Acute Glomerulonephritis (Acute Glomerulonephritis Syndrome)

Post-infectious glomerulonephritis - very high mag[1]

Acute glomerulonephritis (AGN) is an immune-mediated inflammation and destruction of the glomeruli and peri-glomerular tissues including the basement membrane, mesangium, and the capillary endothelium.


AGN is asymptomatic in approximately 50% of patients. In those who present with symptoms, the initial presentation is peripheral edema, low urine volume, and dark-colored urine due to hematuria.The reduction in GFR coupled with the salt and water retention in the distal tubule results in an increased intravascular volume, edema, and systemic hypertension. Edema appears as facial and periorbital swelling initially, before becoming obvious in the lower extremities. Elevated blood pressure progresses with the kidney damage. Non-specific symptoms are also common and include nausea, malaise, and dizziness.

Fever and fatigue are the most frequent presentations of rapidly progressive glomerulonephritis. Other symptoms include nausea, anorexia, vomiting, arthralgia, and abdominal pain. Furthermore in these cases, hypertension is usually absent or mild.

The symptoms of acute post-streptococcal glomerulonephritis include passage of coke-colored or dark brown urine, hypertension, facial puffiness and pedal edema, and proteinuria on urinalysis [11]. Occasionally, the complications of hypertension such as seizures and persistent headaches may be the only presentations of the patient.


No symptom or sign is pathognomonic of AGN. Laboratory tests are, therefore, necessary to confirm a suspected case of AGN.

Urinalysis is necessary and may reveal red blood cell and white blood cell casts. Red blood cell casts are indicative of glomerular damage while the white cell casts are indicative of infection or inflammation of the nephron. Urinalysis also reveals proteinuria. Blood investigations necessary for diagnosis are tests for creatinine and urea levels.

Imaging studies such as abdominal plain radiographs, ultrasonography, and computed tomography (CT) scans may be necessary. However, a kidney biopsy is the definitive diagnostic modality to confirm AGN [12].


The management of AGN involves treatment of the underlying trigger, supportive care, and conservative management of the complications of the disease.

Diuretics are necessary to resolve the edema and antihypertensives are equally vital [13]. Furthermore, dietary modifications should consist of low protein diet and salt restriction. Antibiotics are administered in cases of infectious AGN, however, antibiotics may be ineffective since the nephritis occurs 1 to 6 weeks after the inciting infection. Typically, the infection resolves before the onset of the nephritis, however, if the infection still persists, antibiotics can be administered.

Corticosteroids are administered in cases of AGN triggered by autoimmune disease and in rapidly progressive glomerulonephritis. High dose corticosteroids are administered intravenously for up to 7 days after which they are switched to oral forms. Immunosuppressants may also be beneficial for these patients [14]. Plasmapheresis may also be a beneficial procedure to clear off antibodies from the blood. 

Generally, prompt diagnosis and treatment prevents progression of the disease to ESRD. Renal transplantation is the definitive treatment for ESRD; however, rapidly progressive glomerulonephritis may reappear in the transplanted kidney.


Post-streptococcal glomerulonephritis and IgA nephropathy have a minimal risk of progressing to chronic kidney disease if the underlying pathology is treated well in time. Complete resolution of symptoms is observed in most patients, especially children.

For other glomerular pathologies, the outcome is generally better if the patient presents with asymptomatic hematuria open link and proteinuria and in those with focal instead of diffuse glomerular changes on renal biopsy. Patients with diffuse glomerular involvement usually have a poorer prognosis.

Generally, poor prognostic factors include severe proteinuria, severe renal dysfunction, unresponsiveness to treatment, and extensive fibrotic changes in the glomeruli such as glomerulosclerosis.

If patients having membranoproliferative disease remain untreated, 50-60% of them will lead to ESRD in a period of 10-15 years. The situation in case of Wegener granulomatosis is different because about 20-25% are at risk of leading to ESRD [9] [10]. 


