Overview of Glomerular Disease

An EMQ comparison table: what each disease is, classic associations, complement and serology, LM/IF/EM findings, and the clues that separate similar answers.

Read the stem in this order: syndrome → timing/systemic clues → complement/serology → biopsy. The table covers the major exam diagnoses and selected rarer biopsy labels. Groups are revision aids: diseases can cross the nephritic–nephrotic spectrum, and some rows describe subtypes of the same disease.

Nephrotic: heavy proteinuria (usually ≥3.5 g/day in adults), hypoalbuminaemia and often oedema; lipiduria/oval fat bodies may appear. Nephrotic-range proteinuria alone does not establish the full syndrome.
Nephritic: glomerular haematuria, often dysmorphic RBCs/acanthocytes or RBC casts, with variable proteinuria, hypertension and reduced GFR. RPGN means rapidly deteriorating kidney function over days to weeks with a nephritic sediment; crescents are its characteristic biopsy correlate, not a separate aetiology.
Initial investigations: urine microscopy and quantified ACR/PCR, creatinine/eGFR trend, electrolytes, albumin and blood count. Use the stem to select C3/C4, ANA/anti-dsDNA, PR3/MPO-ANCA, anti-GBM, anti-PLA2R, infection tests or a monoclonal-protein screen. ^[1]

Biopsy key: LM = light microscopy; IF = immunofluorescence; EM = electron microscopy; GBM = glomerular basement membrane. “Normal complement” means circulating C3/C4 are usually normal; it does not mean complement is absent from tissue or uninvolved in the disease.

Glomerular disease comparison table

Podocyte / membranousMetabolic / depositionImmune complex / complementAnti-GBM / pauci-immuneInherited disordersRarer biopsy diagnoses

33 comparisons. Scroll across for investigations and biopsy findings; scroll down for the remaining diseases. The header stays visible; on wider screens, the disease column stays visible too.

