Relevant bibliographies by topics / IgAN

Academic literature on the topic 'IgAN'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "IgAN"

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Zhang, Xue, Xinfang Xie, Sufang Shi, Lijun Liu, Jicheng Lv, and Hong Zhang. "Plasma galactose-deficient immunoglobulin A1 and loss of kidney function in patients with immunoglobulin A vasculitis nephritis." Nephrology Dialysis Transplantation 35, no. 12 (August 3, 2019): 2117–23. http://dx.doi.org/10.1093/ndt/gfz151.

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Abstract Background Immunoglobulin A (IgA) vasculitis nephritis (IgAV-N) is the most common secondary IgA nephropathy (IgAN). Many studies have demonstrated that galactose-deficient IgA1 (Gd-IgA1) in the IgA1 hinge region is associated with the development and also progression of primary IgAN. In this study, we aimed to evaluate the roles of Gd-IgA1 in kidney disease progression in a large Chinese cohort of IgAV-N patients. Methods This cohort study enrolled 112 patients with IgAV-N, 15 patients with IgA vasculitis (IgAV) without kidney involvement and 108 patients with IgAN. Plasma IgA1 and Gd-IgA1 levels at kidney biopsy were measured by enzyme-linked immunosorbent assay. The primary endpoint was a 30% decline in estimated glomerular filtration rate or end-stage renal disease or death. Results The levels of Gd-IgA1 in IgAV-N and IgAN patients were higher than in healthy controls (mean ± SD, 302.86 ± 54.93 U/mL versus 303.16 ± 59.43 U/mL versus 281.30 ± 43.74 U/mL, respectively; P = 0.047), as well as compared with those with IgAV without kidney involvement (272.65 ± 53.14 U/mL; P = 0.036). After adjusting clinical data, higher levels of Gd-IgA1 were found to be independently associated with a greater risk for kidney failure [hazard ratio (HR) = 1.703 per 1 SD, 95% confidence interval (CI) 1.233–2.352; P = 0.001]. Compared with the first Gd-IgA1 quartile group (as reference), the fourth Gd-IgA1 quartile group retained a predictive value for poor renal outcome (HR = 3.740, 95% CI 1.204–11.619; P = 0.023). Conclusions These data indicate that Gd-IgA1 levels were similarly elevated in adult patients with IgAN and those with IgAV-N. Moreover, increased Gd-IgA1 levels were associated with both the development and progression of IgAV-N, as observed in IgAN.
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Khairwa, Anju. "Indian scenario of IgA nephropathy: a systematic review and meta-analysis." African Health Sciences 21, no. 1 (April 16, 2021): 159–65. http://dx.doi.org/10.4314/ahs.v21i1.21.

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Background: IgA nephropathy (IgAN) is most common primary glomerulopathy. There are variations in prevalence of IgAN and its clinical features in different studies from India. Aim: To summarize overall scenario of IgAN in India. Methods: In this systematic review, studies related to IgAN and related renal disease were included. Data searched were PubMed, EMBASE, Google scholar, and Cochrane Database from inception to 31st January 2019. Results: Total 49 studies (N=2480) were included: 21studies (N=2309) of primary IgAN; 19 studies (N=21) of Secondary IgAN; four studies (N=133) of IgA vasculitis nephropathy (IgAVN); and five studies (N=17) of IgA dominant nephropathy (IgADN). Prevalence of IgAN was 16.5% in India. Age of affected persons was ranging from 27.2±16.7 to 48.6±21.3 years . Male female ratio was 1.8:1. Clinical features of Primary IgAN, IgAVN, IgADN & Secondary IgAN were microscopic hematuria (49.6%, 44.4%, 15.6% & 59.5%), macroscopic hematuria (5.1%, 0.4%,40.9%,& 35.7%), Subnephrotic proteinuria (42.1%, 29.4%, 23.2%, & 52.3%), nephrotic proteinuria (16.0%, 4.4%, 76.8%,& 47.6%), and hypertension (25.8%,18.3%, 35.5%,& 47.6%).. The 24 hours proteinuria was ranging from 2.6±1.5 to 4.7±2.3 gm/day and serum creatinine (mg/dl) was ranging from 0.9±0 to 3.5±3.9 mg/dl. Histolomorphologically, all type of IgAN showed mesangial hypercellularity and Immunofluorescence revealed IgA deposition. Conclusion: The overall prevalence of primary IgAN in India was 16.5%. The subnephrotic proteinuria and microscopic hematuria were common clinical features. Keywords: IgA Nephropathy; histomorphology; prevalence; India.
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Suzuki, Hitoshi, Landino Allegri, Yusuke Suzuki, Stacy Hall, Zina Moldoveanu, Robert J. Wyatt, Jan Novak, and Bruce A. Julian. "Galactose-Deficient IgA1 as a Candidate Urinary Polypeptide Marker of IgA Nephropathy?" Disease Markers 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/7806438.

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In patients with IgA nephropathy (IgAN), circulatory IgA1 and IgA1 in mesangial deposits contain elevated amounts of galactose-deficient IgA1 (Gd-IgA1). We hypothesized that a fraction of Gd-IgA1 from the glomerular deposits and/or circulation may be excreted into the urine and thus represent a disease-specific biomarker. Levels of urinary IgA and Gd-IgA1 were determined in 207 patients with IgAN, 205 patients with other renal diseases, and 57 healthy controls, recruited in USA, Japan, and Italy. Urinary IgA was similarly elevated in patients with IgAN and renal-disease controls compared with healthy controls. However, urinary Gd-IgA1 levels were higher in patients with IgAN (IgAN,28.0±17.9; disease controls,20.6±17.4units/mg urinary creatinine;P<0.0001). Lectin western blotting data confirmed these results. In IgAN patients, levels of urinary Gd-IgA1 correlated with proteinuria (P<0.001). When we purified IgA from serum and urine of an IgAN patient, the relative proportion of Gd-IgA1 to total IgA1 was higher in the urine compared with serum, suggesting selective excretion of Gd-IgA1 in IgAN. In summary, urinary excretion of Gd-IgA1 was elevated in patients with IgAN and the urinary Gd-IgA1 levels correlated with proteinuria. Urinary Gd-IgA1 may thus represent a disease-specific biomarker of IgAN.
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Irabu, Hitoshi, Masaki Shimizu, Shuya Kaneko, Natsumi Inoue, Mao Mizuta, Kazuhide Ohta, and Akihiro Yachie. "Clinical Significance of Serum Galactose-Deficient IgA1 Level in Children with IgA Nephropathy." Journal of Immunology Research 2020 (May 21, 2020): 1–10. http://dx.doi.org/10.1155/2020/4284379.