The etiological factors responsible for AGN may be classified into infectious and non-infectious causes. The commonest infections responsible for AGN are streptococcal infections, particularly strep pharyngitis.

Noninfectious causes of AGN are mostly autoimmune diseases and include systemic lupus erythematosus (SLE), goodpasture's syndrome, amyloidosis, Wegener granulomatosis, and polyarteritis nodosa [3].

Prolonged and heavy use of nonsteroidal anti-inflammatory drugs (NSAIDs) have also been suggested as a risk factor for AGN.


AGN accounts for 10-15% cases of glomerular diseases in the United States. However, the incidence rates have been variable, partially because of the asymptomatic nature of this condition in more than 50% of patients. Generally, statistics reveal a decline in the incidence of post-streptococcal glomerulonephritis in the United States. This decline is attributable to improved healthcare delivery and socioeconomic conditions.

In the United States, AGN is responsible for 25-30% of cases of ESRD. In about 25% of cases, the disease progresses to an acute nephritic syndrome. Acute nephritic syndrome, in turn, progresses to end-stage renal failure after several weeks or months.

Worldwide, the commonest cause of AGN is Berger disease or IgA nephropathy. Post-streptococcal glomerulonephritis open link is most commonly seen in Africa, the Caribbean, India, South America, Malaysia, and Pakistan.

In Nigeria's Port Harcourt city, the incidence of AGN in children between the ages of 3 to 16 years was 15.5 cases per year. Furthermore, the incidence of the disease was higher among males than females with a ratio of 1.1:1. However, currently the difference in incidence among males and females is not so significant [4].

Generally, there are more marked variations in geographic and seasonal incidence rates of post-streptococcal glomerulonephritis following pharyngeal infections than those which follow streptococcal skin infections [4] [5].

Sex distribution
Age distribution


AGN presents with both morphological and functional changes in the kidneys. There is cellular proliferation in the glomerular tufts as a result of the excess proliferation of the mesangial, epithelial, and endothelial cells triggered by the immune-complex deposition [6]. The cellular proliferation may be confined to the glomerular capillary, in what's described as endocapillary proliferation. Alternatively, it may occur in the Bowman's capsule beyond the glomerular cells and it is referred to as extra capillary proliferation. Accompanying this cellular proliferation is neutrophilic and monocytic infiltration of the glomerular capillary lumen.

On light microscopy, the glomerular capillary walls appear thickened. A study using electron microscopy clearly shows the basement membrane as thickened due to the deposits of electron-dense particles on the subendothelial, mesangial, and subepithelial parts of the basement membrane. The structural changes in the kidneys may be focal, segmental, diffuse, or global. Morphologically the kidneys appear grossly enlarged as a result of swelling effect in the glomerular tufts.

The main feature of AGN is the deposition or formation of immune complexes in the glomerulus. The deposition of complement factors and immunoglobulins is demonstrable by immunofluorescence.

The triggers for the formation of immune complexes in the glomerulus are largely unclear, except in cases of post-streptococcal glomerulonephritis. In post-streptococcal glomerulonephritis, a streptococcal neuraminidase alters the host immunoglobulin G (IgG) which combines with the host antibodies forming IgG/anti-IgG complexes which subsequently deposit in the glomeruli. Furthermore, the presence of high titers of antistreptolysin O or antihyaluronidase, streptokinase, and DNAase-B strongly suggest a preceding streptococcal infection. Specific antibodies may combine with these antigens to form immune complexes.

Nephritis-associated plasmin receptor (NAPlr) has been described as a glyceraldehyde-3-phosphate dehydrogenase which functions a plasminogen receptor. NAPlr deposition was demonstrated in the initial stages of post-streptococcal glomerulonephritis in immunofluorescence staining of renal biopsy specimens with anti-NAPlr antibodies. This finding links NAPlr with the pathogenesis of post-streptococcal glomerulonephritis [7].

