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Acute proliferative glomerulonephritis

Acute proliferative glomerulonephritis
File:Post-infectious glomerulonephritis - very high mag.jpg
Micrograph of a post-infectious glomerulonephritis. Kidney biopsy. PAS stain.
Classification and external resources
ICD-9 580.0
DiseasesDB 29306
MedlinePlus 000503
eMedicine med/889
NCI Acute proliferative glomerulonephritis
Patient UK Acute proliferative glomerulonephritis

Acute proliferative glomerulonephritis is a disorder of the glomeruli (glomerulonephritis), or small blood vessels in the kidneys. It is a common complication of bacterial infections, typically skin infection by Streptococcus bacteria types 12,4 and 1 (impetigo) but also after streptococcal pharyngitis, for which it is also known as postinfectious or poststreptococcal glomerulonephritis.[1] It can be a risk factor for future albuminuria.[2] In adults, the signs and symptoms of infection may still be present at the time when the kidney problems develop, and the terms infection-related glomerulonephritis or bacterial infection-related glomerulonephritis are also used.[3]

Acute glomerulonephritis resulted in 19,000 deaths in 2013 down from 24,000 deaths in 1990.[4]

Signs and symptoms


  • May be microscopic and not identified by the patient.
  • May be macroscopic and lead to dark brown or smoky urine.
  • Frank hematuria may occur in severe cases.


  • Urine output is less than 400 ml/day (normally 600 to 2500 ml/day). In children it is less than 0.5 mL/kg/h.
  • May not be observed by the patient.


  • Acute onset.
  • Mild to modest severity.
  • Pitting edema.
  • Starts in the eyelids and face then the lower and upper limbs then generalized (e.g. hydrocele, ascites, pericardial, and pleural effusion.)
  • It may be migratory: appearing in eyelid in the morning, disappearing in the afternoon, and reappearing around the ankle in ambulatory patients by the end of the day.


  • It is usually mild to moderate.
  • Hypertensive encephalopathy, heart failure, and acute pulmonary edema may occur in severe cases.
  • Pulmonary congestion and congested neck veins may be present, but is usually due to salt and water retention (and, less commonly, heart failure).


  • Fever, headache, malaise, anorexia, nausea, and vomiting.
  • Pallor due to edema and/or anemia.

Acute renal necrosis due to injury of capillary or capillary thrombosis. Acute tubular obstruction by cast.


Acute proliferative glomerulonephritis can be a complication of streptococcal pharyngitis (strep throat) and impetigo.


The exact pathology remains unclear, but it is believed to be type III hypersensitivity reaction. Immune complexes (antigen-antibody complexes formed during an infection) become lodged in the mesangium and glomerular basement membrane below the podocyte foot processes. This creates a lumpy bumpy appearance on light microscopy and subepithelial humps on electron microscopy. Complement activation leads to destruction of the basement membrane. It has also been proposed that specific antigens from certain nephrotoxic streptococcal infections have a high affinity for basement membrane proteins, giving rise to particularly severe, long lasting antibody response.


Diagnosis rarely requires a renal biopsy since there is usually a classical clinical presentation. There will be an elevated Anti-streptolysin O titre and low complement levels (C3) in the blood.

Mechanism of edema

Diffuse proliferative nephritis (DPN) is a nephritic syndrome; therefore, it causes edema through an increase in hydrostatic pressure and fluid overload secondary to inflammatory damage. Examples of nephritic syndrome include: DPGN, IgA nephropathy, lupus nephritis, and MPGN.

Hypoalbuminemia is the cause of edema in nephrotic syndrome (characterized by heavy proteinuria—greater than 3.5 g/day). Examples include: minimal change disease (MCD), membranous glomerulonephritis (MGN), focal segmental glomerulosclerosis (FSGS), lupus, amyloidosis, and diabetes.

Differential diagnosis

  1. Other causes of acute glomerulonephritis:
  2. Nephrotic syndrome
  3. Other causes of generalized edema:
    • Malnutrition
    • Malabsorption
    • Renal affection
    • Liver cell failure
    • Right side heart failure
    • Angioedema
  4. Other causes of hematuria


Possible complications of acute proliferative glomerulonephritis include kidney failure and hypertensive encephalopathy.


Acute glomerulonephritis resulted in 19,000 deaths in 2013 down from 24,000 deaths in 1990.[4]


  1. ^ Baltimore RS (February 2010). "Re-evaluation of antibiotic treatment of streptococcal pharyngitis". Curr. Opin. Pediatr. 22 (1): 77–82. PMID 19996970. doi:10.1097/MOP.0b013e32833502e7. 
  2. ^ White AV, Hoy WE, McCredie DA (May 2001). "Childhood post-streptococcal glomerulonephritis as a risk factor for chronic renal disease in later life". Med. J. Aust. 174 (10): 492–6. PMID 11419767. 
  3. ^ Nasr SH1, Radhakrishnan J, D'Agati VD (May 2013). "Bacterial infection-related glomerulonephritis in adults". Kidney Int 83 (5): 792–803. PMID 23302723. doi:10.1038/ki.2012.407. 
  4. ^ a b GBD 2013 Mortality and Causes of Death, Collaborators (17 December 2014). "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013.". Lancet. PMID 25530442. doi:10.1016/S0140-6736(14)61682-2. 
  5. ^ Sung HY, Lim CH, Shin MJ et al. (December 2007). "A case of post-streptococcal glomerulonephritis with diffuse alveolar hemorrhage". J. Korean Med. Sci. 22 (6): 1074–8. PMC 2694628. PMID 18162726. doi:10.3346/jkms.2007.22.6.1074. 

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