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This study was aimed at investigating the clinical significance of serum galactose-deficient IgA1 (Gd-IgA1) levels measured by a novel lectin-independent enzyme-linked immunosorbent assay (ELISA) using an anti-Gd-IgA1 monoclonal antibody (KM55) as a disease-specific biomarker for IgA nephropathy (IgAN) in children. Thirty-three children with IgAN, 40 with non-IgA glomerular diseases, and 38 age-matched healthy controls (HCs) were enrolled. Serum Gd-IgA1 levels were quantified by ELISA using KM55. Results were statistically compared with clinical features and pathological findings of IgAN. Serum Gd-IgA1 levels were significantly elevated in children with IgAN compared with children with non-IgA glomerular diseases and HCs. Serum Gd-IgA1 levels in children with IgAN were positively correlated with serum total IgA levels. However, the serum Gd-IgA1/total IgA ratio (Gd-IgA1/IgA) was also significantly elevated in children with IgAN. Serum Gd-IgA1 levels in children with IgAN increased in an age-dependent manner. The cutoff value of serum Gd-IgA1 levels for differentiating IgAN from non-IgA glomerular diseases was 3236 in children<12 years and 5284 in children≥12 years, respectively. In contrast, serum Gd-IgA1/IgA was age-independent. The cutoff value of serum Gd-IgA1/IgA for differentiating IgAN from non-IgA glomerular diseases was 0.2401. Serum Gd-IgA1 levels were negatively correlated with eGFR and positively correlated with mesangial IgA deposition. In contrast, serum Gd-IgA1/IgA levels were not correlated with any clinical parameters of IgAN. In conclusion, serum Gd-IgA1 levels were significantly elevated in children with IgAN. However, those levels were age-dependent; therefore, serum Gd-IgA1 levels classified by age and/or serum Gd-IgA1/IgA might have diagnostic values in children with IgAN.
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Li, Guanhong, Xiaoyan Wang, Zhe Yang, Qing Zhao, Yubing Wen, Xuemei Li, and Ruitong Gao. "Serum Levels of Joining Chain-Containing IgA1 Are Not Elevated in Patients with IgA Nephropathy." Disease Markers 2019 (July 2, 2019): 1–11. http://dx.doi.org/10.1155/2019/9802839.

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Background. It has been suggested that mesangial IgA deposits are dimeric or polymeric in IgA nephropathy (IgAN). However, evidence concerning the molecular form of serum IgA in IgAN is controversial. And there is no direct evidence that the serum levels of joining chain- (J chain-) containing IgA (J-IgA) are elevated in IgAN. In this study, we aimed to measure serum J-IgA and glomerular J chain deposition with anti-J chain monoclonal antibody in IgAN. Methods. BALB/c mice were immunized with human J chain-GST recombinant peptide to obtain anti-J chain monoclonal antibody. The levels of serum total IgA and J-IgA were measured by sandwich enzyme-linked immunosorbent assay in 115 patients with IgAN and 117 healthy volunteers. J chain deposition in kidney specimens was analyzed by immunohistochemistry staining. Results. Serum levels of total IgA1 were elevated in IgAN patients compared to healthy subjects. However, serum levels of IgA, J-IgA, and J chain-containing IgA1 (J-IgA1), the J-IgA to total IgA ratio, and the J-IgA1 to total IgA1 ratio were not significantly different between IgAN patients and healthy subjects. Western blot analysis and gel filtration analysis using purified IgA1 also showed that the proportion of J chain-containing polymeric IgA1 was lower in IgAN patients compared to healthy subjects. No correlation was found between serum J-IgA or J-IgA1 and clinical features in IgAN. Immunohistochemistry analysis showed that glomerular J chain was positive in 12 IgAN patients (57.1%). The values of the J-IgA to IgA ratio and J-IgA1 to IgA ratio were significantly higher in IgAN patients with glomerular J chain deposition than those without. However, the serum levels of J-IgA and J-IgA1 and the J-IgA1 to IgA1 ratio were not significantly higher in two subgroups. Conclusions. Although serum levels of total IgA1 were elevated in IgAN, the serum levels of J-IgA1 were not elevated. And serum J-IgA, serum J-IgA1, and J chain deposition were not correlated with disease severity in IgAN.
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Kim, Jin Sug, Hyeon Seok Hwang, Sang Ho Lee, Yang Gyun Kim, Ju-Young Moon, Ji Yoon Kong, and Kyung Hwan Jeong. "Clinical Relevance of Serum Galactose Deficient IgA1 in Patients with IgA Nephropathy." Journal of Clinical Medicine 9, no. 11 (November 4, 2020): 3549. http://dx.doi.org/10.3390/jcm9113549.

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New biomarkers of IgA nephropathy (IgAN) are needed for non-invasive diagnosis and appropriate treatment. There is emerging evidence that galactose deficient IgA1 (Gd-IgA1) is a pivotal molecule in the pathogenesis of IgAN. However, few studies have investigated the role of Gd-IgA1 as a biomarker in IgAN. In this study, we investigated the clinical relevance of serum Gd-IgA1 levels in patients with IgAN. Two hundred and thirty biopsy-proven IgAN patients, 74 disease controls (patients with non-IgAN nephropathy), and 15 healthy controls were enrolled in this study. Levels of serum Gd-IgA1 were measured using an ELISA kit in serum samples obtained the day of renal biopsy. We compared levels of serum Gd-IgA1 according to the type of glomerular disease and analyzed the association between Gd-IgA1 levels and clinical and pathological parameters in patients with IgAN. We then divided IgAN patients into two groups according to Gd-IgA1 level and investigated the predictive value of Gd-IgA1 for progression of chronic kidney disease (CKD). Serum Gd-IgA1 levels were significantly higher in IgAN patients than disease controls and healthy controls. In patients with IgAN, serum Gd-IA1 levels were significantly correlated with estimated glomerular filtration rate, serum IgA level, and tubular atrophy/interstitial fibrosis. CKD progression was more frequent in IgAN patients with higher serum Gd-IgA1 levels than in those with lower serum Gd-IgA1 levels. Cox proportional hazard models showed that high GdIgA1 level was an independent risk factor for CKD progression after adjusting for several confounders. Our results suggest that serum Gd-IgA1 level is a useful diagnostic and prognostic marker in IgAN patients. Further studies with a larger sample size and longer follow-up duration are needed.
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Sanders, John T., M. Colleen Hastings, Zina Moldoveanu, Jan Novak, Bruce A. Julian, Zoran Bursac, and Robert J. Wyatt. "Serial Galactose-Deficient IgA1 Levels in Children with IgA Nephropathy and Healthy Controls." International Journal of Nephrology 2017 (2017): 1–5. http://dx.doi.org/10.1155/2017/8210641.