A study conducted among adults revealed that the two commonest infectious triggers of AGN were streptococci and staphylococci, occurring in 27.9% and 24.4% of cases, respectively [8]. In infections of groups A, C, and G streptococcus associated with glomerulonephritis, titers of antibodies against nephritis-associated protease (NAPR) are significantly elevated. Anti-NAPR antibodies persist for several years and have been suggested to help prevent further episodes of post-streptococcal glomerulonephritis.


Prevention of AGN may include routine urinalysis done for patients with autoimmune diseases such as SLE.


Acute glomerulonephritis (AGN) is inflammation of the glomeruli which occurs as a result of autoimmune response to an infection or immune complex depositions occurring in autoimmune pathologies. AGN may also affect the various parts of glomerulus such as mesangium, the capillary endothelium and basement membrane.

Generally, the causes of AGN may be infectious or autoimmune diseases. AGN often occurs sequel to a streptococcal infection open link, usually strep throat or strep cutaneous infections [1]. This post-streptococcal glomerulonephritis is often commonly seen in children between 2 and 10 years. Noninfectious causes of AGN include autoimmune diseases such as IgA nephropathy, systemic lupus erythematosus, cryoglobulinemia, goodpasture syndrome, and Wegener granulomatosis [2]. AGN due to these autoimmune diseases is most likely associated with rapidly progressive glomerulonephritis.

The characteristic features of AGN are the formation and deposition of immune complexes in the glomerular tufts, accompanied by polymorphonuclear cellular infiltrates. Functionally, AGN results in hematuria, proteinuria, facial or pedal edema, and systemic hypertension. Nonspecific symptoms are also common in this disease.

Disease prognosis becomes poor due to severe proteinuria, hematuria, and renal damage on presentation, unresponsiveness to appropriate therapy, and the presence of extensive renal fibrosis or sclerosis on biopsy. The main complication of AGN is the end-stage renal disease (ESRD).

Renal biopsy is the main diagnostic tool of choice to confirm AGN. However, other investigations including bloodwork, urinalysis, and imaging studies provide details to corroborate the diagnosis.

Management of AGN comprises of symptomatic control and treatment of the underlying disorder. Antibiotics and corticosteroids are administered for infectious and autoimmune-associated AGN, respectively. Additionally, diuretics are necessary to relieve the edema. 

Patient Information


The kidney is an organ of waste excretion in the form of urine. However, the process of waste excretion is very complex involving several small structures within each kidney. The first stage of urine production is the filtration of the waste products from the blood. Some useful products are also filtered, but are later reabsorbed into the blood. The units which filter the blood are called the glomeruli (singular: glomerulus).

Acute glomerulonephritis (AGN) is an inflammation and consequent destruction of the glomeruli and adjacent tissues. This, in turn, would lead to reduced urine production as well as salt and water retention in the body.


AGN may be caused by infections or certain noninfectious diseases called autoimmune diseases in which the body's antibodies attack certain normal tissues in the body confusing them for foreign harmful substances. The commonest infectious causes of AGN are infections caused by the bacterium streptococcus, which are mostly are responsible for sore throat and skin infections. The common autoimmune diseases which cause AGN includes systemic lupus erythematosus (SLE), Wegener granulomatosis, and Berger disease.


AGN develops when antibodies formed in the body against certain components of the bacterium or infectious agents bind with these agents and deposit in the glomeruli causing destruction of the glomeruli and surrounding tissues.


More than half of the patients with this disease may not show any symptoms. However, those who come down with symptoms may present with swelling of the face and legs, reduced urine volume, passage of coke-colored or dark urine, urine frothiness and a high blood pressure.

The facial and leg swelling results from the kidneys' inability to dilute the urine with water from the blood and so there is an accumulation of excess salt and water in the certain regions of the body such as the feet and face. This is also responsible for the elevated blood pressure in these patients. The dark color of the urine is due to the presence of the blood in it, and the frothiness of the urine is as a result of leakage of small proteins through the damaged glomerular filter into the urine. 

There are other non-specific symptoms of this disease which include fever, weakness, dizziness, and abdominal aches.


