# Glomerulonephritis Classification

> Glomerulonephritis classification for MBBS Pathology: nephritic versus nephrotic, PSGN, IgA nephropathy, RPGN types and PLA2R membranous.

- Canonical URL: https://prepelephant.com/topics/mbbs/pathology/glomerulonephritis-classification
- Exam / course: MBBS · Subject: Pathology
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Glomerulonephritis Classification", PrepElephant, https://prepelephant.com/topics/mbbs/pathology/glomerulonephritis-classification

## 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.