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Ardiles LG, Valderrama G, Moya P, Mezzano SA: Incidence and studies on antigenic specificities of antineutrophil-cytoplasmic autoantibodies (ANCA) in poststreptococcal glomerulonephritis. Clin Nephrol 1997 Jan;47(1):1-5 Division of Nephrology, Faculty of Medicine, Universidad Austral de Chile, Valdivia, Chile. Sera from 210 patients with Acute Poststreptococcal Glomerulonephritis (APSGN) and 14 patients with streptococcal impetigo without glomerular disease were tested for the presence of IgG-ANCA using an indirect immunofluorescence assay (IIF) on ethanol fixed normal human neutrophils. In the group of nephritic patients, ANCA were detected by IIF in 9% (18 out of 210 cases) in an atypical diffuse cytoplasmic pattern (a-ANCA) in 14 cases and in a (p-ANCA) perinuclear staining in the remaining 4 cases. Longitudinal studies performed on six IIF positive patients, showed persistence of the phenomenon for up to six months, without relationship with activity of disease. No patient with streptococcal impetigo showed positivity on the IIF assay. Positive sera were analyzed on ELISA plates for their IgG reactivity against specific purified ANCA antigens: Proteinase-3 (PR3), Myeloperoxidase (MPO). Cathepsin-G and Bactericidal/Permeability Increasing Protein (BPI). Anti-MPO antibodies were present in 4 cases (3 a-ANCA and 1 p-ANCA). No reactivity was identified against PR-3, BPI and Catepsin-G in any of the samples. The presence of ANCA was significantly associated with a more severe glomerular disease as assessed by the serum creatinine and the crescents formation. Further studies are required to identify other antigenic specificities of these autoantibodies. Their absence in the streptococcal impetigo control group might suggest that their presence in APSGN could play some pathogenic role in kidney disease. Sorger K: Postinfectious glomerulonephritis. Subtypes, clinico-pathological correlations, and follow-up studies. Veroff Pathol 1986;125:1-105 APGN (WHO: diffuse endocapillary proliferative glomerulonephritis) has long been considered one of the best described kidney afflictions, clinically characterized by the sudden development of a nephritic syndrome after a latency period following a nasopharyngeal infection or pyoderma. Proliferation of mesangial and endothelial cells in the endocapillary space, aggregation of polymorphonuclear granulocytes in the capillary lumina, and deposition of predominantly subepithelial immune complexes on the glomerular basement membrane (so-called "humps") are to the present day considered characteristic of renal morphology. However, the nature of the antigen (or antigens) as well as the determining mechanisms in the pathogenesis of APGN still are unclear. Considerable disagreement also exists regarding the prognosis. An analysis of APGN is once again presented to elucidate whether the morphological picture of APGN is really as uniform as has been generally assumed. A large number of kidney biopsies was examined and subjected to the triad of light microscopy (LM), immunofluorescence microscopy (IFM) and electron microscopy (EM). The findings, which were recorded at an early stage of APGN in all cases (i.e. during the first 9 weeks), were related to clinical data, age (childhood or adulthood), and etiology (e.g. streptococci, staphylococci). In addition, clinical and morphological follow-up over a period of up to 10 years in those cases, which had been carefully documented in the early stages, afforded an insight into the dynamics and the prognosis of APGN. Light microscopy of APGN showed a certain spectrum of variation even during the rather limited period of 9 weeks, due to the varying number of granulocytes and a varying degree of cell proliferation, as we could show semiquantitatively. With the triad of methods, especially by IFM and EM, three separate morphological patterns were distinguishable: the starry sky pattern, the garland pattern and the mesangial pattern. Based on clinico-pathological correlations, these patterns were shown to permit the nosological subdivision of APGN. The following features merit special emphasis: The starry sky pattern occurred most often during the first few weeks, the mesangial pattern increased in frequency after the 3rd week, and the garland pattern could occur at any time. In the starry sky and garland patterns immunoglobulins (mainly IgG) generally appeared in combination with C 3. The mesangial pattern was characterized by C 3 appearing alone. These three immunohistological patterns, which also showed transitional and combined forms, had certain characteristic features by electron microscopy.
