Contents

SynopsisCodesLook ForDiagnostic PearlsDifferential Diagnosis & PitfallsBest TestsManagement PearlsTherapyDrug Reaction DataReferences

View all Images (2)

Glomerulonephritis
Other Resources UpToDate PubMed

Glomerulonephritis

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

Synopsis

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

Codes

ICD10CM:
N00.9 – Acute nephritic syndrome with unspecified morphologic changes

SNOMEDCT:
36171008 – Glomerulonephritis

Look For

Subscription Required

Diagnostic Pearls

Subscription Required

Differential Diagnosis & Pitfalls

To perform a comparison, select diagnoses from the classic differential

Subscription Required

Best Tests

Subscription Required

Management Pearls

Subscription Required

Therapy

Subscription Required

Drug Reaction Data

Subscription Required

References

Subscription Required

Last Reviewed:03/27/2019
Last Updated:12/04/2019
Copyright © 2024 VisualDx®. All rights reserved.
Glomerulonephritis
Print   View all Images (2)
(with subscription)
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
Copyright © 2024 VisualDx®. All rights reserved.