Glomerular diseases: definitions, presentation, classic associations, investigations, biopsy findings, and exam discriminators.
Disease · what it is	Usual presentation	Classic EMQ associations	Investigations · complement	Biopsy · LM / IF / EM	Best discriminator · exam trap
Podocyte / membranous Minimal change disease (MCD) Podocyte injury with little or no change on LM. ^[1]^[2]	Abrupt nephrotic syndrome. Commonest cause in children; also occurs in adults.	Young child with periorbital oedema after an infection. Hodgkin lymphoma, NSAIDs; atopy is a classic association.	C3/C4 normal. Heavy, often selective albuminuria; low albumin, hyperlipidaemia. Usually bland sediment; adult MCD can cause AKI.	LM: normal / minimal mesangial change. IF: negative or nonspecific. EM: diffuse podocyte foot-process effacement; no immune-complex deposits.	Normal LM + diffuse effacement. Usually steroid-sensitive, especially in children. Typical childhood steroid-sensitive nephrotic syndrome is often treated without an initial biopsy.
Podocyte / membranous Primary focal segmental glomerulosclerosis (FSGS) Podocytopathy with scarring of some glomeruli and part of each affected tuft. ^[1]^[3]	Nephrotic syndrome, often abrupt; hypertension, microscopic haematuria or reduced GFR may coexist.	Nephrotic adult with an FSGS lesion and no secondary or genetic explanation. Rapid recurrence after transplantation is a classic clue to primary disease.	C3/C4 normal. Heavy proteinuria + hypoalbuminaemia. Review secondary causes; consider genetic testing in selected patients.	LM: focal, segmental sclerosis/hyalinosis. IF: nonspecific IgM/C3 trapping in scars. EM: usually diffuse foot-process effacement in primary FSGS.	FSGS is a lesion, not one cause. Primary disease requires the clinical context. Focal sampling can miss scars; effacement alone does not distinguish MCD from FSGS.
Podocyte / membranous Secondary / adaptive FSGS Podocyte loss from hyperfiltration or another identifiable insult. ^[1]^[3]	Gradual proteinuria, sometimes nephrotic-range without marked hypoalbuminaemia or oedema.	Obesity, reduced nephron mass, reflux nephropathy, sickle cell disease. Drug-associated forms include interferon, pamidronate and anabolic steroids; heroin is a classic exam association.	C3/C4 normal. Look for obesity, a small/scarred or solitary kidney, exposure history and the underlying condition.	LM: segmental sclerosis; glomerulomegaly/perihilar lesions favour adaptive disease. IF: nonspecific trapping. EM: often patchy effacement in adaptive FSGS; viral/drug forms may differ.	Heavy proteinuria ≠ automatically primary FSGS. Treat the cause and proteinuria; secondary FSGS is not an indication for empiric primary-FSGS immunosuppression.
Podocyte / membranous HIV-associated nephropathy (HIVAN) Classically a collapsing glomerulopathy with substantial tubular/interstitial injury. ^[1]^[6]	Heavy proteinuria with rapid loss of kidney function; often a relatively bland sediment.	Untreated/advanced HIV. APOL1 high-risk genotypes, most frequent in people with recent African ancestry, increase susceptibility.	C3/C4 usually normal. HIV testing, viral load/CD4 count. Kidneys may be enlarged and echogenic.	LM: collapsed capillary tufts with overlying epithelial proliferation; tubular microcysts. IF: nonspecific. EM: extensive effacement; endothelial tubuloreticular inclusions may occur.	HIV + rapid decline + collapsing lesion. HIV also causes immune-complex kidney disease; not every HIV-associated renal lesion is HIVAN.
Podocyte / membranous Genetic podocytopathy / congenital nephrotic syndrome Inherited defects in filtration-barrier proteins; congenital refers to onset in the first 3 months. ^[3]^[19]	Congenital/infantile nephrotic syndrome or familial steroid-resistant nephrotic syndrome/FSGS.	NPHS1 (nephrin): classic Finnish-type congenital nephrosis. NPHS2 (podocin): recessive steroid-resistant disease. WT1: syndromic disease with genital abnormalities and/or Wilms tumour risk.	C3/C4 usually normal. Genetic panel guided by age, family history and syndromic features. Congenital nephrosis also has non-genetic causes, including infections.	LM: may show FSGS or diffuse mesangial sclerosis, depending on the defect. IF: generally no immune deposits. EM: podocyte effacement.	Very early onset / family history / steroid resistance → genetic cause. A histological label alone does not identify the mutation.
