Capacity of Group a (Type M12) Streptococci to Bind Immune Complexes and Their Role in Pathogenesis of Post-Streptococcal Glomerulonephritis

Bürova, Larissa A.; Gavrilova, E. A.; Pigarevskii, P. V.; Seliverstova, Valentina; Нагорнев, В. А.; Shalen, K; Artem, A Totolian

doi:10.15789/1563-0625-2006-5-6-623-630

Cited by 4 publications

(1 citation statement)

References 8 publications

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“…В многочисленных исследованиях доказано, что у молодых ОПСГН развивается спустя 7-21 день после тонзиллита, фарингита, или стрептодермии [2,8,14]. Основное клиническое проявление ОПСГН -это остронефритический синдром (ОНС) (отеки, гипертония, гематурия), который может осложниться острым почечным повреждением (ОПП) [4,9,12]. Первичное действие этиологических факторов, как правило сопровождается повышением температуры тела, по поводу чего больные принимают нестероидные противовоспалительные препараты, в основном парацетамол и диклофенак, которые имеют гепато-и нефротоксические эффекты [6,10,16].…”

Section: актуальность проблемыunclassified

Hepatorenal and renocardial syndrome in young patients with acute glomerulonephritis

Sargsyan,

Melikyan,

Melikyan

2023

jour

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In this paper we discuss classical types of acute glomerulonephritis in young adults, when the intake of paracetamol and diclofenac led to a dysfunctional and organic liver injury, at the same time it negatively affected the course of acute glomerulonephritis. To study the characteristics of the development of acute reno-cardial syndrome (ARCS) Goal: Assessment of cause and effect relations of renal, hearts and liver injuries in young adults in acute post-streptococcal glomerulonephritis (APSG). With acute nephritic syndrome (ANS) complicated by acute kidney injury (AKI) and without it, to identify the role of the etiological factor on the course of APSG. Methods and Material: 220 male patients with APSG with ANS aged 18-20 were examined. The patients were divided into 2 groups based on the functional state of kidneys. The first group included 140 patients with APSG without ANS, the second group included 80 patients with AKI. Results: Out 66 patients had subclinical liver injury, which resulted from the effect of antipyretic hepatotoxic drugs taken in the initial stage of the disease. Due to the toxic and immunological liver injury, levels of transaminases increase, and albumin levels decrease. These changes occur along with the development of APSG and are correlated with some laboratory values. Impairment of cardiovascular function was observed in all 220 patients. ECG and Echocardiography studies conducted during the cardiac asthma attacks occurred as a decrease of voltage, broadening of the P wave, lengthening of the PQ interval, broadening of the QRS complex, dilatations of the right and left atrium. The severity of clinical manifestations of AKI and ARCS correlates with the degree of macrohematuria, GFR decrease, complement C3 fraction, monocyte. Conclusion. In APSG liver injury has a toxicoallergic character. Frequency of liver injury depends on specific features of a particular organism, it does not depend on the dose of the taken drug. In case of any type of acute glomerulonephritis it is necessary to assess the functional state of liver and after the treatment of the main disease hepatologist follow-up of patients is recommended. Thus in the development of acute reno-cardial syndrome (ARCS) the degree of manifestation of hypervolemia with hypertension, as a result of active immune inflammation of the glomerular apparatus with the development of AKI, plays the main role in the development of ARCS with APSG.. As a rule ARCS in case of APSG with ANS in young adults has a successful outcome.

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Section: актуальность проблемыunclassified

Hepatorenal and renocardial syndrome in young patients with acute glomerulonephritis

Sargsyan,

Melikyan,

Melikyan

2023

jour

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A role of streptokinase in experimental post-streptococcal glomerulonephritis

