Acute proliferative glomerulonephritis

Acute proliferative glomerulonephritis
Classification and external resources

Micrograph of a post-infectious glomerulonephritis. Kidney biopsy. PAS stain.
ICD-9 580.0
DiseasesDB 29306
MedlinePlus 000503
eMedicine med/889

Acute proliferative glomerulonephritis is a disorder of the glomeruli (glomerulonephritis), or small blood vessels in the kidneys. It is a common complication of infections, typically streptococcal skin infection (impetigo) rather than streptococcal pharyngitis, for which it is also known as postinfectious or poststreptococcal glomerulonephritis.[1]

It can be a risk factor for future albuminuria.[2]

Contents

Causes

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

Pathophysiology

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 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

Diagnosis rarely requires a renal biopsy since there is usually a classical clinical presentation. There will be elevated levels of ASOT Ab and low complement levels (C3 and C4) in the blood.

Presentation

1) Hematuria:[3]

2) Oliguria

3) Edema

4) Hypertension.

5) General

6) Acute renal necrosis due to injury of capillary or capillary thrombosis.

Mechanism of edema

Diffuse Proliferative Glomerulonephritis (DPGN) 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 3.5g/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

Complications

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

References

  1. ^ Baltimore RS (February 2010). "Re-evaluation of antibiotic treatment of streptococcal pharyngitis". Curr. Opin. Pediatr. 22 (1): 77–82. doi:10.1097/MOP.0b013e32833502e7. PMID 19996970. 
  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. http://www.mja.com.au/public/issues/174_10_210501/white/white.html. 
  3. ^ 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. doi:10.3346/jkms.2007.22.6.1074. PMID 18162726. http://jkms.org/contents/jkms.php?pubyear=2007&vol=22&fpage=1074. 

External links