Podocyte / membranous Primary / antigen-associated membranous nephropathy Antibodies against podocyte antigens produce subepithelial immune deposits; PLA2R is the commonest target. ^[1]^[4]	Adult nephrotic syndrome, often with initially preserved GFR.	Middle-aged/older adult; venous thrombosis, including renal vein thrombosis, is a classic nephrotic complication with a strong membranous association.	C3/C4 usually normal. Anti-PLA2R strongly supports PLA2R-associated disease. Negative anti-PLA2R does not exclude membranous nephropathy; other antigens exist.	LM: diffuse capillary-wall thickening; silver-stain spikes. IF: granular IgG/C3 along capillary loops. EM: subepithelial deposits and effacement ('spike and dome').	PLA2R + subepithelial deposits. Selected patients with nephrotic syndrome and positive anti-PLA2R can be diagnosed without biopsy; still evaluate associated conditions.
Podocyte / membranous Secondary membranous nephropathy The membranous pattern associated with infection, autoimmunity, drugs or malignancy. ^[1]^[4]^[10]	Nephrotic syndrome with clues to an underlying condition.	HBV, solid-organ malignancy, SLE class V; NSAIDs, gold and penicillamine are classic drug associations. Syphilis is another recognised cause.	Complement depends on cause: often normal, may be low with SLE. HBV serology, ANA/anti-dsDNA, medication review and age-/risk-appropriate malignancy evaluation.	LM/EM: membranous pattern with subepithelial deposits. IF: granular staining; mesangial deposits or a full-house pattern suggest lupus. Histology/antigen staining helps refine the cause.	Adult nephrosis + cancer/HBV/drug exposure → consider membranous. An association is a clue, not proof of causation. Class V lupus has its own row below.
Metabolic / deposition Diabetic kidney disease / diabetic glomerulosclerosis Metabolic and haemodynamic injury thickens the GBM and expands mesangial matrix. ^[1]^[14]	Gradual albuminuria and/or falling GFR; may become nephrotic. Non-albuminuric diabetic kidney disease also occurs.	Longstanding diabetes, often with diabetic retinopathy and neuropathy. The association with retinopathy is especially helpful in type 1 diabetes.	C3/C4 normal. HbA1c, serial ACR and eGFR; usually bland sediment. Sudden nephrosis, active sediment or rapid decline suggests an additional diagnosis.	LM: diffuse mesangial expansion; Kimmelstiel–Wilson nodules; afferent and efferent arteriolar hyalinosis. IF: nonspecific linear IgG/albumin staining can occur. EM: thickened GBM, expanded matrix.	Diabetes + nodular sclerosis, but nodules also occur in LCDD. Nonspecific linear IgG in diabetes is not, by itself, anti-GBM disease.
Metabolic / deposition AL amyloidosis A clonal plasma-cell/B-cell disorder produces amyloid-forming immunoglobulin light chains. ^[1]^[14]	Often heavy albuminuria / nephrotic syndrome; progressive CKD.	Macroglossia, periorbital purpura, restrictive cardiomyopathy or autonomic neuropathy. A plasma-cell clone may be small; overt myeloma is not required.	C3/C4 usually normal. Serum free light chains + serum/urine immunofixation. Confirm amyloid in tissue and type the deposits, preferably by mass spectrometry when available.	LM: amorphous deposits; Congo red positive with apple-green birefringence. IF: light-chain restriction may be demonstrable, often λ. EM: randomly arranged nonbranching fibrils, typically about 8–12 nm.	Nephrosis + plasma-cell/systemic clues + Congo red positivity. A monoclonal blood protein alone does not prove the amyloid is AL.
Metabolic / deposition AA amyloidosis Chronic inflammation drives serum amyloid A production and AA fibril deposition. ^[1]	Proteinuria, often nephrotic, followed by CKD.	Longstanding inflammatory disease or chronic infection: rheumatoid arthritis, bronchiectasis, tuberculosis; familial Mediterranean fever.	C3/C4 usually normal. Inflammatory markers and search for the driver; tissue typing identifies AA, not immunoglobulin light chain.	LM: Congo red-positive amyloid with apple-green birefringence. Typing: AA protein. EM: nonbranching fibrils, as in other amyloid types.	Chronic inflammation + amyloid → think AA. Congo red identifies amyloid, not its precursor protein. Control of the inflammatory cause is central.
Metabolic / deposition Monoclonal immunoglobulin deposition disease (especially LCDD) Non-amyloid monoclonal light/heavy chains deposit along renal basement membranes. ^[14]	Proteinuria ± nephrotic syndrome, hypertension and declining GFR.	Monoclonal gammopathy of renal significance (MGRS) or myeloma. LCDD commonly involves κ light chains.	C3/C4 usually normal in LCDD. Serum/urine immunofixation and serum free light chains; haematological assessment of the clone.	LM: nodular glomerulosclerosis; Congo red negative. IF: linear monotypic light chain along glomerular and tubular basement membranes. EM: finely granular powdery, nonfibrillar deposits.	Diabetes-like nodules + κ restriction + Congo red negative. Contrast AL amyloid's fibrils and Congo red positivity; cast nephropathy is primarily tubular.
