Acute proliferative glomerulonephritis

Acute proliferative glomerulonephritis
Micrograph of a post-infectious glomerulonephritis. Kidney biopsy. PAS stain.
Classification and external resources
Specialty
ICD-10	N00.8
ICD-9-CM	580.0
DiseasesDB	29306
MedlinePlus	000503
eMedicine	med/889
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. 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. Acute glomerulonephritis resulted in 19,000 deaths in 2013 down from 24,000 deaths in 1990.

Signs and symptoms

Among the signs and symptoms of acute proliferative glomerulonephritis are:

• Hematuria:
• Oliguria
• Edema
• Hypertension
• Fever, headache, malaise, anorexia, nausea.

Causes

Acute proliferative glomerulonephritis (post-streptococcal glomerulonephritisis) is caused by an infection with streptococcus bacteria. The infection causes blood vessels in the kidneys to develop inflammation, this hampers the renal organs ability to filter urine.This disorder can occur 3 weeks after a skin infection, the disorder occurs most often in children .

Pathophysiology

The pathophysiology of this disorder is consistent with an immune complex mediated mechanism, a type III hypersensitivity reaction. This disorder produces proteins that have different antigenic determinants, which in turn have an affinity for sites in the glomerulus. As soon as binding occurs to the glomerulus, via interaction with properdin, complement is activated. Complement fixation causes the generation of additional inflammatory mediators

Complement activation is very important in acute proliferative glomerulonephritis. Apparently immunoglobulin (Ig)-binding proteins bind C4BP. Complement regulatory proteins (FH and FHL-1),may be removed by SpeB, and therefore restrain FH and FHL-1 recruitment in the process of infection.

Diagnosis

Acute Glomerulonephritis.

In terms of the diagnosis of acute proliferative glomerulonephritis (poststreptococcal glomerulonephritis) can be prevented by early antibiotic treatment, this decision is immediate with skin infections due to the fact that the differential diagnosis is between staphylococcal and streptococcal impetigo.

Via serological markers a diagnosis can be done. The streptozyme test measures different streptococcal antibodies: Antistreptolysin,Antihyaluronidase,Antistreptokinase, Antinicotinamide-adenine dinucleotidase,and Anti-DNAse B antibodies

Differential diagnosis

2

Treatment

Treatment of acute proliferative glomerulonephritis consists of blood pressure (BP) control:also a renal biopsy may be needed to be performed at some point. A low-sodium, diet may be needed when hypertension is present.In individuals with oliguric acute kidney injury, the amount of potassium should be controlled.

Epidemiology

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

External links

• Post-infectious glomerulonephritis - Mayo Clinic
• Group A Streptococcal Infections - National Institute of Allergy and Infectious Diseases