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Galactose-deficient IgA1 (Gd-IgA1) is a key pathogenic factor for IgA nephropathy (IgAN) and a potential biomarker for the disease. This study examined serial serum Gd-IgA1 levels over 1 year in 13 children with IgAN and 40 healthy children, to determine whether or not serum Gd-IgA1 levels changed over time. Subjects were younger than 18 years of age. Follow-up measurements were scheduled 6 and/or 12 months later. Analysis of variance and regression models for repeated measures were used to estimate group and time effects. Serum Gd-IgA1 level was higher in initial samples for IgAN patients compared to those of healthy children (P<0.0001). Serum Gd-IgA1 levels did not change over time for healthy controls but increased for IgAN patients (P=0.001). Serum Gd-IgA1 level was elevated for 9 children with IgAN at study entry and remained elevated. Two of the 4 IgAN patients with initially normal Gd-IgA1 levels had a subsequent elevated level. The persistent elevation of the serum Gd-IgA1 level in children with IgAN enhances its utility as a potential diagnostic test for IgAN.
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Fukao, Yusuke, Hitoshi Suzuki, Jin Sug Kim, Kyung Hwan Jeong, Yuko Makita, Toshiki Kano, Yoshihito Nihei, et al. "Galactose-Deficient IgA1 as a Candidate Urinary Marker of IgA Nephropathy." Journal of Clinical Medicine 11, no. 11 (June 2, 2022): 3173. http://dx.doi.org/10.3390/jcm11113173.

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In patients with IgA nephropathy (IgAN), circulatory IgA1 and IgA1 in the mesangial deposits contain galactose-deficient IgA1 (Gd-IgA1). Some of the Gd-IgA1 from the glomerular deposits is excreted in the urine and thus urinary Gd-IgA1 may represent a disease-specific marker. We recruited 338 Japanese biopsy-proven IgAN patients and 120 patients with other renal diseases (disease controls). Urine samples collected at the time of renal biopsy were used to measure Gd-IgA1 levels using a specific monoclonal antibody (KM55 mAb). Urinary Gd-IgA1 levels were significantly higher in patients with IgAN than in disease controls. Moreover, urinary Gd-IgA1 was significantly correlated with the severity of the histopathological parameters in IgAN patients. Next, we validated the use of urinary Gd-IgA1 levels in the other Asian cohorts. In the Korean cohort, urinary Gd-IgA1 levels were also higher in patients with IgAN than in disease controls. Even in Japanese patients with IgAN and trace proteinuria (less than 0.3 g/gCr), urinary Gd-IgA1 was detected. Thus, urinary Gd-IgA1 may be an early disease-specific biomarker useful for determining the disease activity of IgAN.
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Cho, Won-Hee, Seon-Hwa Park, Seul-Ki Choi, Su Woong Jung, Kyung Hwan Jeong, Yang-Gyun Kim, Ju-Young Moon, et al. "Characterization of IgA Deposition in the Kidney of Patients with IgA Nephropathy and Minimal Change Disease." Journal of Clinical Medicine 9, no. 8 (August 12, 2020): 2619. http://dx.doi.org/10.3390/jcm9082619.

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Approximately 5% of patients with IgA nephropathy (IgAN) exhibit mild mesangial lesions with acute onset nephrotic syndrome and diffuse foot process effacement representative of minimal change disease (MCD). It is not clear whether these unusual cases of IgAN with MCD (IgAN-MCD) are variant types of IgAN or coincidental deposition of IgA in patients with MCD. In a retrospective multicenter cohort study of 18 hospitals in Korea, we analyzed 46 patients with IgAN-MCD. Patients with endocapillary proliferation, segmental sclerosis, and crescent were excluded, and the clinical features and prognosis of IgAN-MCD were compared with those of pure MCD. In addition, we performed galactose-deficient IgA1 (KM55) staining to characterize IgAN-MCD. Among the 21,697 patients with glomerulonephritis enrolled in the database, 46 patients (0.21%) were diagnosed with IgAN-MCD, and 1610 patients (7.4%) with pure MCD. The 46 patients with IgAN-MCD accounted for 0.6% of primary IgAN patients (n = 7584). There was no difference in prognosis between patients with IgAN-MCD and those with only MCD. IgA and KM55 showed double positivity in all patients with IgAN-MCD (n = 4) or primary IgAN (n = 5) under double immunofluorescent staining. However, in four patients with lupus nephritis, mesangial IgA was deposited, but galactose-deficient-IgA1 (Gd-IgA1) was not. These findings suggest that IgAN-MCD is a dual glomerulopathy in which MCD was superimposed on possibly indolent IgAN. We confirmed by KM55 staining that IgAN-MCD is true IgAN, enabling better characterizations of the disease. Furthermore, IgAN-MCD shows a good prognosis when treated according to the usual MCD treatment modality.
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Rizk, Dana V., Manish K. Saha, Stacy Hall, Lea Novak, Rhubell Brown, Zhi-Qiang Huang, Huma Fatima, Bruce A. Julian, and Jan Novak. "Glomerular Immunodeposits of Patients with IgA Nephropathy Are Enriched for IgG Autoantibodies Specific for Galactose-Deficient IgA1." Journal of the American Society of Nephrology 30, no. 10 (August 23, 2019): 2017–26. http://dx.doi.org/10.1681/asn.2018111156.

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BackgroundIgA nephropathy (IgAN) is the leading primary GN worldwide. The disease is thought to result from glomerular deposition of circulating immune complexes of IgG bound to galactose-deficient IgA1 (Gd-IgA1). However, routine immunofluorescence microscopy fails to detect IgG in many kidney biopsies from patients with IgAN and the specificity of IgG in immunodeposits has not been tested.MethodsWe used remnant frozen kidney-biopsy specimens from 34 patients with IgAN; 14 were IgG-positive and 20 were IgG-negative by routine immunofluorescence microscopy. Six patients with primary membranous nephropathy (MN) and eight with lupus nephritis (LN) served as controls. IgG in the kidney tissue was extracted and its amount determined by ELISA. IgG molecular integrity was assessed by SDS-PAGE immunoblotting. Antigenic specificity of extracted IgG was determined by ELISA using phospholipase A2 receptor (PLA2R) or Gd-IgA1 as antigen. In addition, ten other IgAN cases, six IgG-positive and four IgG-negative by routine immunofluorescence, were used for colocalization studies by confocal microscopy.ResultsIgG extracted from MN but not IgAN immunodeposits reacted with PLA2R. Conversely, IgG extracted from IgAN but not MN or LN immunodeposits reacted with Gd-IgA1. Even IgAN kidney-biopsy specimens without IgG by routine immunofluorescence microscopy had IgG specific for Gd-IgA1. Confocal microscopy confirmed the presence of IgG in the IgAN biopsies with colocalization of glomerular IgA and IgG.ConclusionsThese results reveal for the first time that IgAN kidney biopsies, with or without IgG by routine immunofluorescence, contain Gd-IgA1–specific IgG autoantibodies. These findings support the importance of these autoantibodies in the pathogenesis of IgAN.
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Dissertations / Theses on the topic "IgAN"