Immune complex / complement IgA nephropathy (Berger disease) IgA-containing immune complexes accumulate predominantly in the mesangium. ^[1]^[8]	Recurrent visible or persistent microscopic haematuria ± proteinuria; occasionally nephrotic syndrome or RPGN.	Young adult with synpharyngitic haematuria: during or within roughly 1–3 days of a mucosal infection. IgA deposition may also accompany liver disease or coeliac disease.	C3/C4 usually normal. Serum IgA may be raised but is neither sensitive nor diagnostic. Kidney biopsy establishes IgAN; no validated serum test replaces it.	LM: mesangial hypercellularity ± segmental sclerosis/crescents. IF: dominant/co-dominant mesangial IgA, often C3. EM: mesangial electron-dense deposits.	Haematuria with the infection + normal C3. PSGN follows a latent interval. Oxford MEST-C describes biopsy lesions; it is not a serum diagnostic test.
Immune complex / complement IgA vasculitis nephritis (IgAV; formerly HSP) Renal involvement in systemic IgA-mediated small-vessel vasculitis. ^[1]^[8]	Haematuria/proteinuria with systemic vasculitis; severe cases can be nephrotic or crescentic.	Palpable purpura on legs/buttocks + abdominal pain + arthralgia; often a child after URTI. Intussusception is a classic complication.	C3/C4 usually normal. Platelet count usually normal (non-thrombocytopenic purpura). Monitor BP, urine protein and kidney function; skin biopsy can show IgA vasculitis.	Kidney LM/IF/EM: resembles IgA nephropathy, including mesangial IgA ± crescents. Skin: leukocytoclastic vasculitis with IgA deposition.	IgA renal disease + purpura/gut/joints → IgAV. Renal biopsy alone cannot reliably separate IgAN from IgAV nephritis.
Immune complex / complement Post-streptococcal glomerulonephritis (PSGN) Immune-mediated GN after nephritogenic group A streptococcal infection. ^[1]^[6]^[11]	Acute nephritic syndrome: cola urine, periorbital oedema, hypertension and oliguria.	Child about 1–3 weeks after pharyngitis or 3–6 weeks after impetigo. The latent interval distinguishes it from synpharyngitic IgAN.	Low C3; C4 usually normal. ASO supports prior throat infection; anti-DNase B is useful after skin infection. C3 usually recovers within 6–8 weeks.	LM: diffuse endocapillary proliferation with neutrophils. IF: coarse granular C3 ± IgG ('starry sky' / 'lumpy-bumpy'). EM: subepithelial humps.	Post-infectious delay + transient low C3 + humps. Persistently low C3 or an atypical course prompts reassessment for C3G or another immune-complex GN.
Immune complex / complement Other infection-related GN (including endocarditis-associated GN) Glomerular immune injury during or after infection; not restricted to streptococci. ^[1]^[6]	Nephritic AKI or mixed nephritic/nephrotic disease, often during active infection.	Older adult with diabetes and Staphylococcus infection (may be IgA-dominant). Fever + murmur + embolic signs suggests infective endocarditis; also infected shunts/deep abscesses.	C3 often low; C4 variable. Blood/site cultures and echocardiography when indicated. Endocarditis can produce positive ANCA and rheumatoid factor.	LM: endocapillary/exudative GN ± crescents. IF: C3-dominant/co-dominant immune deposits; staphylococcal GN may be IgA-dominant. EM: deposits may include subepithelial humps.	Active infection changes the answer. IgA staining is not automatically primary IgAN, and ANCA positivity does not exclude endocarditis. Identify and treat the infection.
Immune complex / complement Proliferative lupus nephritis (class III / IV) SLE immune-complex GN: class III involves <50% and class IV ≥50% of glomeruli. ^[1]^[10]	Nephritic or mixed syndrome, sometimes RPGN; class IV is diffuse proliferative disease.	SLE context: photosensitive rash, oral ulcers, arthritis, cytopenias or serositis; renal disease may be the first presentation.	C3 and C4 often low. ANA, anti-dsDNA, urine protein/sediment and creatinine trend. Anti-dsDNA may track activity but is not a substitute for biopsy.	LM: proliferative lesions ± necrosis/crescents; wire loops from large subendothelial deposits. IF: full house (IgG, IgA, IgM, C3, C1q). EM: mesangial/subendothelial deposits; tubuloreticular inclusions may occur.	SLE + active sediment + low C3/C4. Biopsy class, activity and chronicity guide management. Full-house staining strongly suggests lupus but is not completely specific.
