What are the causes of glomerulonephritis?

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Last updated: September 11, 2026 • View editorial policy

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Causes of Glomerulonephritis

Glomerulonephritis occurs as either primary (idiopathic) kidney disease or secondary to systemic autoimmune diseases, infections, drugs, or malignancy. 1

Primary Glomerulonephritis (Two-thirds of cases)

Primary glomerular diseases account for approximately 60-70% of all glomerulonephritis cases and include:

  • IgA nephropathy - the most common primary GN worldwide
  • Membranous nephropathy - now proven to be autoimmune in nature with pathogenic autoantibodies
  • Minimal change disease (MCD)
  • Focal segmental glomerulosclerosis (FSGS) - can be mediated by soluble factors or represent adaptive/genetic forms
  • Complement-mediated diseases - including C3 glomerulopathy and dense deposit disease

These conditions arise from intrinsic kidney immune dysregulation without identifiable systemic triggers. 1

Secondary Glomerulonephritis (One-third of cases)

Secondary GN develops in the context of identifiable systemic conditions:

Autoimmune/Systemic Diseases

  • Lupus nephritis - the predominant secondary cause (76% of secondary GN cases) 2
  • ANCA-associated vasculitis - involving complement activation and neutrophil extracellular traps 3
  • Anti-GBM antibody disease - causing rapidly progressive GN
  • IgA vasculitis (Henoch-Schönlein purpura)

Infectious Causes

  • Post-streptococcal GN - the leading cause of acute GN in children globally, particularly in low- and middle-income countries 4
  • Staphylococcus-associated GN - including infective endocarditis and shunt nephritis 4
  • Hepatitis B virus - associated with membranous nephropathy and mesangiocapillary GN in endemic areas 5
  • Hepatitis C virus - causes cryoglobulinemia-mediated GN and various other forms 5
  • HIV - associated with collapsing FSGS, particularly in individuals of African descent 5
  • Parvovirus B19 - implicated in some cases of collapsing FSGS 5
  • Hantavirus and SARS-CoV-2 - can cause acute kidney injury with glomerular involvement 5

Other Secondary Causes

  • Drugs and toxins
  • Malignancy-associated GN
  • Metabolic disorders
  • Hematologic conditions 1

Pathogenic Mechanisms

The current understanding has evolved from older concepts of passive immune complex deposition to recognition that most GN is autoimmune in nature, mediated by both antibodies and T cells reactive with self-antigens 6. The pathogenesis involves:

  • Environmental insults (particularly infections) triggering host responses in genetically susceptible individuals
  • Complement activation, including locally produced renal complement
  • Fc receptor-driven myeloid effector functions
  • Neutrophil extracellular traps with nucleic acid sensing
  • IL-23/IL-17 pathways and type 1 interferon-primed T cell cytotoxicity
  • Epithelial stress responses in podocytes and parietal epithelial cells 6, 3

Clinical Caveat

Kidney biopsy remains the gold standard for definitive diagnosis since clinical presentations overlap significantly across different etiologies. Look specifically for: proteinuria >0.5 g/day, dysmorphic erythrocytes, red blood cell casts, declining kidney function, or new-onset hypertension as indicators requiring further evaluation. 7 Serologic testing is essential for identifying secondary forms, but tissue diagnosis guides prognosis and treatment decisions. 1, 7

References

2
Research

Medical causes and histological pattern of glomerulonephritis.

Mymensingh medical journal : MMJ, 2008

3
Research

Pathophysiology of glomerulonephritis in autoimmune diseases.

Current opinion in rheumatology, 2026

5
Research

Viral nephropathy.

Nature clinical practice. Nephrology, 2006

6
Research

Pathogenesis and treatment of glomerulonephritis-an update.

Jornal brasileiro de nefrologia, 2016

7
Research

[Approach to suspected glomerulonephritis].

Innere Medizin (Heidelberg, Germany), 2026

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.