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Mohey, Hesham. "Le risque rénal absolu (RRA) de dialyse ou décès chez les patients adultes avec néphropathie à IgA primaire (NIgA) : étude d'une cohorte prospective de néphropathie à IgA recrutée à Saint-Etienne (IGAN -STET-CO)." Phd thesis, Université Jean Monnet - Saint-Etienne, 2010. http://tel.archives-ouvertes.fr/tel-00675243.

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La NIgA primaire est la plus fréquente des glomérulonéphrites. Elle représente, selon l'origine géographique et ethnique des populations, 10 à 40% des glomérulonéphrites primitives. Le diagnostic de NIgA est fait nécessairement sur la ponction biopsie rénale (PBR) en immunofluorescence. La grande difficulté dans cette maladie se trouve dans la prédiction au moment du diagnostic par les facteurs pronostiques de l'évolution vers l'insuffisance rénale chronique terminale à 10 et 20 ans après le début de la maladie. L'hypertension artérielle, la protéinurie ≥l g/24 h et la sévérité des lésions histologiques sur la biopsie rénale sont les facteurs de risque majeurs qui permettent la prédiction initiale. Objectifs de l'étude : confirmer et valider dans notre cohorte de NIgA les 3 facteurs de risque (FdR) comme facteurs significatifs et indépendants prédictifs d'une évolution ultérieure vers la Dialyse ou le Décès (avant dialyse) et utiliser ces 3 FdR pour développer un modèle simple de Risque Rénal Absolu (RRA) dont le score évalué au moment du diagnostic permettrait une prédiction du devenir à long terme (10 et 20 ans). Notre cohorte de patients (332) avec NIgA a été recrutée par le Service de Néphrologie, Dialyse, et Transplantation Rénale du CHU de Saint Etienne à l'Hôpital Nord (IGAN-STET-CO). La cohorte est prospective et inclut tous les patients avec diagnostic de Néphropathie à IgA primaire dont la biopsie rénale diagnostique a été réalisée entre le 1er janvier 1990 et le 31 décembre 1999. Le diagnostic histologique de NIgA est défini par la présence de dépôts mésangiaux d'IgA, d'intensité au moins 1+ comme immunoglobuline dominante ou codominante en immunofluorescence. L'intervalle de temps entre le début la maladie et la PBR diagnostique a été de : moyenne (déviation standard, DS) = 5.7 (8.5) ans et médiane (extrêmes) = 2.5 (0.1-46.9) ans. La durée totale d'exposition au risque principal entre le début de NIgA et le dernier recul ou le l'évènement principal était: moyenne (DS) = 12.9 (9.5) ans et médiane (extrêmes) = 11.3 (0.l-56.0) ans; chez 44 patients cette durée d'exposition était supérieure à 20 ans (l3.3%). La progression de la NIgA a été basée sur l'apparition de deux évènements : l'évènement principal (primary end-point) était la dialyse (Di; correspondant à la mort rénale avec un DFG de stade V autour de 8 ml/mn/1.73m2S) ou le décès du patient (De; s'il survenait avant le début de la dialyse), et représenté par Di/De ou plus simplement par D/D; l'évènement secondaire (secondary end-point) était la survenue d'un DFGe<60 ml/mn/1.73m2S marquant le début de l'IRC et correspondant à l'entrée dans le stade III de la maladie rénale chronique (MRC-3+). Les facteurs de risque majeurs étudiés dans cette étude sont l'hypertension artérielle (supérieure à 140/90 mmHg), la protéinurie (≥1g/24 h), et le score optique global (GOS ≥8). Le risque rénal absolu (RRA) de dialyse/décès (D/D) a été calculé à partir de ces trois facteurs simplifiés et dichotomiques après avoir confirmé leur caractère indépendant (les uns des autres) et que leur poids spécifique dans cette prédiction était quantitativement très similaire. 0 pour aucun de ces FdR, 3 pour leur présence simultanée et un score intermédiaire de 1 ou de 2 pour la présence de 1 ou 2 parmi ces 3 facteurs. Ce RRA a été utilisé comme une variable qualitative avec 4 catégories. Nous avons utilisé les courbes de survie sans l'évènement étudié selon Kaplan-Meier (KM) et la méthode de régression de Cox qui permet d'étudier l'influence d'une variable sur la survie sans l'évènement et permet ainsi d'isoler des facteurs pronostiques. Le DFG estimé au moment du diagnostic est de: moyenne(DS) = 74.7 (28.3) et médiane = 80 ml/mn/1.73m2S contre au dernier recul: moyenne (DS) = 68.0 (3 l .3) et médiane = 72.5 avec un P très significatif. La répartition des patients selon le RRA était la suivante: 151 patients (45,5%) avec un score de 0, 69 (20,8%) avec un score de 1,65 (19,6%) avec un score de 2, et 47 patients (14,2%) avec un score de 3. Le taux d'incidence cumulative de D/D, respectivement à 10 ans et 20 ans, a été de 2% (81 à risque) et 4% (15 à risque) pour RRA = 0,2% (38 à risque) et 9% (12 à risque) pour RRA = 1,7% (42 à risque) et 18% (9 à risque) pour RRA = 2, et 29% (27 à risque) et 64% (8 à risque) pour RRA = 3 (test du Logrank global; Chi2 = 62,1; P <0,0001). Les courbes de survie des patients sans D/D, selon Kaplan-Meier ont montré une meilleure survie avec un contrôle effectif de l'HTA. Le taux d'incidence cumulée pour dialyse/décès à 10 et à 20 ans était respectivement, pour le groupe non hypertendu de 4% (84 patients à risque) et 5% (17 patients à risque); pour le groupe des patients avec HTA contrôlée de 1% (54 patients à risque) et 19% (14 patients à risque), et pour le groupe des hypertendus non- contrôlés de 19% (50 patients à risque) et 42% (13 patients à risque) avec une différence significative entre les groupes des non hypertendus et des hypertendus contrôlés avec le groupe des hypertendus non contrôlés (P <0,0001). Pour la protéinurie, les courbes de survie des patients sans D/D, selon Kaplan-Meier, ont montré une amélioration significative (p<0,0001) en cas de réduction effective de la protéinurie. Ainsi, le taux d'incidence cumulée pour dialyse/décès à 10 et 20 ans était de 3% (118 à risque) et 5% (25 à risque) pour le groupe avec protéinurie faible/absente, 2% (40 à risque) et 2% (10 à risque) pour le groupe avec " protéinurie réduite", et 29% (30 à risque) et 67% (9 à risque) pour le groupe avec protéinurie non-réduite. Le contrôle des lésions histologiques graves est difficile à estimer à partir de notre cohorte en l'absence de biopsies répétées. Notre score de Risque Rénal Absolu est basé sur trois facteurs de risque majeurs, indépendants et simplifiés prédictifs de la progression vers la MRC-3+, puis vers la dialyse/décès. Ces FdR avaient finalement un poids identique dans cette prédiction à long terme, comme en témoignent : - une valeur de β/SE comprise entre 4 et 5 dans l'analyse monofactorielle et entre 2 et 3 dans l'analyse multifactorielle de Cox, - ainsi que des paramètres d'exactitude quasi similaires: même valeur prédictive négative autour de 0,95 et même valeur prédictive positive autour de 0,30; de même la probabilité de survenue de dialyse/décès était d'environ 31% en leur présence, mais seulement de 3 à 6% en leur absence. Au moment du diagnostic, 47 patients présentaient les 3 FdR ensemble (RRA = 3) et 28 (60%) sont arrivés en dialyse ou sont décédés. La probabilité de l'évolution à long terme vers la dialyse/décès était de 60% chez les patients avec RRA = 3 contre seulement 6% chez les patients avec RRA =0. Nous sommes les premiers à publier sur le Risque Rénale Absolu de dialyse e/o de décès et de proposer un score global avec une application clinique importante. L'utilisation de ce score RRA, nous permet de prédire à 10 et 20 ans après le début de la maladie, le taux d'incidence cumulative de dialyse/décès en retenant les chiffres arrondis à 20ans de 5% si RRA=0, de 10% si RRA=1, de 20% si RRA= 2, et de 60% si RRA=3, et cela dans une population activement traitée. Notre RRA est très simple à calculer par une simple addition des FdR présents au diagnostic, ne nécessite pas de calcul et s'affranchit des autres facteurs de risque (cliniques, biologiques, pathologiques et génétiques) décrits chez les patients avec NIgA comme le sexe ou l'âge du patient au moment de la biopsie ou l'indice de masse corporelle, IMC . Le point important est que l'utilisation du RRA, permettrait de bien sélectionner les patients à inclure dans des essais randomisés et contrôlés L'autre avantage sera dans les études génétiques de démontrer l'impact d'un génotype / allèle spécifique lié à la progression de la maladie en montrant une augmentation pas à pas de la fréquence du génotype/allèle dans les sous- groupes de RRA= 0 à RRA=3
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Mohey, Hesham. "Le risque rénal absolu (RRA) de dialyse ou décès chez les patients adultes avec néphropathie à IgA primaire (NIgA) : étude d’une cohorte prospective de néphropathie à IgA recrutée à Saint-Etienne (IGAN -STET-CO)." Thesis, Saint-Etienne, 2010. http://www.theses.fr/2010STET010T/document.