Immune complex / complement Membranous lupus nephritis (class V) Lupus immune-complex disease with a predominantly subepithelial/membranous pattern. ^[1]^[10]	Nephrotic syndrome; pure class V may have a relatively bland sediment.	Known or newly recognised SLE with heavy proteinuria. Class V can coexist with class III or IV.	C3/C4 variable; may be normal in pure class V. ANA/anti-dsDNA and kidney biopsy. Serology alone cannot distinguish proliferative from membranous lupus.	LM: thickened capillary walls ± spikes. IF: typically full-house capillary-loop and mesangial staining. EM: subepithelial and mesangial deposits; substantial subendothelial proliferative lesions suggest mixed class.	Lupus can be nephrotic. Full-house/mesangial deposits and the systemic context distinguish it from a typical PLA2R-associated pattern.
Immune complex / complement Immune-complex GN with an MPGN pattern Membranoproliferative GN describes mesangial/endocapillary proliferation and capillary-wall duplication, not a single disease. ^[1]^[5]	Mixed nephritic–nephrotic picture with hypertension and variable CKD.	Chronic infections (HBV/HCV, endocarditis), autoimmunity and monoclonal gammopathy. Search for a cause before using an idiopathic label.	C3 often low; C4 may also be low. HBV/HCV tests, autoimmune studies, infection evaluation and monoclonal-protein screen as indicated.	LM: lobular hypercellularity, double contours / tram tracks. IF: immunoglobulins plus complement. EM: commonly subendothelial and mesangial deposits.	Tram tracks identify a pattern; IF directs the cause. Current classification separates immunoglobulin-associated GN from complement-dominant C3G; historical MPGN I/II/III is not the preferred organising system.
Immune complex / complement Cryoglobulinaemic glomerulonephritis Cryoglobulin-containing immune complexes injure glomeruli, commonly with an MPGN pattern. ^[1]^[14]	Nephritic or mixed disease, sometimes rapidly progressive.	HCV + palpable purpura + arthralgia + weakness, often neuropathy. Also autoimmune/B-cell disorders. Mixed cryoglobulins often have rheumatoid-factor activity.	Very low C4, often with low C3. Cryoglobulins, rheumatoid factor, HCV antibody/RNA and clonal work-up. Keep blood warm until serum separation to avoid a false-negative cryoglobulin result.	LM: MPGN ± intracapillary pseudothrombi. IF: IgM/IgG and complement (depends on cryoglobulin type). EM: subendothelial/mesangial deposits, sometimes organised.	Disproportionately depressed C4 + HCV/purpura/neuropathy. Purpura also occurs in IgAV, but IgAV usually has normal complement.
Immune complex / complement C3 glomerulopathy (C3GN / dense deposit disease) Alternative complement-pathway dysregulation causing C3-dominant GN; EM separates C3GN from DDD. ^[1]^[5]	Haematuria + proteinuria, nephritic/mixed syndrome; sometimes infection-triggered.	Persistent low C3 after presumed infection-related GN; complement autoantibodies (e.g. C3 nephritic factor) or genetic defects. DDD can accompany acquired partial lipodystrophy/drusen.	C3 often low, C4 usually normal; normal C3 does not exclude C3G. Specialist complement work-up; investigate monoclonal gammopathy, especially in older adults.	LM: variable, often MPGN. IF: C3-dominant, with little/no immunoglobulin. EM: DDD = very dense ribbon-like intramembranous deposits; C3GN = less dense mesangial/capillary-wall deposits.	C3 dominance + sustained complement abnormality. DDD was historically 'MPGN type II'; neither all MPGN nor all C3-dominant biopsies are C3G (infection must be considered).
Anti-GBM / pauci-immune Anti-GBM disease Autoantibodies target the α3 chain NC1 domain of type IV collagen in glomerular/alveolar basement membranes. ^[1]^[7]	RPGN ± pulmonary haemorrhage. Kidney-only disease occurs.	Haemoptysis, falling haemoglobin, pulmonary infiltrates and rapidly rising creatinine. Smoking can precipitate lung involvement. 'Goodpasture syndrome' is the classic pulmonary–renal presentation.	C3/C4 usually normal. Serum anti-GBM antibodies; also test ANCA because dual positivity occurs. Chest imaging and urgent renal evaluation.	LM: necrotising crescentic GN. IF: strong, smooth linear IgG along GBM ± C3. EM: GBM breaks; no typical immune-complex deposits.	Linear IgG + anti-GBM + RPGN. Suspected disease is an emergency; appropriate treatment should not wait for every confirmatory result. Pulmonary–renal syndrome can also be ANCA vasculitis.
