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Contributors: Peter Joo MD, Christine Osborne MD, Michael W. Winter MD
Other Resources UpToDate PubMed


Glomerulonephritis is inflammation of the glomerular capillaries from immune complex deposition (ie, immunoglobulin A [IgA] nephropathy), autoimmune activation, or inflammatory agents secreted by bacteria, viruses, or fungi, leading to damage of glomerular cells. Progressive damage leads to worsening renal function caused by interstitial nephritis, fibrosis, and tubular atrophy.

Patients typically present with hematuria, dysmorphic red blood cells on urine microscopy, proteinuria from mild to nephrotic range, edema, hypertension, and decline in renal function. This disease frequently affects young adults and is the most common cause of end-stage renal disease in this population.

There are groups of glomerulonephritis that can be classified based on clinical presentations, with overlap among groups depending on presentation:
  • Acute nephritic syndromes – Patients present with non-nephrotic range proteinuria, hematuria with red blood cell casts, pyuria, hypertension, fluid retention, and a rise in serum creatinine associated with a reduction in glomerular filtration, which can be progressive or rapid in onset. Diseases include membranoproliferative glomerulonephritis, lupus nephritis (see systemic lupus erythematosus), and post-streptococcal glomerulonephritis.
  • Pulmonary-renal syndromes – Patients develop rapidly progressive renal decline with hematuria, proteinuria, and edema and have associated pulmonary hemorrhage, vasculitis, or antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis. Examples include Goodpasture syndrome (see antiglomerular basement membrane [anti-GBM] disease) and granulomatosis with polyangiitis. Up to one-third of patients with anti-GBM antibodies also have ANCAs, and approximately 5% of those initially positive for ANCAs also have anti-GBM antibodies. Known as double antibody–positive disease, this combination often generates the sudden renal decline of anti-GBM disease and the extrarenal manifestations of ANCA-associated disease.
  • Nephrotic syndromes – Patients present with heavy proteinuria defined as more than 3.5 g per 24 hours, edema, hypertension, hypercholesterolemia, hypoalbuminemia, and microscopic hematuria. There may be a decline in glomerular filtration over time, leading to progressive renal dysfunction. Examples include minimal change disease, focal segmental glomerulosclerosis, and light-chain deposition disease.
  • Basement membrane syndromes – Patients present with microscopic hematuria, mild to heavy proteinuria, hypertension, and variable declines in renal function due to either genetically abnormal glomerular basement membranes or autoimmune responses to glomerular basement membrane collagen. Examples include Alport syndrome and anti-glomerular basement membrane disease.
  • Glomerular-vascular syndromes – Patients present with hematuria and moderate proteinuria, and disease is secondary to underlying vasculitis, thrombotic microangiopathy, antiphospholipid syndrome, or other systemic disease such as sickle cell disease, atherosclerosis, or hypertension. Examples include atherosclerotic nephropathy, hypertensive nephropathy, and sickle cell disease.
  • Infectious disease-associated syndromes – In the developing world, infectious disease-related glomerulonephritis is the most common cause of glomerular disease. Patients present with varying degrees of glomerular inflammation with a combination of hematuria and proteinuria on urinalysis. Examples include human immunodeficiency virus nephropathy, hepatitis B, hepatitis C, malaria, and post-streptococcal glomerulonephritis.
Related topic: Membranous glomerulonephritis


N00.9 – Acute nephritic syndrome with unspecified morphologic changes

36171008 – Glomerulonephritis

Look For

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Diagnostic Pearls

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Differential Diagnosis & Pitfalls

Most clinical and laboratory findings in the workup for glomerulonephritis portend a wide differential diagnosis. These include:
  • Congestive heart failure – edema, orthopnea, elevated jugular venous pulse
  • Acute liver failure – anasarca, hyperammonemia, jaundice, uremia
  • Cystitis – hematuria, suprapubic pain
  • Bladder cancer – painless hematuria, constitutional symptoms
  • Pyelonephritis – flank pain, pyuria
  • Renal calculus – flank pain, hematuria, crystals on urinalysis
  • Acute kidney injury – from various causes; oliguria, casts, possible hematuria
  • Acute interstitial nephritis – typically from medications (NSAIDs, antibiotics); eosinophils in urinalysis
There are a number of causes of glomerulonephritis (see Synopsis above).

Best Tests

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Management Pearls

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Drug Reaction Data

Below is a list of drugs with literature evidence indicating an adverse association with this diagnosis. The list is continually updated through ongoing research and new medication approvals. Click on Citations to sort by number of citations or click on Medication to sort the medications alphabetically.

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Last Reviewed:03/27/2019
Last Updated:12/04/2019
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A medical illustration showing key findings of Glomerulonephritis (Acute) : Dark urine, Facial edema, Fatigue, Creatinine elevated, Hematuria, Malaise, Proteinuria, RBC casts, Anorexia, Peripheral leg edema, Hypertension
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