Glomerulonephritis Classification
On this page
Direct answer
Nephritic versus nephrotic is the split that organises all glomerulonephritis: the nephritic pattern (haematuria with dysmorphic red cells and red-cell casts, hypertension, oliguria, modest proteinuria) reflects proliferative injury, while the nephrotic pattern (proteinuria above 3.5 grams daily with hypoalbuminaemia, oedema and hyperlipidaemia) reflects a leaky filtration barrier. Post-streptococcal glomerulonephritis follows pharyngitis by one to three weeks with low complement and subepithelial humps; IgA nephropathy — the world's most common glomerulonephritis — bleeds within a day or two of a sore throat with normal complement; crescentic (rapidly progressive) glomerulonephritis splits into anti-glomerular basement membrane, immune-complex and pauci-immune ANCA-associated types. Among nephrotic causes, minimal change disease owns childhood, membranous nephropathy owns adulthood.
What you must remember
- PSGN: 1-3 weeks after streptococcal pharyngitis (longer after skin infection); low C3, raised ASO and anti-DNase B; granular lumpy-bumpy subepithelial deposits and electron-dense humps; children recover, a small adult minority progress.
- IgA nephropathy (Berger disease): synpharyngitic haematuria — concurrent with the mucosal infection, no latent period; mesangial IgA deposition on immunofluorescence; complement normal; the commonest glomerulonephritis worldwide.
- RPGN types: type I anti-GBM with linear immunofluorescence and pulmonary haemorrhage in Goodpasture disease; type II immune-complex; type III pauci-immune, ANCA-positive — the commonest in older adults.
- Minimal change disease: commonest nephrotic cause in children; light microscopy normal, electron microscopy shows podocyte foot-process effacement; highly selective proteinuria; steroid responsive.
- Membranous nephropathy: commonest nephrotic cause in adults; anti-PLA2R antibodies mark the primary form; spike-and-dome basement membrane with subepithelial deposits; screen for hepatitis B, lupus, drugs and solid tumours.
- Focal segmental glomerulosclerosis: steroid-resistant nephrotic syndrome in adolescents and young adults; collapsing variant associates with HIV.
- Lupus nephritis: full-house immunofluorescence (IgG, IgA, IgM, C3, C1q); class IV diffuse proliferative is the commonest and severest.
Using complement to split the syndromes
A single number, C3, prunes the differential more than any biopsy report summary. The child with periorbital swelling and Coca-Cola urine one week after a sore throat has a low C3: post-streptococcal glomerulonephritis, and the biopsy is usually unnecessary. The adult with nephrotic-range proteinuria and a normal C3 travels the membranous or minimal-change pathway, with anti-PLA2R separating primary membranous from the hepatitis B- or malignancy-driven secondary form. Persistently low C3 beyond eight weeks points instead to membranoproliferative glomerulonephritis or dense deposit disease, with their tram-track basement membranes. Meanwhile the young adult who reports that urine turns red during every cold has IgA nephropathy — the timing, not the complement, is the clue: concurrent with the infection, unlike the streptococcal week-long gap. Add a rapidly rising creatinine with crescents on biopsy, and the immunofluorescence pattern alone — linear, granular, or nothing — assigns anti-GBM disease, immune-complex disease, or ANCA-associated vasculitis, each with a different plasmapheresis and immunosuppression algorithm.
The latent-period trap
The examination question turns on the interval between infection and haematuria: one to three weeks (post-streptococcal, complement low) versus same-day to 48 hours (IgA nephropathy, complement normal). The second trap is the child versus adult answer to "commonest cause of nephrotic syndrome": minimal change disease before roughly age fifteen, membranous nephropathy after — with diabetic nephropathy overtaking both in older Indian adults, which is why every nephrotic adult gets glycated haemoglobin along with the biopsy form.
Frequently asked questions
What distinguishes nephritic from nephrotic syndrome?
Nephritic syndrome features haematuria with red-cell casts, hypertension and oliguria from proliferative glomerular injury; nephrotic syndrome features proteinuria over 3.5 g daily, hypoalbuminaemia, oedema and hyperlipidaemia.
Which glomerulonephritis is most common worldwide?
IgA nephropathy, presenting with synpharyngitic haematuria and mesangial IgA deposits with a normal complement level.
What are the three types of rapidly progressive glomerulonephritis?
Type I anti-GBM (linear immunofluorescence, Goodpasture), type II immune-complex (granular), and type III pauci-immune ANCA-associated — the commonest in the elderly.
What is the role of anti-PLA2R antibody testing?
It identifies primary membranous nephropathy, tracks disease activity and immunosuppression response, and spares the patient a biopsy in classic cases.
Why is minimal change disease so named?
Light microscopy and immunofluorescence are normal; only electron microscopy shows podocyte foot-process effacement — yet it causes the child's nephrotic syndrome and responds to steroids.