Anti-GBM / pauci-immune Granulomatosis with polyangiitis (GPA) Necrotising small-vessel vasculitis with granulomatous respiratory-tract inflammation. ^[1]^[9]	Nephritic AKI / RPGN, often with ENT and lung disease.	Chronic sinusitis/otitis, nasal crusting or saddle nose + cavitating lung nodules + GN. May have pulmonary haemorrhage.	C3/C4 usually normal. PR3-ANCA is the classic association (often c-ANCA pattern); MPO positivity or negative ANCA is possible. Chest/ENT imaging guided by symptoms.	Kidney LM: necrotising crescentic GN. IF: pauci-immune (little/no staining). EM: few/no immune deposits. Granulomas are usually sought in respiratory tissue, not expected in the renal glomerulus.	Destructive ENT disease + cavitating nodules → GPA. PR3 is an association, not an absolute diagnostic rule; antigen-specific PR3/MPO testing is more informative than c-/p-ANCA labels alone.
Anti-GBM / pauci-immune Microscopic polyangiitis (MPA) Necrotising small-vessel vasculitis without the granulomatous inflammation of GPA. ^[1]^[9]	RPGN ± pulmonary capillaritis/haemorrhage; purpura or neuropathy may occur.	Pulmonary–renal syndrome without destructive ENT disease or granulomatous nodules. Interstitial lung disease can occur, particularly with MPO-ANCA.	C3/C4 usually normal. MPO-ANCA is the classic association (often p-ANCA pattern); some cases are PR3-positive or ANCA-negative.	LM: necrotising crescentic GN. IF: pauci-immune. EM: few/no deposits. No granulomatous inflammation as a defining systemic feature.	Pulmonary–renal + MPO + no GPA-type ENT clues → MPA. MPA and GPA kidney biopsies can look the same.
Anti-GBM / pauci-immune Eosinophilic granulomatosis with polyangiitis (EGPA) Eosinophil-rich inflammation and small-vessel vasculitis associated with asthma. ^[18]	Systemic eosinophilic/vasculitic illness; renal GN is less frequent than in GPA/MPA.	Adult-onset asthma + eosinophilia + nasal polyps, migratory lung infiltrates, mononeuritis multiplex or cardiac involvement.	C3/C4 usually normal. Eosinophilia; IgE may rise. ANCA is positive in a minority overall, usually MPO, and renal vasculitis is more frequent in that subgroup.	Kidney: when vasculitic GN occurs, usually pauci-immune necrotising/crescentic GN. Eosinophilic interstitial inflammation or other renal patterns may coexist.	Asthma + eosinophilia + neuropathy → EGPA. Negative ANCA does not exclude it. Asthma/eosinophilia distinguish it from a typical MPA stem.
Anti-GBM / pauci-immune Renal-limited pauci-immune GN Pauci-immune necrotising/crescentic GN without recognised extrarenal vasculitis. ^[1]^[9]	Rising creatinine with glomerular haematuria, often RPGN.	Often an older adult with no obvious rash, ENT or lung findings. Hydralazine and propylthiouracil are important exposures when considering drug-associated ANCA vasculitis.	C3/C4 usually normal. MPO-ANCA often positive; PR3-positive and ANCA-negative cases occur. Exclude anti-GBM disease and infection mimics.	LM: necrosis and crescents. IF: pauci-immune. EM: few/no immune deposits.	No systemic signs does not exclude renal vasculitis. Normal complement and negative ANCA do not rule out severe crescentic GN; biopsy is decisive in seronegative cases.
Inherited disorders Alport syndrome / COL4A-associated nephropathy Inherited α3/α4/α5 type IV collagen defects: COL4A3, COL4A4 or COL4A5. ^[12]	Persistent haematuria, later proteinuria and progressive CKD; severity varies by genotype.	Sensorineural hearing loss + ocular abnormalities, especially anterior lenticonus, with familial kidney disease. COL4A5 disease is X-linked; COL4A3/4 forms have other inheritance patterns.	C3/C4 normal. COL4A3/4/5 genetic testing, audiology, eye examination and family assessment. Women with COL4A5 variants are affected individuals, not necessarily asymptomatic carriers.	LM: may be normal early; later sclerosis. IF: no immune-complex pattern; collagen-chain staining may be abnormal. EM: irregular thinning/thickening and GBM splitting/lamellation ('basket weave').	Haematuria + hearing/eye disease + family history. Early disease can show only thin GBM, so absence of basket weaving does not exclude Alport.
Inherited disorders Thin-basement-membrane phenotype Diffuse GBM thinning; often associated with heterozygous COL4A3/COL4A4 variants and overlaps the Alport spectrum. ^[12]	Usually persistent isolated microscopic haematuria with initially preserved GFR and little proteinuria.	Incidental/familial haematuria, often without the hearing or ocular features of classic Alport syndrome.	C3/C4 normal. Assess family history, BP, ACR and eGFR; consider genetic testing. Follow-up matters if albuminuria, hypertension or familial kidney failure is present.	LM: often normal. IF: negative for immune deposits. EM: diffusely thin GBM, without the established multilamination of classic Alport.	Isolated familial haematuria + thin GBM. Avoid 'benign familial haematuria': some patients develop proteinuria/CKD, and the clinical/genetic spectrum overlaps Alport.