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La NIgA primaire est la plus fréquente des glomérulonéphrites. Elle représente, selon l’origine géographique et ethnique des populations, 10 à 40% des glomérulonéphrites primitives. Le diagnostic de NIgA est fait nécessairement sur la ponction biopsie rénale (PBR) en immunofluorescence. La grande difficulté dans cette maladie se trouve dans la prédiction au moment du diagnostic par les facteurs pronostiques de l’évolution vers l'insuffisance rénale chronique terminale à 10 et 20 ans après le début de la maladie. L’hypertension artérielle, la protéinurie ≥l g/24 h et la sévérité des lésions histologiques sur la biopsie rénale sont les facteurs de risque majeurs qui permettent la prédiction initiale. Objectifs de l’étude : confirmer et valider dans notre cohorte de NIgA les 3 facteurs de risque (FdR) comme facteurs significatifs et indépendants prédictifs d’une évolution ultérieure vers la Dialyse ou le Décès (avant dialyse) et utiliser ces 3 FdR pour développer un modèle simple de Risque Rénal Absolu (RRA) dont le score évalué au moment du diagnostic permettrait une prédiction du devenir à long terme (10 et 20 ans). Notre cohorte de patients (332) avec NIgA a été recrutée par le Service de Néphrologie, Dialyse, et Transplantation Rénale du CHU de Saint Etienne à l’Hôpital Nord (IGAN-STET-CO). La cohorte est prospective et inclut tous les patients avec diagnostic de Néphropathie à IgA primaire dont la biopsie rénale diagnostique a été réalisée entre le 1er janvier 1990 et le 31 décembre 1999. Le diagnostic histologique de NIgA est défini par la présence de dépôts mésangiaux d’IgA, d’intensité au moins 1+ comme immunoglobuline dominante ou codominante en immunofluorescence. L’intervalle de temps entre le début la maladie et la PBR diagnostique a été de : moyenne (déviation standard, DS) = 5.7 (8.5) ans et médiane (extrêmes) = 2.5 (0.1-46.9) ans. La durée totale d’exposition au risque principal entre le début de NIgA et le dernier recul ou le l’évènement principal était: moyenne (DS) = 12.9 (9.5) ans et médiane (extrêmes) = 11.3 (0.l-56.0) ans; chez 44 patients cette durée d’exposition était supérieure à 20 ans (l3.3%). La progression de la NIgA a été basée sur l’apparition de deux évènements : l’évènement principal (primary end-point) était la dialyse (Di; correspondant à la mort rénale avec un DFG de stade V autour de 8 ml/mn/1.73m2S) ou le décès du patient (De; s’il survenait avant le début de la dialyse), et représenté par Di/De ou plus simplement par D/D; l’évènement secondaire (secondary end-point) était la survenue d’un DFGe<60 ml/mn/1.73m2S marquant le début de l’IRC et correspondant à l’entrée dans le stade III de la maladie rénale chronique (MRC-3+). Les facteurs de risque majeurs étudiés dans cette étude sont l’hypertension artérielle (supérieure à 140/90 mmHg), la protéinurie (≥1g/24 h), et le score optique global (GOS ≥8). Le risque rénal absolu (RRA) de dialyse/décès (D/D) a été calculé à partir de ces trois facteurs simplifiés et dichotomiques après avoir confirmé leur caractère indépendant (les uns des autres) et que leur poids spécifique dans cette prédiction était quantitativement très similaire. 0 pour aucun de ces FdR, 3 pour leur présence simultanée et un score intermédiaire de 1 ou de 2 pour la présence de 1 ou 2 parmi ces 3 facteurs. Ce RRA a été utilisé comme une variable qualitative avec 4 catégories. Nous avons utilisé les courbes de survie sans l’évènement étudié selon Kaplan-Meier (KM) et la méthode de régression de Cox qui permet d’étudier l’influence d’une variable sur la survie sans l’évènement et permet ainsi d’isoler des facteurs pronostiques. Le DFG estimé au moment du diagnostic est de: moyenne(DS) = 74.7 (28.3) et médiane = 80 ml/mn/1.73m2S contre au dernier recul: moyenne (DS) = 68.0 (3 l .3) et médiane = 72.5 avec un P très significatif. La répartition des patients selon le RRA était la suivante: 151 patients (45,5%) avec un score de 0, 69 (20,8%) avec un score de 1,65 (19,6%) avec un score de 2, et 47 patients (14,2%) avec un score de 3. Le taux d'incidence cumulative de D/D, respectivement à 10 ans et 20 ans, a été de 2% (81 à risque) et 4% (15 à risque) pour RRA = 0,2% (38 à risque) et 9% (12 à risque) pour RRA = 1,7% (42 à risque) et 18% (9 à risque) pour RRA = 2, et 29% (27 à risque) et 64% (8 à risque) pour RRA = 3 (test du Logrank global; Chi2 = 62,1; P <0,0001). Les courbes de survie des patients sans D/D, selon Kaplan-Meier ont montré une meilleure survie avec un contrôle effectif de l’HTA. Le taux d'incidence cumulée pour dialyse/décès à 10 et à 20 ans était respectivement, pour le groupe non hypertendu de 4% (84 patients à risque) et 5% (17 patients à risque); pour le groupe des patients avec HTA contrôlée de 1% (54 patients à risque) et 19% (14 patients à risque), et pour le groupe des hypertendus