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Glomerulonephritis (GN) is a renal disease characterised by inflammation and damage to the glomeruli.

This glomerular damage allows protein (with or without blood) to leak into the urine (proteinuria and haematuria respectively).

Glomerulonephritis can present with any of the following:

  • Isolated haematuria or proteinuria
  • Nephrotic syndrome
  • Nephritic syndrome 
  • Acute renal failure
  • Chronic renal failure

Glomerulonephritis (GN) can be broadly categorised into proliferative and non-proliferative disease.

This article provides a brief overview of the various subtypes of both proliferative and non-proliferative GN.

Nephrotic and nephritic syndrome

Nephrotic syndrome is a condition involving the loss of significant volumes of protein via the kidneys (proteinuria) which results in hypoalbuminaemia. The definition of nephrotic syndrome includes both massive proteinuria (≥3.5 g/day) and hypoalbuminaemia (serum albumin ≤30 g/L).

Nephritic syndrome is a condition involving haematuria, mild to moderate proteinuria (typically less than 3.5g/L/day), hypertensionoliguria and red cell casts in the urine.

For more information, see the Geeky Medics article on nephrotic vs nephritic syndrome and our deep dive into glomerulonephropathies.

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Non-proliferative glomerulonephritis

Non-proliferative glomerulonephritis is characterised by a lack of glomerular cell proliferation and typically presents with nephrotic syndrome.

Minimal change glomerulonephritis

Minimal change glomerulonephritis (also called minimal change disease) presents with nephrotic syndrome and accounts for 80% of all nephrotic syndrome in children and 20% of nephrotic syndrome in adults.

The underlying cause of minimal change glomerulonephritis is unknown. The name minimal change glomerulonephritis comes from the lack of changes seen on light microscopy. 


Typical investigation findings include:1,2

  • Urinalysis: proteinuria
  • Light microscopy: no visible abnormalities
  • Immunofluorescence: no immunoglobulins or complement deposits bound to the kidney tissue
  • Electron microscopy: diffuse loss of visceral epithelial cells’ foot processes (i.e. podocyte effacement), vacuolation, and growth of microvilli on the visceral epithelial cells, allowing for excess protein loss in the urine


Management of minimal change glomerulonephritis includes:1

  • Supportive care: nutritional support, salt and fluid restriction
  • Corticosteroids: first-line treatment in both adults and children (more data for efficacy in children)
  • Other immunosuppressants (e.g. calcineurin inhibitor, mycophenolate mofetil, rituximab): these are second-line management options, and their effectiveness is unclear

Focal segmental glomerulosclerosis (FSGS)

Focal segmental glomerulosclerosis typically presents with nephrotic syndrome. It is the most common cause of nephrotic syndrome in adults. 

It can be divided into primary FSGS (unknown cause with a possible genetic element) and secondary FSGS (caused by another disease process, e.g. HIV, lupus, reflux nephropathy).


Typical findings on renal biopsy are segmental scarring of some glomeruli and fusion of foot processes.


Management of focal segmental glomerulosclerosis includes:

  • Supportive care: salt restriction and fluid management
  • High-dose prednisolone: approximately 50% of patients respond and treatment can be up to four months in adults
  • Cyclophosphamide or ciclosporin is used in some cases to reduce proteinuria


Typically progresses to end-stage kidney disease over the course of several years in up to 50% of patients. Corticosteroids can halt progression in some cases.

Membranous glomerulonephritis

Membranous glomerulonephritis typically presents with nephrotic syndrome. It is a slowly progressive disease primarily affecting individuals between the ages of 30 – 50.

Membranous glomerulonephritis is commonly idiopathic but can be associated with hepatitis B, malaria and systemic lupus erythematosus (SLE).

Immune complex deposition results in complement activation against glomerular basement membrane proteins.