Inherited disorders Fabry nephropathy X-linked GLA-related α-galactosidase A deficiency causes lysosomal glycosphingolipid accumulation. ^[13]	Proteinuria and progressive CKD; renal-predominant variants occur.	Burning extremity pain, angiokeratomas, reduced sweating, cornea verticillata, unexplained LV hypertrophy or early stroke.	C3/C4 normal. α-galactosidase A activity (particularly useful in males), lyso-Gb3 and GLA testing. Normal enzyme activity does not exclude disease in females.	LM: vacuolated podocytes ± sclerosis. IF: no typical immune-complex deposits. EM: lamellated lysosomal inclusions (zebra/myelin bodies).	Proteinuria + neuropathic pain/angiokeratomas + zebra bodies. Drug-induced phospholipidosis can mimic the EM appearance; integrate genetic/biochemical results.
Rarer biopsy diagnoses Fibrillary glomerulonephritis (FGN) Glomerular deposition of organised fibrils, usually containing polyclonal IgG and DNAJB9. ^[15]	Proteinuria, haematuria and reduced GFR; often a mixed or nephrotic presentation.	Usually middle-aged/older adults. May accompany autoimmune disease, HCV or malignancy; no single association is diagnostic.	Complement usually normal. Renal biopsy with DNAJB9 immunohistochemistry; assess infection/autoimmune/clonal clues as appropriate.	LM: variable proliferative/MPGN pattern. IF: smudgy IgG/C3; DNAJB9 usually positive. EM: randomly arranged fibrils, typically 12–24 nm. Congo red usually negative.	DNAJB9 + randomly arranged fibrils larger than amyloid. Rare Congo red-positive FGN exists; staining and ultrastructure should be interpreted together.
Rarer biopsy diagnoses Immunotactoid glomerulopathy Organised immunoglobulin deposits form microtubules, often from a monoclonal B-cell process. ^[15]	Proteinuria ± nephrotic syndrome, haematuria and CKD.	CLL / B-cell lymphoproliferative disease or monoclonal gammopathy.	Complement variable. Serum/urine immunofixation, free light chains and haematological evaluation. DNAJB9 negative.	LM: often MPGN. IF: commonly monotypic IgG plus complement. EM: parallel, hollow microtubules, usually >30 nm; Congo red negative.	Parallel microtubules + a B-cell clone. FGN has randomly arranged smaller fibrils and is usually DNAJB9-positive; size ranges can overlap.
Rarer biopsy diagnoses PGNMID Proliferative GN with monoclonal immunoglobulin deposits; a form of MGRS. ^[14]	Proteinuria, haematuria and impaired GFR; nephrotic or mixed syndrome.	Usually adults; a pathogenic monoclonal immunoglobulin can be present even when a circulating clone/protein cannot be detected.	Complement can be low. Serum/urine immunofixation, free light chains and haematological work-up. A negative blood screen does not exclude it.	LM: proliferative / MPGN pattern. IF: deposits restricted to one IgG subclass and one light-chain type (often IgG3κ). EM: granular, non-organised mesangial/subendothelial deposits.	Monotypic granular immune deposits. Distinguish from LCDD's linear basement-membrane deposits and immunotactoid microtubules.
Rarer biopsy diagnoses IgM nephropathy A debated clinicopathological label for dominant/co-dominant diffuse mesangial IgM deposition. ^[16]	Often nephrotic syndrome; microscopic haematuria or isolated proteinuria can occur.	Child or adult with a podocytopathy-like presentation; steroid response is variable.	Complement usually normal. A biopsy diagnosis after excluding secondary/systemic causes; serum IgM is not diagnostic.	LM: minimal-change, mesangial proliferative or FSGS pattern. IF: diffuse mesangial IgM dominance. EM: mesangial deposits may be seen with foot-process effacement.	Diffuse mesangial IgM ≠ focal IgM trapped in FSGS scars. Definitions and its status as a distinct disease remain unsettled.
Rarer biopsy diagnoses C1q nephropathy A histological label for dominant/co-dominant mesangial C1q deposits without evidence of SLE. ^[17]	Often childhood/young-adult proteinuria or nephrotic syndrome; variable haematuria.	May resemble MCD/FSGS clinically; steroid-resistant disease is a recognised presentation.	Serum complement often normal. Evaluate ANA/anti-dsDNA and systemic features to exclude lupus; no diagnostic serum C1q test.	LM: MCD, FSGS or proliferative pattern. IF: dominant/co-dominant mesangial C1q. EM: mesangial electron-dense deposits ± foot-process effacement.	C1q-dominant tissue staining without SLE. C1q in lupus full-house staining does not make the diagnosis C1q nephropathy.

