Internal Medicine (Theory) · MU Sofia

28. Glomerulonephritis

Covers glomerulonephritis as a group of kidney diseases marked by glomerular inflammation, then goes through its infectious, autoimmune and hereditary causes and how it is classed by clinical course and by cause. A side-by-side table sets acute and chronic forms against each other on onset, symptoms, urinalysis, blood tests, imaging, biopsy findings, treatment and prognosis. It then outlines immune-mediated pathogenesis, symptoms, examination and laboratory and imaging findings, kidney biopsy, and treatment by type.

Inside: 8 sections · 3 labelled pictures · 2 tables · 14 flashcards · 5 min

Topic 26 of 58 in the MU Sofia syllabus for Internal Medicine (Theory) (Medicine, Year 3). The free AceMed note covers it in 8 sections, about 427 words (5 min of reading), with 14 flashcards.

In this note

  1. Glomerulonephritis
  2. Definition:
  3. Etiology:
  4. Classification:
  5. Pathogenesis:
  6. Symptoms:
  7. Diagnosis:
  8. Treatment:

Definition:

Glomerulonephritis (GN) refers to a group of kidney diseases characterized by inflammation of the glomeruli, leading to varying degrees of hematuria, proteinuria, reduced glomerular filtration rate (GFR), hypertension, and edema.

It can present as acute, rapidly progressive, or chronic disease and may be primary (limited to kidneys) or secondary (as part of systemic illness).

Etiology:

Infectious causes:

  • Group A beta-hemolytic streptococci (post-streptococcal GN)
  • Bacterial endocarditis
  • Hepatitis B, C
  • HIV, syphilis

Autoimmune / Immune-mediated:

  • Systemic lupus erythematosus (SLE)
  • IgA nephropathy (Berger disease)

Others:

  • Hereditary disorders (e.g., Alport syndrome)

Classification:

A. Based on Clinical Course:

  • Acute glomerulonephritis (e.g., PSGN)
  • Rapidly progressive glomerulonephritis (RPGN)
  • Chronic glomerulonephritis

C. Based on Cause:

  • Primary GN (renal-limited)
  • Secondary GN (associated with systemic disease)

Pathogenesis:

  • Immune-mediated injury is the primary mechanism.
  • Antibodies or immune complexes deposit in the glomeruli.
  • This triggers complement activation and inflammation.
  • Leads to damage of the filtration barrier → hematuria, proteinuria, decreased GFR.
  • In some types (e.g., RPGN), aggressive injury leads to crescent formation and rapid loss of renal function.

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