Typical findings on renal biopsy include:

  • Microscopic analysis: shows thickened glomerular basement membrane
  • Immunofluorescence: shows diffuse uptake of IgG 
Figure 1. A renal biopsy in membranous nephropathy showing glomerular basement membrane thickening.4


Management of membranous glomerulonephritis includes: 

  • Supportive care: salt restriction and fluid management
  • Corticosteroids are often used to treat progressive disease


The rule of thirds describes the broad prognosis of membranous glomerulonephritis: 

  • 1/3 have chronic membranous glomerulonephritis
  • 1/3 go into remission
  • 1/3 progress to end-stage renal failure

Proliferative glomerulonephritis

Proliferative glomerulonephritis is characterised by increased numbers of cells in the glomerulus. It typically presents with nephritic syndrome.

IgA nephropathy

IgA nephropathy is also known as Berger’s disease. It is the most common form of glomerulonephritis in adults worldwide.

IgA nephropathy typically presents as nephritic syndrome (macroscopic haematuria), 24-48 hours after an upper respiratory tract infection.


Microscopically the disease is characterised by:

  • Increased numbers of mesangial cells
  • Increased matrix (the cellular scaffolding that holds everything together)

Immunohistochemistry will show IgA deposition in the matrix.


Management of IgA nephropathy includes:

  • High-dose prednisolone: can reduce proteinuria and delay renal impairment
  • Other immunosuppressive drugs: can be used in patients with deteriorating renal function


Prognosis is variable, with 20 – 30% of patients progressing to end-stage renal failure.

Post-infectious glomerulonephritis

Post-infectious glomerulonephritis (PIGN) is an immunologically mediated glomerular injury triggered by an infection.

PIGN is most commonly associated with streptococcal infections (referred to as post-streptococcal glomerulonephritis)

The disease typically presents approximately 2 weeks after infection with nephritic syndrome (i.e. gross haematuria, oliguria, oedema).


Typical findings on renal biopsy include:

  • Diffuse proliferative and exudative glomerular histology
  • Dominant C3 staining and subepithelial humps


Diagnosis is typically based on the presence of:

  • Symptoms and signs of glomerulonephritis
  • History of recent infection (e.g. streptococcal)
  • Raised streptococcal titres 


Management is largely supportive, with careful monitoring of fluid balance.


PIGN is usually a self-limited disease, especially in children. However, long-term follow-up studies indicate persistent low-grade renal abnormalities in a sizeable proportion of patients.3

Membranoproliferative glomerulonephritis

Membranoproliferative glomerulonephritis is a group of immune-mediated disorders characterised histologically by glomerular basement membrane (GBM) thickening and proliferative changes on light microscopy.

It should not be confused with membranous glomerulonephritis, a condition in which the basement membrane is thickened, but the mesangium is not.

The disease is associated with hepatitis C and several autoimmune conditions including systemic lupus erythematosus (SLE).


Typical findings on renal biopsy include:

  • Thickened basement membrane
  • Thickened mesangium
  • “Tram tracking” appearance

Immunofluorescence shows subendothelial deposition of IgG.


Management of membranoproliferative glomerulonephritis includes:

  • Children (with nephrotic-range proteinuria): corticosteroids
  • Adults: dipyridamole and aspirin
  • Kidney transplantation for patients with end-stage renal disease

Rapidly progressive glomerulonephritis (crescentic glomerulonephritis)

Rapidly progressive glomerulonephritis (RPGN) is acute nephritic syndrome accompanied by microscopic glomerular crescent formation with progression to renal failure within weeks to months.

RPGN is relatively uncommon, affecting 10 to 15% of patients with glomerulonephritis. It primarily occurs in patients aged 20 to 50 years. 

RPGN can be caused by anti-glomerular basement membrane antibody disease and vasculitic disorders (covered below). 

