Pathology — segmental sclerosis in some glomeruli; podocyte foot-process effacement.
- Variants — collapsing (HIV, parvovirus B19), tip lesion (best prognosis), perihilar (obesity-related), cellular, NOS.
- Secondary FSGS causes — HIV, heroin, obesity, reflux nephropathy, sickle cell, pamidronate.
- Genetic forms — NPHS1 (nephrin), NPHS2 (podocin), APOL1 (high risk in African ancestry).
- Treatment — high-dose steroids; cyclosporine or tacrolimus (calcineurin inhibitors) in steroid-resistant. Rituximab as third-line.
Membranous nephropathy
The most common nephrotic cause in white adults above 50. Approximately 70 to 80 percent of primary cases are anti-PLA2R positive.
- Pathology — diffuse subepithelial immune deposits; spike-and-dome pattern on silver stain (Jones methenamine); GBM thickening.
- Secondary causes — malignancy (especially solid tumours in older adults), hepatitis B, SLE (class V), drugs (gold, penicillamine, captopril, NSAIDs).
- Treatment — KDIGO 2021 favours rituximab over cyclosporine and over modified Ponticelli regimen (alternating monthly steroid and cyclophosphamide) for moderate-risk patients.
- Clinical pearl — highest risk of renal vein thrombosis among all nephrotic syndromes (about 30 percent). Always image the renal veins if AKI develops.
Membranoproliferative glomerulonephritis (MPGN)
Now reclassified by mechanism into immune-complex MPGN, C3 glomerulopathy (dense deposit disease and C3 GN), and thrombotic microangiopathy-associated.
- Pathology — tram-track double-contour appearance of GBM on silver stain (mesangial interposition); mixed nephritic-nephrotic picture.
- Causes — hepatitis C plus cryoglobulinaemia, chronic infection (endocarditis, malaria, schistosomiasis), autoimmune.
- Treatment — treat underlying cause; immunosuppression for idiopathic.
Diabetic nephropathy
Most common cause of nephrotic-range proteinuria and end-stage renal disease in adults overall.
- Pathology — Kimmelstiel-Wilson nodules (nodular glomerulosclerosis), GBM thickening, mesangial expansion.
- Treatment — glycaemic control, ACEi or ARB, SGLT2 inhibitor (now Class I in CKD with proteinuria irrespective of diabetes — DAPA-CKD, EMPA-KIDNEY trials), finerenone (FIDELIO-DKD).
Amyloidosis
AL (light-chain, plasma cell dyscrasia) or AA (chronic inflammation, TB, rheumatoid).
- Pathology — Congo red apple-green birefringence under polarised light.
- Treatment — daratumumab plus CyBorD for AL; treat underlying inflammation for AA.
Nephritic syndrome — causes
Post-streptococcal glomerulonephritis (PSGN)
Classical paediatric vignette — child aged 5 to 12 years with sudden cola-coloured urine, hypertension, periorbital edema, 1 to 3 weeks after strep pharyngitis or 3 to 6 weeks after impetigo.
- Lab — low C3 (normalises in 6 to 8 weeks), normal C4. Elevated ASO (post-pharyngitic) or anti-DNase B (post-skin).
- Pathology — endocapillary proliferation, neutrophil infiltration, subepithelial humps on EM ("starry-sky" on IF — granular IgG and C3).
- Treatment — supportive (salt restriction, diuretics, antihypertensives). Antibiotics for active infection but no effect on GN course.
- Prognosis — over 95 percent of children recover fully; adults may progress.
IgA nephropathy (Berger disease)
The most common primary glomerulonephritis worldwide.
- Clinical — synpharyngitic haematuria (gross haematuria within 24 to 48 hours of upper respiratory infection — distinguishes from PSGN's 1 to 3 week latent period).
- Pathology — mesangial IgA deposits on immunofluorescence (diagnostic).
- Treatment — ACEi or ARB to reduce proteinuria; KDIGO 2021 reserves immunosuppression for high-risk progressive disease (proteinuria above 1 g per day despite optimised RAS blockade); newer options include sparsentan and budesonide-targeted release.
Henoch-Schönlein purpura (IgA vasculitis)
Children with palpable purpura on lower limbs, abdominal pain, arthritis, haematuria. Same mesangial IgA deposits as IgA nephropathy.