Bürova

Gavrilov²,

Pigarevsky

et al. 2021

Russian Journal of Infection and Immunity

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Post-streptococcal glomerulonephritis (PSGN) refers to the sequela of the acute infection, caused by Streptococcus pyogenes (group A streptococcus, GAS). This pathology has been studied for a long time, and today attempts are being made to identify the products of their life activity, able to initiate an immunopathological process in kidneys. Most attention has been paid to streptokinase, the enzyme transforming blood plasminogen into plasmin, capable, together with the plasmin receptor (NAPlr), of damaging the glomerular tissue, as well as activating the complement system. The aim of the study was to consider two tasks: to study the ability of the GAS-obtained enzyme to transform plasminogen of different species into plasmin as well as to study its role in the development of PSGN in rabbits having subcutaneously implanted tissue chambers. The animals were infected by inoculating GAS cultures into the chambers. Materials and methods. GAS strains of M types 1, 12, 22 and their ska– isogenic mutants were used in the study. Purified plasminogen preparations were isolated from fresh human, rabbit or mouse plasma by using chromatographic column with Lysine Sepharose 4B. To reveal the ability of streptokinase to activate plasminogen into plasmin, its preparation at a concentration of 1 mg/ml was added to 10 ìg of purified human, rabbit or mouse plasminogen. The concentration of plasmin was defined photometrically using S-2251 (Chromogenix, USA). To reproduce PSGN, four chambers were implanted under the skin in each rabbit; after the complete wound healing animals were infected and observed for three weeks. On day 14, the animals were treated with benzylpenicillin. The kidneys from survived rabbits were subjected to immunohistology analysis. Results. During in vitro experiments, M1, M12 and M22 GAS streptokinase showed distinct functional activity on human plasminogen, transforming it into plasmin: optical density indicators at ë = 405 nm were 0.4–0.7 compared with the negative control (ОD < 0.001). Streptokinase did not activate mouse plasminogen (ОD = 0.001) and exerted quite a weak effect on transformation of the rabbit plasminogen into plasmin (ОD = 0.002). In experiments on PSGN induction in rabbits, we failed to detect streptokinase involvement, because no differences between initiation of glomerulonephritis by wild strains or ska– isogenic mutants were identified. Mutant strains deficient in the gene responsible for streptokinase synthesis but retained ability to bind rabbit and human IgG, caused morphological changes in kidney tissue, specific for PSGN. In addition, a comparative analysis of PSGN “rabbit” and “mouse” models developed by the same technology, was carried out and led to opposing conclusions regarding a role of streptokinase in pathogenesis of experimental glomerulonephritis. The role of IgG Fc-binding activity of GAS in development of experimental PSGN is discussed.

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Autoimmune streptococcal glomerulonephritis: the problem of nephritogenicity of <i>Streptococcus pyogenes</i>

Burova,

Suvorov,

Pigarevsky

et al. 2023

Russian Journal of Infection and Immunity

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Acute post-streptococcal glomerulonephritis usually occurs as a complication after a streptococcal infection due to untimely or inadequate antibiotic therapy. The etiology of post-streptococcal glomerulonephritis has been studied rather comprehensively. Today, both clinicians and microbiologists do not deny the dominant role of Streptococcus pyogenes (streptococcus attributed to serological group A, GAS). Usually, emergence of acute post-streptococcal glomerulonephritis (APSGN) is associated with the so-called GAS-related "nephritogenicity" often judged by appearance and accumulation of antibodies to the antigens and extracellular products of streptococcal cells in patient blood. This interpretation is quite loose and most likely evidence about a link to the bacterial strain, rather than its nephritogenicity. Many studies refer and still attribute a leading role of "nephritogenic" factors to various streptococcal antigens and related biologically active products. Streptococcal nephritogenic factors include cross-reacting antigens, streptokinase, cysteine proteinase, endostreptosin a GAS cell membrane protein as well as plasmin-tropic enzyme glyceraldehyde-3-phosphate dehydrogenase. Nephritogenicity of all such streptococcal products is suspected to result from the fact that they are found in renal biopsies like specific patient blood serum antibodies. Regarding a term of nephritogenicity, it has been evidenced that it cannot be attributed to any specific streptococcal cell product. This review attempted to analyze a number of bacterial products as starting factors triggering this process. APSGN can be reproduced experimentally in rabbits by intravenous administration of a heat-killed Streptococcus pyogenes culture. In our experiments, strains of serotypes 1, 4, 12, 15, 22 were used. They produced M-proteins and had the ability to bind human and rabbit immunoglobulin G by interacting with the Fc part of the IgG molecule. In numerous series of experiments, evidence was obtained regarding the initiating role of GAS IgGFc-receptor proteins in developing APSGN. Recent studies confirmed the role of streptococcal IgGFc-binding proteins in the initiation of glomerulonephritis after animals were inoculated with temperature-killed IgGFc-positive GAS. This approach excluded a large group of bacterial extracellular agents from the list of APSGN-initiating candidates. An unconventional view on the pathogenesis of GAS-infection-coupled complications may allow approaching their prevention or new treatment strategies.

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Capacity of Group a (Type M12) Streptococci to Bind Immune Complexes and Their Role in Pathogenesis of Post-Streptococcal Glomerulonephritis

Cited by 4 publications

References 8 publications

Hepatorenal and renocardial syndrome in young patients with acute glomerulonephritis

Hepatorenal and renocardial syndrome in young patients with acute glomerulonephritis

A role of streptokinase in experimental post-streptococcal glomerulonephritis

Autoimmune streptococcal glomerulonephritis: the problem of nephritogenicity of <i>Streptococcus pyogenes</i>

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