Fast EMQ elimination rules

Stem clue	Best direction	What separates it from the distractor
Blood in urine during a sore throat	IgA nephropathy	PSGN follows a latent interval and usually lowers C3.
Low C3, C4 relatively preserved	PSGN / infection-related GN / C3G	Infection context and C3 recovery distinguish transient infection-related consumption from persistent complement dysregulation.
Low C3 + low C4 with SLE clues	Lupus nephritis	Cryoglobulinaemia often produces a particularly profound C4 reduction. Complement patterns are clues, not diagnostic rules.
Linear IgG with crescentic GN	Anti-GBM disease	Pauci-immune suggests ANCA-associated disease; granular deposits suggest immune-complex GN.
Granular versus linear versus pauci-immune RPGN	Immune-complex versus anti-GBM versus pauci-immune GN	The classic types II, I and III respectively. Dual anti-GBM/ANCA positivity occurs. ^[7]^[9]
Spikes / humps / tram tracks	Membranous / infection-related GN / MPGN pattern	Both membranous deposits and infection-related humps are subepithelial; the clinical context and overall biopsy pattern decide.
Nephrotic syndrome + Hodgkin lymphoma	MCD	Solid-organ malignancy is the classic membranous association.
Congo red+ fibrils / powdery κ deposits / DNAJB9+ fibrils	Amyloid / LCDD / FGN	Type amyloid; Congo red positivity alone does not establish AL.
Haematuria + deafness / lenticonus	Alport syndrome	Thin-GBM phenotypes often lack extrarenal signs but overlap genetically and are not uniformly benign.
MAHA + thrombocytopenia + AKI	Thrombotic microangiopathy (e.g. HUS/TTP)	Glomerular endothelial/vascular injury can mimic GN; schistocytes and haemolysis redirect the work-up. This is not a primary immune-complex GN.

Two classification traps: lupus I = minimal mesangial; II = mesangial proliferative; III/IV = focal/diffuse proliferative; V = membranous; VI = advanced sclerosis (≥90% globally sclerosed glomeruli without residual activity). A crescent or an MPGN pattern can result from several diseases—neither identifies the cause by itself. ^[5]^[10]

Other common distractors: hypertensive nephrosclerosis usually causes a gradual CKD course with a bland sediment; reflux nephropathy can produce secondary FSGS. Myeloma cast nephropathy is predominantly tubular (light-chain casts), whereas AL amyloid and LCDD can cause glomerular proteinuria. ^[1]^[14]

Sources

The existing GC 057 teaching notes provide the local exam framework. The linked guidance and pathology literature support the diagnostic distinctions and current terminology; older names appear only where useful for recognising an EMQ option.

Overview of Glomerular Disease

Glomerular disease comparison table

Fast EMQ elimination rules

Sources

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