Anti-GBM disease (Goodpasture)
- Clinical — pulmonary-renal syndrome (hemoptysis plus glomerulonephritis).
- Lab — anti-GBM antibodies (against alpha-3 chain of type IV collagen).
- Pathology — linear IgG deposition along GBM on immunofluorescence; crescents.
- Treatment — pulse methylprednisolone, cyclophosphamide, plasmapheresis (until antibody negative). Smoking exacerbates pulmonary haemorrhage.
ANCA-associated vasculitis (small-vessel)
- GPA (granulomatosis with polyangiitis) — c-ANCA / anti-PR3; saddle-nose, sinusitis, lung cavities, glomerulonephritis.
- MPA (microscopic polyangiitis) — p-ANCA / anti-MPO; pulmonary capillaritis, GN, no granulomas.
- EGPA (eosinophilic granulomatosis with polyangiitis) — asthma, eosinophilia, p-ANCA in 40 percent.
- Pathology — pauci-immune crescentic GN (no immunoglobulin deposits).
- Treatment — pulse steroids plus cyclophosphamide or rituximab; plasmapheresis for severe disease.
Lupus nephritis
ISN/RPS classification I to VI:
- Class I — minimal mesangial.
- Class II — mesangial proliferative.
- Class III — focal proliferative.
- Class IV — diffuse proliferative (most common, worst prognosis, full-house IF).
- Class V — membranous.
- Class VI — advanced sclerosing.
Class III and IV need pulse steroids plus mycophenolate or cyclophosphamide. Class V mimics membranous and may need calcineurin inhibitor or rituximab.
Rapidly progressive GN (RPGN, crescentic GN)
Clinical syndrome of rapid loss of renal function over days to weeks. Three pathologic types:
- Type I — anti-GBM (linear IF).
- Type II — immune complex (granular IF — PSGN, IgA, lupus, MPGN).
- Type III — pauci-immune (ANCA-associated).
Crescents on more than 50 percent of glomeruli. Treat aggressively with pulse steroids plus cyclophosphamide or rituximab; plasmapheresis for type I and severe type III.
Complications of nephrotic syndrome
Infection
- Loss of urinary IgG, factor B, and properdin predisposes to encapsulated organisms.
- Streptococcus pneumoniae peritonitis is the classic paediatric complication.
- Pneumococcal vaccination (PCV13 plus PPSV23), varicella vaccination, and influenza vaccination are mandatory.
Thromboembolism
- Loss of antithrombin III, protein S, and increased fibrinogen.
- Renal vein thrombosis is most common in membranous nephropathy (about 30 percent), often unilateral, presents with flank pain and haematuria.
- Anticoagulation is initiated for confirmed thrombosis; prophylactic anticoagulation considered when albumin below 2 to 2.5 g/dL in adult membranous.
AKI
- Pre-renal from intravascular volume depletion or aggressive diuresis.
- Acute interstitial nephritis from NSAIDs.
- Renal vein thrombosis.
- Bilateral cortical necrosis in severe cases.
Dyslipidaemia
- Liver upregulates apolipoprotein synthesis; both LDL and lipoprotein(a) rise.
- Statin therapy reasonable in adults with persistent disease.
Vitamin D deficiency
- Loss of vitamin D-binding protein; supplementation needed.
Anaemia
- Loss of transferrin and erythropoietin in severe cases.
Pediatric-specific considerations
| Feature | Pediatric MCD | Adult MCD |
|---|
| Empiric steroids without biopsy | Yes (1 to 10 years) | No (biopsy first) |
| Steroid response | Above 90 percent | About 80 percent |
| Frequent relapsing | Common | Less common |
| Biopsy indications | Steroid resistance, age outside 1 to 12 years, atypical features | All cases at presentation |
Steroid-response classification (key NEET PG terminology):
- Steroid-sensitive nephrotic syndrome (SSNS) — remission within 4 weeks of daily prednisolone.
- Steroid-dependent (SDNS) — relapse during taper or within 14 days of stopping.
- Frequently relapsing (FRNS) — 2 or more relapses in 6 months or 4 or more in a year.
- Steroid-resistant (SRNS) — no remission after 4 to 6 weeks of daily prednisolone — biopsy.
