Acute proliferative glomerulonephritis
|Acute proliferative glomerulonephritis|
|Classification and external resources|
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 (impetigo) but also after streptococcal pharyngitis, for which it is also known as postinfectious or poststreptococcal glomerulonephritis. It can be a risk factor for future albuminuria. 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.
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.
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.
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.
- Other causes of acute glomerulonephritis:
- Nephrotic syndrome
- Other causes of generalized edema:
- Renal affection
- Liver cell failure
- Right side heart failure
- Other causes of hematuria
Acute glomerulonephritis resulted in about 84,000 deaths in 2010 down from 135,000 in 1990.
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- Post-infectious glomerulonephritis - Mayo Clinic
- Group A Streptococcal Infections - National Institute of Allergy and Infectious Diseases