Circulating immune complexes and complement levels in relation to the clinical presentation of Nigerian children with acute poststreptococcal glomerulonephritis.

Abstract

SUMMARY Circulating immune complexes have been detected in the sera of 24 Nigerian children with acute poststreptococcal glomerulonephritis using two methods. There was a significant correlation between levels of soluble complexes, detected in samples taken from patients in the oliguric phase of acute nephritis, and severity of disease, as judged by blood urea levels. Serial estimation of immune complexes was more useful than serial C3 estimation in predicting the onset of anuria in two patients admitted with mild disease who subsequently deteriorated. With one exception. C4 values were normal. Factor B levels were low in 90 % of cases, in keeping with activation of the alternate complement pathway.

What is the Role of Mannose-Binding Lectin Gene Polymorphism in the Development of Acute Post-Streptococcal Glomerulonephritis?

“…In this defect, MBL levels are less than 100 ng/ml. MBL deficiency is not a classic primary immunodeficiency, it has various regulatory mutations, and its clinical penetrance is significantly low (2,14) .…”

“…APSGN is known as immune-mediated disease that occurs following skin and pharyngeal infections which are related to nephritogenic strains of group a streptococci; however, the pathologic process has not been clarified yet (1) . The role of lectin cascade, which is triggered by MBL (the third pathway of complement system) in the development of APSGN has received considerable attention (2)(3)(4)(5) . MBL recognizes high levels of mannose and N-acetylglucosamine (G1cNAc) derivatives, which are located on the surface of micro-organisms.…”

“…None of the studies have addressed the role of the lectin pathway (LP) (1) . Renal biopsies performed in typical cases involving APSGN within the 4 th week following the onset of symptoms have demonstrated MBL, C4d, and MAPS-1-positivities inside the mesangium (2) . It has been proposed that the LP, which is the third pathway of the complement system, can activate APSGN which takes place by the recognition of glucosamine residues on the bacterial wall by MBL; however, patients with defects in MBL may also develop glomerulonephritis (3) .…”

“…Streptococcal contents and products are known to trigger this process, while the process has not been precisely defined. Although the mechanism of renal damage is not known, theories, such as glomerular localization of circulatory immune complexes, the molecular similarity between streptococcal and renal antigens, immune complex formation between in situ anti-streptococcal antibodies and glomerular antigens, and complement activation directly induced by deposit streptococcal antigens inside the glomerulus have been proposed (1)(2)(3)(4) .…”

Circulating and deposited immune complexes in renal disease and their clinical correlation.

“…A number of workers have described varying levels of CIC in several histological types of glomerulonephritis (Johnson et al, 1975;Rossen et al, 1976;Stuhlinger et al, 1976;Ooi et al, 1977;Woodroffe et al, 1977;Cohen et al, 1978;Levinsky et al, 1978;Onyewotu and Mee, 1978;Pussell et al, 1978). The purpose of this study was (a) to investigate whether CIC could be detected at the time of renal biopsy and correlated with histological findings, and (b) to see if serial measurements of levels of CIC indicated any correlation with the clinical course.…”