Crescentic glomerulonephritis
Figure 2. A renal biopsy showing crescentic glomerulonephritis.5

Anti-glomerular basement membrane antibody disease (Anti-GBM)

Anti-GBM disease is an immune-mediated pathology involving antibodies directed against glomerular basement membrane antigens (anti-GBM antibodies). These antigens are located in the glomeruli and in the alveoli of the lungs.

A cell-mediated inflammatory response occurs as a result of the anti-GBM antibodies which can affect both the kidneys (nephritic syndrome) as well as the lungs (alveolar haemorrhage presenting with haemoptysis).

If the lungs and kidneys are involved the condition is known as Goodpasture’s syndrome.

Anti-GBM disease accounts for approximately 10% of RPGN. Progression to renal failure is often rapid without medical intervention.


Typical investigation findings include:

  • Immunohistochemistry: IgG deposits along the basement membrane of the glomerulus
  • Antibodies: anti-GBM antibodies


Management of anti-GBM disease includes high dose immunosuppression, options include IV prednisolone, cyclophosphamide and plasmapheresis.

Vasculitic disorders

Vasculitic disorders which may cause proliferative glomerulonephritis include granulomatosis with polyangiitis (GPA) and microscopic polyangiitis.

Granulomatosis with polyangiitis

Granulomatosis with polyangiitis (GPA), previously known as Wegener’s granulomatosis, is an extremely rare long-term systemic disorder that involves the formation of granulomas and inflammation of blood vessels (vasculitis).

It is a form of vasculitis that affects both small and medium-sized vessels in many organs (commonly the upper respiratory tract, lungs and kidneys). 5

Symptoms are highly variable, depending on which vessels are affected. The vasculitis is caused by anti-neutrophil cytoplasmic antibodies (c-ANCA).

A biopsy (e.g. of kidney or cutaneous tissue) will show leukocytoclastic vasculitis with necrotic changes and granulomatous inflammation (clumps of typically arranged white blood cells) on microscopy.

Management involves immunosuppression. Remission is induced with rituximab or cyclophosphamide in combination with high dose corticosteroids. Maintenance therapy may include methotrexate and corticosteroids. 

Microscopic polyangiitis

Microscopic polyangiitis is a systemic small-vessel vasculitis without clinical or pathological evidence of necrotising granulomatous inflammation.

Clinical features can include weight loss, fevers, fatigue and renal failure. Ongoing inflammation is driven by anti-neutrophil cytoplasmic antibodies (p-ANCA), which is positive in almost all cases. 

Management involves long-term prednisolone and cyclophosphamide therapy (often cycled). Plasmapheresis can be helpful acutely to remove p-ANCA antibodies.

Key points

  • Glomerulonephritis (GN) is a renal disease characterised by inflammation and damage to the glomeruli.
  • The clinical presentation is variable and ranges from isolated haematuria/proteinuria to acute renal failure.
  • Non-proliferative glomerulonephritis is characterised by a lack of glomerular cell proliferation and typically presents with nephrotic syndrome.
  • Proliferative glomerulonephritis is characterised by increased numbers of cells in the glomerulus. It typically presents with nephritic syndrome.


  1. Johnson, Richard J.; Feehally, John; Floege, Jürgen (2018-06-26). Comprehensive clinical nephrology (Sixth ed.). Edinburgh. ISBN 9780323547192. OCLC 1047958109.
  2. Fogo, Agnes B.; Lusco, Mark A.; Najafian, Behzad; Alpers, Charles E. (Aug 2015). “AJKD Atlas of Renal Pathology: Minimal Change Disease”. American Journal of Kidney Diseases. 66 (2): 376–377. doi:10.1053/j.ajkd.2015.04.006. ISSN 1523-6838. PMID 26210726.
  3. Kambham N. Postinfectious glomerulonephritis. Published September 2012. Available from: [LINK]
  4. Nephron. Membranous nephropathy. Licence: [CC BY-SA]
  5. Nephron. Crescentic glomerulonephritis. Licence: [CC BY-SA]


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