non- contrôlés de 19% (50 patients à risque) et 42% (13 patients à risque) avec une différence significative entre les groupes des non hypertendus et des hypertendus contrôlés avec le groupe des hypertendus non contrôlés (P <0,0001). Pour la protéinurie, les courbes de survie des patients sans D/D, selon Kaplan-Meier, ont montré une amélioration significative (p<0,0001) en cas de réduction effective de la protéinurie. Ainsi, le taux d'incidence cumulée pour dialyse/décès à 10 et 20 ans était de 3% (118 à risque) et 5% (25 à risque) pour le groupe avec protéinurie faible/absente, 2% (40 à risque) et 2% (10 à risque) pour le groupe avec « protéinurie réduite», et 29% (30 à risque) et 67% (9 à risque) pour le groupe avec protéinurie non-réduite. Le contrôle des lésions histologiques graves est difficile à estimer à partir de notre cohorte en l'absence de biopsies répétées. Notre score de Risque Rénal Absolu est basé sur trois facteurs de risque majeurs, indépendants et simplifiés prédictifs de la progression vers la MRC-3+, puis vers la dialyse/décès. Ces FdR avaient finalement un poids identique dans cette prédiction à long terme, comme en témoignent : - une valeur de β/SE comprise entre 4 et 5 dans l’analyse monofactorielle et entre 2 et 3 dans l’analyse multifactorielle de Cox, - ainsi que des paramètres d’exactitude quasi similaires: même valeur prédictive négative autour de 0,95 et même valeur prédictive positive autour de 0,30; de même la probabilité de survenue de dialyse/décès était d'environ 31% en leur présence, mais seulement de 3 à 6% en leur absence. Au moment du diagnostic, 47 patients présentaient les 3 FdR ensemble (RRA = 3) et 28 (60%) sont arrivés en dialyse ou sont décédés. La probabilité de l'évolution à long terme vers la dialyse/décès était de 60% chez les patients avec RRA = 3 contre seulement 6% chez les patients avec RRA =0. Nous sommes les premiers à publier sur le Risque Rénale Absolu de dialyse e/o de décès et de proposer un score global avec une application clinique importante. L'utilisation de ce score RRA, nous permet de prédire à 10 et 20 ans après le début de la maladie, le taux d’incidence cumulative de dialyse/décès en retenant les chiffres arrondis à 20ans de 5% si RRA=0, de 10% si RRA=1, de 20% si RRA= 2, et de 60% si RRA=3, et cela dans une population activement traitée. Notre RRA est très simple à calculer par une simple addition des FdR présents au diagnostic, ne nécessite pas de calcul et s’affranchit des autres facteurs de risque (cliniques, biologiques, pathologiques et génétiques) décrits chez les patients avec NIgA comme le sexe ou l’âge du patient au moment de la biopsie ou l’indice de masse corporelle, IMC . Le point important est que l'utilisation du RRA, permettrait de bien sélectionner les patients à inclure dans des essais randomisés et contrôlés L’autre avantage sera dans les études génétiques de démontrer l'impact d'un génotype / allèle spécifique lié à la progression de la maladie en montrant une augmentation pas à pas de la fréquence du génotype/allèle dans les sous- groupes de RRA= 0 à RRA=3
For the individual patient with primary IgA nephropathy (IgAN), it remains a challenge to predict accurately the long term outcome at 10 and 20 years after disease onset. We studied it in a prospective cohort of 332 (237 males, 71.4%) biopsy-proven IgAN patients, the IGAN-STET-CO, aged at diagnosis of mean = 41.4 (SD=15.1) years, with a total exposure time of mean = 12.9 (9.5) y. Using three consensual risk factors (RF) simplified as dichotomous covariates : occurrence of hypertension, proteinuria ≥1 g/d, and severe pathological lesions (global optical score ≥8), we calculated an absolute renal risk (ARR) of dialysis/death (D/D), in analogy to the absolute cardiovascular risk. The ultimate prediction according to the number of RF present at diagnosis (ARR score: 0, 1, 2, or 3) was done by the Cox regression and the Kaplan-Meier survival methods. Overall, this ARR scoring permitted significant (P<0.0001) stratification of the risk. The cumulative incidence rate of D/D events (N=45), respectively at 10 and 20y, was 2 and 4% for ARR=0 (45.5% of all cases), 2 and 9% for ARR=1 (20.8%), 7 and 18% for ARR=2 (19.6%), and 29 and 64% for ARR=3 (N=47; 14.1%) in adequately treated patients. Effective control of hypertension and reduction of proteinuria improved survival without D/D when achieved. This absolute renal risk score evaluated at diagnosis, allowed accurate prediction of ultimate dialysis/death risk and was also validated in another cohort. This is a significant progress in the management of the individual patient with lgA nephropathy
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Gomes, Michelle Marie. "Molecular characterization of IgA1-receptor interactions implicated in IgA nephropathy." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1242938515.