Edelstein CL, Bates WD: Subtypes of acute postinfectious glomerulonephritis: a clinico-pathological correlation. Clin Nephrol 1992 Dec;38(6):311-7 Department of Internal Medicine, University of Stellenbosch, Tygerberg, Cape Province, South Africa. The case records and histopathology of 42 adults with the characteristic light and electron microscopic features of Acute Postinfectious Glomerulonephritis (APGN) were studied. The biopsies were divided into three subtypes depending on the form and distribution of subepithelial "humps" and other immune-complex deposits on electron microscopy (EM): the "starry sky", "garland" and "mesangial" patterns. There was no significant difference between the three subtypes with regard to age, hypertension, creatinine, anti-streptolysin 0 titer and low serum complement levels on presentation. The "garland" subtype had significantly more proteinuria than both the "starry sky" (p = 0.04) and "mesangial" (p = 0.003) subtypes. The "mesangial" pattern had a lesser degree of cellular proliferation and leukocytosis in the glomeruli than the other subtypes. The "starry sky" subtype was present in 4 of the 5 cases of crescentic nephritis and in 6 of the 7 patients with a chronic course. Our study suggests that the higher degree of proteinuria in the "garland" subtype and the chronic course of the "starry sky" subtype are the main clinical features that distinguish the three histological subtypes. Our patients, from a developing community with poor socio-economic conditions, had a poor prognosis.
Montseny JJ, Meyrier A, Kleinknecht D, Callard P: The current spectrum of infectious glomerulonephritis. Experience with 76 patients and review of the literature. Medicine (Baltimore) 1995 Mar;74(2):63-73 Service de Nephrologie, Hopital Avicenne, Faculte de Medecine de Bobigny (Universite Paris-XIII), France. To identify the demographic, clinical, and pathologic features and the prognosis of renal disease in a series of patients with infectious or postinfectious proliferative glomerulonephritis (GN), data were collected from records of 76 adult patients admitted from 1976 to 1993 to 2 neighboring suburban hospital nephrology units, whose catchment population consists of patients living in a suburban borough of Paris with a below-average socioeconomic status. Thirty-four patients (45%) were alcoholics, diabetics, or intravenous illicit-drug users. Sixty-six patients presented with acute nephritic and/or nephrotic syndrome. Acute renal failure was present in 56 (76%) and required dialysis in 14. The diagnostic workup comprised at least 1 renal biopsy in each case. The patient's background, site of infection, clinical course, laboratory variables, and, when available, bacteriologic findings were analyzed in each case to interpret the evolution of the disease. Initial renal biopsy disclosed endocapillary GN in 44 patients, crescentic GN in 26, and membranoproliferative GN in 6. Ten patients had endocarditis. Staphylococci and Gram-negative strains, not streptococci, were the most common bacteria identified. The origin of sepsis was mainly the oropharynx (21), the skin (19) and the lung (14); 19 cases involved multiple sites of infection. Eight patients died (11%), and 20 (26%) recovered renal function, but GN followed a chronic course in 38 (50%), rapidly requiring maintenance dialysis in 6. Poor prognostic factors included age over 50 years, purpura, endocarditis, and glomerular extracapillary proliferation. Twenty-six patients underwent repeat renal biopsy 1 month to 11 years after the initial presentation. The main finding, irrespective of the interval since the first biopsy, was that ongoing or new iatrogenic infection acquired during hospitalization was almost invariably acquired during hospitalization was almost invariably associated with developing glomerular proliferative changes. This study shows that infectious proliferative GN remains common, but that its epidemiology has changed from what was observed until 2 decades ago. The responsible bacteria, when identified, now comprise a majority of staphylococci and Gram-negative strains, in contrast to the streptococci which predominated 3 decades ago. Infectious GN affects with increasing frequency patients with an underlying condition responsible for immunosuppression, especially alcoholism, even in the absence of cirrhosis. Destructive glomerular proliferation persists, especially but not exclusively until infection has been eradicated, and despite rescue treatment with corticosteroids and/or cytostatic drugs. Thus, the prognosis is poor, and infectious GN often ends in renal death. Infection continues in this decade to represent a frequent and probably often overlooked cause of end-stage renal failure.
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