A diagnosis of AGN is made by way of investigations which include blood tests and urinalysis: which involves examining a sample of the patient's urine and analyzing it's contents. Results of urinalysis in AGN usually show presence of white and red blood cells which indicate infective damage or inflammation of the kidney tubules and damage to the glomeruli, respectively.

The main diagnostic tool for confirming the diagnosis of AGN is kidney biopsy. This procedure involves using a big needle to take a sample of the kidney through the patient's trunk, then analyzing the sample under a microscope.


Prompt diagnosis and treatment of AGN is necessary to avoid the major complication which is called end-stage renal disease which indicates that the kidney is too damaged to function at all.

Treatment of AGN involves treating the predisposing condition and correcting the symptoms. A class of drugs called diuretics are prescribed to remove excess fluids from the sites where they accumulate. Drugs which lower blood pressure are also necessary. If an infection is determined as the trigger of AGN, antibiotics are administered and for autoimmune-related cases, drugs called corticosteroids such as prednisolone are administered.

In cases of end-stage renal disease, kidney transplant is considered.


Ask Question

5000 Characters left Format the text using: # Heading, **bold**, _italic_. HTML code is not allowed.


  1. Tejani A, Ingulli E. Poststreptococcal glomerulonephritis: current clinical and pathological concepts. Nephron. 1990; 55:1-5.
  2. Emancipator SN. IgA nephropathy: morphological expression and pathogenesis. Am J Kidney Dis. 1994; 23:451-462.
  3. Kalluri R, Wilson CV, Weber M, et al. Identification of the α-3 chain of type IV collagen as the common autoantigen in anti-glomerular basement membrane disease and Goodpasture’s syndrome. J Am Soc Nephrol. 1995; 6:1178-1184.
  4. Anochie I, Eke F, Okpere A. Childhood acute glomerulonephritis in Port Harcourt, Rivers State, Nigeria. Niger J Med. 2009; 18(2):162-167.
  5. Wong W, Morris MC, Zwi J. Outcome of severe acute post-streptococcal glomerulonephritis in New Zealand children. Pediatr Nephrol. 2009; 24(5):1021-1026.
  6. Wen YK, Chen ML. The significance of atypical morphology in the changes of spectrum of postinfectious glomerulonephritis. Clin Nephrol. 2010; 73(3):173-179. 
  7. Oda T, Yoshizawa N, Yamakami K, et al. The role of nephritis-associated plasmin receptor (NAPlr) in glomerulonephritis associated with streptococcal infection. J Biomed Biotechnol. 2012; 2012:417675.
  8. Nasr SH, Markowitz GS, Stokes MB, et al. Acute postinfectious glomerulonephritis in the modern era: experience with 86 adults and review of the literature. Medicine (Baltimore). 2008; 87(1):21-32.
  9. Donadio JV Jr, Offord KP. Reassessment of treatment results in membranoproliferative glomerulonephritis, with emphasis on life-table analysis. Am J Kidney Dis. 1989; 14:445-451.
  10. Andrassy K, Erb A, Koderisch J, et al. Wegener's granulomatosis with renal involvement: patient survival and correlations between initial renal function, renal histology, therapy and renal outcome. Clin Nephrol. 1991; 35:139-147.
  11. Sad RA, Said SM. Hypertension in Jordanian children: a retrospective analysis of 70 cases Pediatr. Nephrol. 1990; 4:520-522.
  12. Nebuloni M, Barbiano di Belgiojoso G, Genderini A, et al. Glomerular lesions in HIV-positive patients: a 20-year biopsy experience from Northern Italy. Clin Nephrol. 2009; 72(1):38-45.
  13. Tapaneyaand O. AGN in children: a prospective study. J Med Assoc Thai. 1989; 72(suppl):35-38.
  14. Wong W, Morris MC, Zwi J. Outcome of severe acute post-streptococcal glomerulonephritis in New Zealand children. Pediatr Nephrol. 2009; 24(5):1021-1026.

Media References

  1. Post-infectious glomerulonephritis - very high mag, CC BY-SA 3.0