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Wehbe, Batoul. "IgA et rein : destructrice ou protectrice ? : Rôles de l'immunoglobuline A (IgA) dans deux pathologies rénales." Thesis, Limoges, 2018. http://www.theses.fr/2018LIMO0034/document.

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L’immunoglobuline A (IgA) est l’immunoglobuline la plus abondamment synthétisée chez les mammifères. Ses propriétés ambivalentes l’impliquent non seulement dans des fonctions de protection contre les agents pathogènes mais aussi dans des phénomènes de tolérance immunitaire vis-à-vis des germes commensaux du microbiote. Toutefois, les IgA peuvent développer des propriétés pathogènes. Dans la première partie de mon travail de thèse, nous avons étudié les effets pathogènes de l’IgA. Les dépôts d’IgA sur le mésangium sont la caractéristique de l’IgAN. La physiopathologie de cette maladie est mal connue. L’hypothèse d’un défaut de glycosylation de l’IgA est souvent retenue ; ce défaut peut être la cause de sa polymérisation et de son antigénicité, il peut aussi favoriser le clivage du récepteur CD89. Nous avons analysé l’effet du défaut d’affinité de la région variable des IgA, de la substitution de la chaîne légère ainsi que de l’association des IgA à leur récepteur, le CD89 sur l’induction des lésions et le dysfonctionnement rénal chez quatre modèles murins différents générés au laboratoire et suivis pendant 12 mois. Nous avons également étudié les propriétés physico-chimiques des IgA de 28 patients ayant une dysglobulinémie et de 28 IgA produites par des hybridomes ; la relation entre ces propriétés et la capacité des IgA à se déposer a été observée. Dans une seconde partie, nous avons étudié l’aspect immunomodulateur et les propriétés antiinflammatoires conférées par l’IgA humaine surexprimée chez un modèle murin de lupus systémique (souris MRL/lpr). Dans la dernière partie du travail, nous avons contribué à la caractérisation d’un modèle de souris transgénique exprimant l’IgA de classe 2 et à l’étude de l’effet de signalisation médiée par cette IgA2 sur le développement des populations lymphocytaires. L’ensemble de ces travaux a montré l’effet pathogène des IgA naturelles ayant une faible affinité sur le développement de la néphropathie à IgA ; ainsi les analyses des IgA des patients et des hybridomes montrent que c’est la stabilité moléculaire de préférence au profil de glycosylation qui joue un rôle crucial dans leur capacité de dépôt. L’expression des IgA humaines chez les souris lupiques a considérablement prolongé leur durée de vie et a ralenti la survenue de l’auto-immunité et de l’atteinte rénale ce qui témoigne du rôle anti-inflammatoire des IgA. L’étude du modèle murin exprimant l’IgA2 humaine a montré que la signalisation via l’IgA2 joue un rôle inhibiteur sur le développement précoce de certaines sous-populations de cellules B. L’ensemble de ces résultats montrent la multitude d’effets de l’IgA lui permettant d’intervenir d’une part dans la pathogenèse d’une maladie complexe (l’IgAN) et d’autre part dans la protection de l’auto-immunité, témoignant de la complexité des interactions mises en jeu et du caractère régulateur de cette immunoglobuline
Immunoglobulin A (IgA) is the most synthetized immunoglobulin in mammals. IgA has ambivalent properties: it is implicated in the mechanisms of defense against pathogens but also in the immune tolerance of commensal microbiota. However, IgA can develop pathogenic properties. In the first part of my thesis, we studied the pathogenic effects of IgA. IgA deposits are the main characteristic of IgA nephropathy (IgAN). IgAN physiopathology is not yet clearly understood. The hypothesis of a glycosylation defect is strongly adapted. This defect can be due to IgA polymerization or antigenicity. It can also induce shedding of CD89 (IgA Fc receptor) or other factors. We studied the effect of variable region altered affinity, the light chain substitution and the association of IgA with CD89 on the development of kidney lesions and impairment of kidney function in four mouse models followed up during 12 months. In addition, we studied the physico-chemical properties of 28 IgA purified from patients with dysglobulinaemia and 28 chimeric IgA produced by hybridomas. The effect of these properties on the propensity of IgA for mesangial deposition was explored. In the second part, we studied the immunomodulatory and anti-inflammatory properties conferred by the overexpression of human IgA in a mouse model with systemic lupus (MRL/lpr model). In the last part, we contributed to the characterization of a transgenic mouse model producing IgA class 2 and to the study of the effect of IgA2-mediated signaling on B lymphocyte development. Altogether, obtained results show the pathogenic effect of low affinity-IgA on the development of IgA nephropathy. In addition, different analyses showed that molecular stability but not glycosylation profile is the determining factor for IgA deposition. On the other hand, IgA expression in lupus-prone mice extended their survival, delayed the onset of auto-immunity and ameliorated kidney functions in these animals which supports IgA anti-inflammatory properties. The study of IgA2-mediated signaling in the transgenic model showed the inhibitory effect of IgA2 on the early development of several B cell sub-populations. All of these results show the multiple effects of IgA which contribute on one hand to the pathogenesis of a complex disease (IgAN) and on the other hand to protection from autoimmunity, demonstrating the complexity of interactions and the regulatory character of this immunoglobulin
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Günther, Ellen. "Examen igen?" Thesis, Södertörn University College, Lärarutbildningen, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:sh:diva-1999.

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This paper will discuss the proposed reintroducing of a final degree in upper secondary school. In a public government inquiry that was released in March 2008 a proposal about reintroducing a final degree in upper secondary school was presented. A final degree has not been a part of the upper secondary school science 1968. Why was the system with a final degree abounded and why do the government want to reintroduce it?

Research in pedagogy has through the years presented numbers of theories about assessment. In last decades a great part of the discussion has been focused on formative assessment. In formative assessment the assessment is used as a pedagogy tool. The purpose is to help the student develop their learning process and to learn to work independently. The contrary to formative assessment is assessment which only purpose is to summarise and control the level of knowledge a student possesses.

