eMedicine Specialties > Nephrology > Glomerular Diseases
Glomerulonephritis, Acute
Updated: Jul 2, 2008
Introduction
Background
Bright initially described acute glomerulonephritis (GN) in 1927. Acute poststreptococcal glomerulonephritis (PSGN) is the archetype of acute GN. Acute nephritic syndrome is the most serious and potentially devastating form of various renal syndromes. Acute GN is characterized by the abrupt onset of hematuria and proteinuria, often accompanied by azotemia (ie, decreased glomerular filtration rate [GFR]) and renal salt and water retention.
Pathophysiology
Acute GN has 2 components: structural changes and functional changes.
Structural changes
- Cellular proliferation: This leads to an increase in the number of cells in the glomerular tuft because of the proliferation of endothelial, mesangial, and epithelial cells. The proliferation could be endocapillary (ie, within the confines of the glomerular capillary tufts) or extracapillary (ie, in the Bowman space involving the epithelial cells). In extracapillary proliferation, proliferation of parietal epithelial cells leads to the formation of crescents, a feature characteristic of certain forms of rapidly progressive GN.
- Leukocyte proliferation: This is indicated by the presence of neutrophils and monocytes within the glomerular capillary lumen and often accompanies cellular proliferation.
- Glomerular basement membrane thickening: This development appears as thickening of capillary walls using light microscopy. Using electron microscopy, this may appear as the result of thickening of basement membrane proper (eg, diabetes) or deposition of electron-dense material, either on the endothelial or epithelial side of the basement membrane.
- Hyalinization or sclerosis: These conditions indicate irreversible injury.
- Electron-dense deposits: Such deposits could be subendothelial, subepithelial, intramembranous, or mesangial, and they correspond to an area of immune complex deposition.
- These structural changes could be focal, diffuse or segmental, and global.
Functional changes
Functional changes include proteinuria, hematuria, reduction in GFR (ie, oligoanuria), and active urine sediment with RBCs and RBC casts. The decreased GFR and avid distal nephron salt and water retention result in expansion of intravascular volume, edema, and, frequently, systemic hypertension.
Poststreptococcal glomerulonephritis
M-protein of the organism was previously believed to be responsible for PSGN. These studies have been discounted recently. Nephritis-associated streptococcal cationic protease and its zymogen precursor (NAPR) have been identified as a glyceraldehyde-3-phosphate dehydrogenase that functions as a plasmin(ogen) receptor. This binds to plasmin and activates complement via alternate pathway. Antibody levels to NAPR are elevated in streptococcal infections (of group A, C, and G) associated with glomerulonephritis but are not elevated in streptococcal infections without glomerulonephritis, whereas anti-streptolysin-O titers are elevated in both circumstances. These antibodies to NAPR persist for years and perhaps are protective against further episodes of PSGN. In a recent study in adults, the 2 most frequently identified infectious agents were streptococcus (27.9%) and staphylococcus (24.4%).1
Frequency
United States
GN comprises 25-30% of all cases of end-stage renal disease (ESRD). About one fourth of patients present with acute nephritis syndrome. Most cases that progress do so relatively quickly, and end-stage renal failure may occur within weeks or months of acute nephritic syndrome onset. Asymptomatic episodes of PSGN exceed symptomatic episodes by a ratio of 3-4:1.
International
Geographic and seasonal variations in the prevalence of PSGN are more marked for pharyngeally associated GN than for cutaneously associated disease.
Race
Postinfectious GN has no predilection for any racial or ethnic group. A higher incidence (related to poor hygiene) may be observed in some socioeconomic groups.
Sex
Acute GN predominantly affects males (ie, 2:1 male-to-female ratio).
Age
Postinfectious GN can occur at any age but usually develops in children. Outbreaks of PSGN are common in children aged 6-10 years.
Clinical
History
Taking a proper history is important and helpful.
- Determine onset of disease: Ask the patient about onset and duration of illness.
- Identify a possible etiologic agent (eg, streptococcal throat infection [pharyngitis], skin infection [pyoderma]): Recent fever, sore throat, joint pains, hepatitis, travel, valve replacement, and/or intravenous drug use may be causative factors. Rheumatic fever rarely coexists with acute PSGN.
- Identify systemic disease (eg, arthralgia, diabetes).