Second-line agents in SDNS / FRNS / SRNS — levamisole, cyclophosphamide, calcineurin inhibitors (cyclosporine, tacrolimus), mycophenolate mofetil, rituximab.
NEET PG MCQ traps
- PSGN vs IgA timing — PSGN follows infection by 1 to 3 weeks (post-pharyngeal) or 3 to 6 weeks (post-skin); IgA is synpharyngitic (within 24 to 48 hours).
- Low C3 — PSGN, MPGN type I, lupus, cryoglobulinaemia, endocarditis. Normal C3 — IgA, anti-GBM, ANCA, HSP.
- Anti-PLA2R — primary membranous nephropathy biomarker; does not need biopsy if positive plus typical features.
- Spike-and-dome on silver stain — membranous.
- Tram-track on silver stain — MPGN.
- Linear IF along GBM — anti-GBM.
- Full-house IF (IgG, IgM, IgA, C3, C1q) — lupus nephritis class IV.
- Renal vein thrombosis presents as flank pain plus AKI plus elevated LDH — most common in membranous.
- Steroid-resistant child — biopsy reveals FSGS in many; consider genetic testing for NPHS1, NPHS2, APOL1.
- Albright orientation — fixed: any MPGN-like patient should be screened for hepatitis C and cryoglobulinaemia.
Recent updates and Indian context
- KDIGO 2021 Glomerular Diseases guideline — rituximab elevated to first-line in moderate-risk membranous; SGLT2 inhibitors recommended for proteinuric CKD.
- DAPA-CKD and EMPA-KIDNEY trials — dapagliflozin and empagliflozin reduce CKD progression and cardiovascular events independently of diabetes.
- Sparsentan — dual endothelin-A and angiotensin receptor antagonist; approved for IgA nephropathy and FSGS.
- Indian context — PSGN remains common given high streptococcal pyoderma prevalence; tropical infection-associated MPGN (filariasis, schistosomiasis, hepatitis B) is over-represented; APOL1-associated FSGS is uncommon in Indians but South Asian-specific genetic FSGS variants are emerging. ISPN 2021 paediatric guideline retains the 6-week induction protocol for empirical steroid trial in childhood nephrotic syndrome.
Frequently asked questions
What are the diagnostic criteria for nephrotic syndrome?
Nephrotic syndrome requires proteinuria above 3.5 g per 24 hours (or urine protein-to-creatinine ratio above 3.5 g/g) plus serum albumin below 3 g/dL plus edema and hyperlipidaemia. In children, the cutoff is 40 mg per square metre per hour or urine PCR above 2 g/g, often with cholesterol above 200 mg/dL.
What is the most common cause of nephrotic syndrome in children versus adults?
In children aged 1 to 10 years, minimal change disease (MCD) accounts for over 80 percent and is highly steroid-responsive. In adults, focal segmental glomerulosclerosis (FSGS) is the most common primary cause overall, while membranous nephropathy is the leading cause in white adults above 50. Diabetic nephropathy is the most common secondary cause in all adults.
What distinguishes nephritic from nephrotic syndrome on urinalysis?
Nephritic syndrome shows haematuria with red cell casts and dysmorphic red cells, mild-to-moderate proteinuria (under 3 g per day), hypertension, oliguria, and AKI. Nephrotic syndrome shows heavy proteinuria above 3.5 g per day, oval fat bodies and fatty casts, hypoalbuminaemia, and edema, typically without hypertension or AKI initially.
When is renal biopsy indicated in nephrotic syndrome?
In children aged 1 to 10 years with classic features, an empirical steroid trial is given without biopsy because MCD is overwhelmingly likely. Biopsy is performed for steroid-resistant disease, atypical features (haematuria, hypertension, AKI), age below 1 year or above 12 years, or frequent relapse. In adults, biopsy is performed at presentation in nearly all cases.
What are the major complications of nephrotic syndrome?
The four major complications are infection (especially Streptococcus pneumoniae peritonitis from urinary IgG loss), thromboembolism (especially renal vein thrombosis in membranous nephropathy from antithrombin III loss), AKI, and dyslipidaemia with accelerated atherosclerosis. Children also lose vitamin D-binding protein, causing vitamin D deficiency.
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: May 2026
