Acute Proliferative Glomerulonephritis

( “Pign”; Post-Strptokokken glomerulonephritis; non-streptococcal “Pign”

The post-infectious glomerulonephritis after infection occurs mostly with a strain of nephritogenic betahämolysierenden streptococci (group A). The diagnosis is suspected by history and urine findings and confirmed by a low complement levels and sometimes antibody test. The prognosis is excellent. Treatment is supportive.

The post-infectious glomerulonephritis after infection occurs mostly with a strain of nephritogenic betahämolysierenden streptococci (group A). The diagnosis is suspected by history and urine findings and confirmed by a low complement levels and sometimes antibody test. The prognosis is excellent. Treatment is supportive. Etiology The post-infectious glomerulonephritis (Pign), a nephritic syndrome, the most common cause of glomerular disorder in children aged 5 to 15 years. In children <2 years and adults> 40 years it rarely. Most cases are caused by strains nephritogene betahämolysierender group A streptococci, mostly type 12 (which causes pharyngitis) and type 49 (of impetigo caused). An estimated 5-10% of patients with streptococcal pharyngitis and about 25% with impetigo develop Pign. A latency period of 6-21 days between infection and onset of GN is typical, but it can also extend up to 6 weeks. Less common pathogens are non-streptococcal bacteria, viruses, parasites, rickettsia and fungi (see Table: Causes of glomerulonephritis). Furthermore, a Pign may also develop on the floor of a bacterial endocarditis, and an infection of a ventrikuloatialen shunts; less susceptible to infection are ventriculoperitoneal shunts. The mechanism of the disease is unknown, but it is believed that microbial antigens to the glomerular basement membrane binding, primarily activate the alternate complement pathway (direct and through interaction with circulating antibodies) and thereby cause glomerular damage which circumscribed or may be diffuse. Alternatively, circulating immune complexes can precipitate the glomerular basement membrane. Symptoms and signs The symptoms and complaints can range from asymptomatic hematuria (in about 50% of cases) and weak proteinuria to a fully formed nephritis with micro- or gross hematuria (cola color, brown, smoky or pure bloody urine), proteinuria (sometimes in nephrotic range), oliguria rich, edema, hypertension and renal insufficiency. Fever is rare and suggests a persistent infection. Kidney failure that causes fluid overload with heart failure and severe hypertension and requires dialysis, affects 1-2% of patients and can be represented as pulmorenales syndrome with hematuria and hemoptysis. Rarely can a nephrotic syndrome consist in the aftermath of serious illness. Clinical manifestations of non-streptococcal Pign can pretend other disorders (polyarteritis nodosa, kidney embolism, antibiotic-induced acute interstitial nephritis). Diagnosis Clinical evidence of recent infection urinalysis typically showing dysmorphic red blood cells, red blood cell casts, proteinuria, white blood cells and renal tubular cells often hypocomplementemia A streptococcal Pign is because of past pharyngitis or impetigo excl. Either typical symptoms of Pign or incidental findings on urinalysis suspected. Evidence of a hypocomplementemia is an important confirmation. Tests that are performed to confirm the diagnosis depends on clinical findings. Antistreptolysin O, Antihyaluronidase- and Antideoxyribonuclease- (anti-DNAase) antibodies are often measured. Serum creatinine and complement levels (C3 and overall hemolytic complement activity) also be measured as a rule, however, can be omitted in patients with typical clinical findings on some tests. Sometimes other tests also are performed. The biopsy confirmed the diagnosis but is rarely required. Antistreptolysin-O-mirror, the most common detection of a previous streptococcal infection, the patient increases in 75% of patients with pharyngitis and 50% with impetigo and remains elevated for several months, but is not specific. The Streptozym test which also measures Antihyaluronidase, Antideoxyribonuclease and other titers detected 95% of recent streptococcal pharyngitis and 80% of skin infections. Urinalysis typically shows proteinuria (0.5-2 g / m2 / day), dysmorphic red cells, renal tubular cells, and possibly erythrocyte, leukocyte and Granulozytenzylinder. The random ( “spot”) protein / creatinine ratio in urine is usually between 0.2 and 2 (normal, <0.2), but can occasionally be in the nephrotic range (? 3). Serum creatinine can rise quickly, but increases usually only to values ??below the dialysis need. The C3 and the gesamthämolytischen Komplementaktivitätsspiegel (CH 50) fall during the active phase, and return of 80% of Pign cases within 6-8 weeks to normal values ??back. The C1q, C2 and C4 levels are only minimally reduced or remain normal. Cryoglobulinemia may also occur and persist for several months while circulating immune complexes are detectable only for a few weeks. The biopsy samples are magnified and hyper cellular glomeruli, beginning with neutrophil infiltration and later with mononuclear infiltration. An epithelial cell hyperplasia is usually an early temporary signs. There may be a micro-thrombosis. If the damage is severe, cause hemodynamic changes due to cellular proliferation and edema of the glomerulus to oliguria, often in conjunction with crescent formation (by proliferation of Bowman's Kapselepithels). Endothelial and mesangial cells proliferate; mesangial areas are often significantly expanded by edema and include neutrophils, dead cells, cell debris and subepithelial deposits of electron dense material. Immunofluorescence microscopy shows mostly immune complex deposits of IgG and complement in granular form. In electron microscopy, this localized in the subepithelial region deposits are crescent or hump-shaped. The presence of these deposits and small subendothelial and mesangial deposits initiated complement-inflammatory response that causes the glomerular damage. The main antigen is likely zymogen cysteine ??proteinase exotoxin B (zymogen / SPE B). Acute proliferative glomerulonephritis (hypercellularity with neutrophil infiltration) Figure provided by Agnes Fogo, M.D., and the American Journal of Kidney Disease, Atlas of Renal Pathology (see var model = {thumbnailUrl: '/-/media/manual/professional/images/postinfectious_glomerulonephritis_hypercellularity_neutrophilic_infiltration_high_de.jpg?la=de&thn=0&mw=350' imageUrl: '/-/media/manual/professional/images/postinfectious_glomerulonephritis_hypercellularity_neutrophilic_infiltration_high_de.jpg?la = en & thn = 0 ', title:' acute proliferative glomerulonephritis (hypercellularity with neutrophil infiltration) 'description:' u003Ca id = "v38396890 " class = ""anchor "" u003e u003c / a u003e u003cdiv class = ""para "" u003e u003cp u003eEndotheliale and mesangial hypercellularity with neutrophil infiltration (silver staining according to Jones

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