- Assess the consequences of the disease process (eg, uremic symptoms): Inquire about loss of appetite, generalized itching, tiredness, listlessness, nausea, easy bruising, nose bleeds, facial swelling, leg edema, and shortness of breath.
- Identify clinical features: Inquire about edema, decreased volume and frequency of urination, systemic hypertension, uremic symptoms, costovertebral tenderness (ie, enlarged kidneys [rare]), and gross hematuria. Gross hematuria is the most common abnormality observed in patients with acute PSGN and often manifests as smoky-, coffee-, or cola-colored urine.
Physical
- Signs of fluid overload
- Periorbital and/or pedal edema
- Edema and hypertension due to fluid overload (in 75% of patients)
- Crackles (ie, if pulmonary edema)
- Elevated jugular venous pressure
- Ascites and pleural effusion (possible)
- Rash (ie, vasculitis, Henoch-Schönlein purpura)
- Pallor
- Renal angle (ie, costovertebral) fullness or tenderness, joint swelling, or tenderness
Causes
The causal factors that underlie this syndrome can be broadly divided into infectious and noninfectious groups.
- Infectious
- Streptococcal: Poststreptococcal GN usually develops 1-3 weeks following acute infection with specific nephritogenic strains of group A beta-hemolytic streptococcus. The incidence of GN is approximately 5-10% in persons with pharyngitis and 25% in those with skin infections.
- Nonstreptococcal postinfectious glomerulonephritis
- Bacterial - Infective endocarditis, shunt nephritis, sepsis, pneumococcal pneumonia, typhoid, secondary syphilis, meningococcemia, and infection with methicillin-resistant Staphylococcus aureus (MRSA)
- Viral - Hepatitis B, infectious mononucleosis, mumps, measles, varicella, vaccinia, echovirus, parvovirus, and coxsackievirus
- Parasitic - Malaria, toxoplasmosis
- Noninfectious
- Multisystem systemic diseases - Systemic lupus erythematosus, vasculitis, Henoch-Schönlein purpura, Goodpasture syndrome, Wegener granulomatosis
- Primary glomerular diseases - Membranoproliferative GN (MPGN), Berger disease (ie, immunoglobulin A [IgA] nephropathy), "pure" mesangial proliferative GN
- Miscellaneous - Guillain-Barré syndrome, radiation of Wilms tumor, diphtheria-pertussis-tetanus vaccine, serum sickness
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References
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Baldwin DS, Gluck MC, Schacht RG, et al. The long-term course of poststreptococcal glomerulonephritis. Ann Intern Med. Mar 1974;80(3):342-58. [Medline].
Bazzi C, Petrini C, Rizza V, et al. A modern approach to selectivity of proteinuria and tubulointerstitial damage in nephrotic syndrome. Kidney Int. Oct 2000;58(4):1732-41. [Medline].
Dodge WF, Spargo BH, Travis LB, et al. Poststreptococcal glomerulonephritis. A prospective study in children. N Engl J Med. Feb 10 1972;286(6):273-8. [Medline].
Neugarten J, Gallo GR, Baldwin DS. Glomerulonephritis in bacterial endocarditis. Am J Kidney Dis. Mar 1984;3(5):371-9. [Medline].
Oda T, Yamakami K, Omasu F, et al. Glomerular plasmin-like activity in relation to nephritis-associated plasmin receptor in acute poststreptococcal glomerulonephritis. J Am Soc Nephrol. Jan 2005;16(1):247-54. [Medline].
Rodriguez-Iturbe B. Nephritis-associated streptococcal antigens: where are we now?. J Am Soc Nephrol. Jul 2004;15(7):1961-2. [Medline].
Rodríguez-Iturbe B. Epidemic poststreptococcal glomerulonephritis. Kidney Int. Jan 1984;25(1):129-36. [Medline].
Ronco P, Verroust P, Morel-Maroger L. Viruses and Glomerulonephritis. Nephron. 1982;31(2):97-102. [Medline].
Yoshizawa N, Yamakami K, Fujino M, et al. Nephritis-associated plasmin receptor and acute poststreptococcal glomerulonephritis: characterization of the antigen and associated immune response. J Am Soc Nephrol. Jul 2004;15(7):1785-93. [Medline].
Further Reading
Keywords
acute glomerulonephritis, acute nephritis, Bright disease, acute poststreptococcal glomerulonephritis, PSGN, acute postinfectious glomerulonephritis