The public government inquiry that led to abolish of a final degree in upper secondary school in 1968 shared many thoughts with theories about formative assessment. Forty years later the government has grown sick of all the formative assessment, which they think has led to a “muddled” school. The public government inquiry presented in 2008 wants to reintroduce a final degree and create a school where the student’s knowledge is orderly controlled and summarised.

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Layward, Lorna. "IgA in IgA nephropathy." Thesis, University of Leicester, 1992. http://hdl.handle.net/2381/34129.

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IgA in IgA Nephropathy Lorna Layward IgA nephropathy is a common glomerulonephritis of unknown pathogenesis, characterised by the presence of IgA within the glomerular mesangium. The predominant subclass of deposited IgA is known to be of the subclass IgA1 and is, at least in part, polymeric. IgA subclass measurements showed that raised serum IgA levels were restricted to the IgAl subclass, and that increased IgA levels were only observed in the systemic (not mucosal) compartment of the IgA immune system. In vitro production of IgA by peripheral blood lymphocytes was increased, with a concomitant decrease in IgG production. The response to systemic challenge with tetanus toxoid demonstrated a bias towards serum IgA1 antibody production; an enhanced circulating antigen-specific B cell response; and a positive saliva response where none was observed in controls. Serum polymeric IgA antibody production in response to systemic antigen challenge was significantly elevated in IgA nephropathy. Patients with IgA nephropathy were more likely to have an IgG subclass antibody deficiency than controls, showing dysregulation of other isotypes besides IgA. The affinity of serum IgA antibodies produced was lower than controls, while IgG affinity was normal. The production of low affinity IgA antibodies may result in the formation of nephritogenic immune complexes and explain the predominance of IgA within the glomerular mesangium. Gut permeability was normal in IgA nephropathy, and the response to mucosal antigen challenge did not differ from controls except for a higher antigen-specific in vitro B cell response. These results suggest an enhanced overlap of circulating IgA immunocompetent IgA B cells between the two sites in IgA nephropathy, regardless of the route of antigen administration. These data show abnormalities of mainly systemic IgA lending support to the hypothesis that the source of IgA overproduction is the systemic rather than the mucosal compartment of the IgA immune system.
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Allen, Alice. "IgA glycosylation in IgA nephropathy." Thesis, University of Leicester, 1995. http://hdl.handle.net/2381/35028.

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IgA nephropathy (IgAN) is a common glomerulonephritis characterised by deposition of IgA1 in the glomerular mesangium The underlying abnormality lies within the IgA system rather than the kidney, and modest irregularities of IgA biology have been described, but the mechanisms involved in IgA1 deposition and glomerular injury remain elusive. A few reports have suggested an abnormality of the carbohydrate component of IgA1 in IgAN. These studies sought to confirm and further characterise the putative glycosylation defect and to identify its biochemical basis. Lectin binding assays were developed and used to analyse the N- and O-linked glycans of IgA1 in IgAN and controls. No gross abnormality of N-glycosylation was detected in IgAN, though these studies were subject to technical limitations. IgA1 in IgAN displayed significantly increased binding to lectins with affinity for O-linked N-acetylgalactosamine (Ga1NAc) as compared to controls. One explanation for this finding is reduced terminal galactosylation of the O-linked sugars of IgA1. A novel assay was developed to measure the functional activity of alpha1,3 galactosyltransferase (alpha1,3GT), the enzyme responsible for O-galactosylation, in cell lysates. In IgAN, peripheral blood B cells appeared to show significantly lower alpha1,3GT activity than controls, and this was inversely proportional to Ga1NAc expression of serum IgA1 as measured by lectin binding. These studies confirm an abnormality of O-linked glycosylation of serum IgA1 in IgAN, which may be attributed to low B cell alpha1,3GT activity. Altered O-glycosylation of IgA1 may be relevant to the pathogenesis of IgAN.
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Mattsson, Madeleine, and Emma Liljefeldt. "MKB Vågade - igen?" Thesis, Malmö högskola, Fakulteten för kultur och samhälle (KS), 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-21945.

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Studien avser att belysa dels ett historiskt perspektiv hos MKB Fastighets AB:s organisationsförändring under Allan Karlssons ledning på 1990-talet, dels avser studien att undersöka hur dagens organisationskultur yttrar sig och dels hur den rådande kulturen förmodas integrera med en leanimplementering. Syftet är att utifrån dessa tre perspektiv skildra den rådande organisationskulturen samt genomföra en tolkning om organisationskulturen är enhetlig eller splittrad med existerande subkulturer. Frågeställningarna berör kulturen på 1990-talet, hur förvaltningsområdena framställs, respondenternas skildring av samhörighet och konsensus i organisationen, hur respondenterna ser på organisationsförändringen samt respondenternas syns på ledningen. Den teoretiska referensramen i studien lyfter fram vikten av att en organisationsförändring påverkar flera organisatoriska dimensioner. Organisationskulturen har makten att påverka organisationsförändringar och skapa inkonsekvenser som utvecklar subkulturer. Förändringsledarskapet lyfts fram som en viktig del i att kontrollera motståndet och påverka både organisationsförändring och organisationskulturen. Leanfilosofin innebär att införa en ny organisationskultur som genererar tydligare struktur och ökad delaktighet.Undersökningen är en kvalitativ fallstudie med en hermeneutikisk och en fenomenologisk ansats. Datainsamlingen grundades i ett strategiskt urval av elva respondenter, varav tio förvaltare och en styrgruppsmedlem. Det empiriska materialet sammanställdes utifrån intervjuer med respondenterna, resultatet bygger även på projektbeskrivningen, årsredovisningen och MKB Vågade (Aunér, 2001). Analysen av empirin gav insikt om att det fanns en stark självbestämmande kultur, bristande vetskap om leanimplementeringen, stora meningsskiljaktigheter mellan ledning och operativ personal samt att ett nätverkande kommunikationssystem i form av lobbyverksamhet som existerar i organisationen.
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Wallin, Pérez Carolina. "Snurra min jord igen." Thesis, Kungl. Musikhögskolan, Institutionen för jazz, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:kmh:diva-105.

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Bilaga: 1 CD. Medverkande: Carolina Wallin Pérez - sång, Mattias Fjellström - gitarrer, Joakim Simonsson - piano, Markus Hängsel - kontrabas, Fredrik Okazaki Bergström - trummor/klockspel/producent, Thomas Backman - barytonsaxofon/basklarinett, Stockholm Strings (Hanna Ekström - violin/viola, Victoria Lundell - violin, Erik Holm - viola, Anna Dager - cello).
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Millet, Isabelle. "Récepteurs pour les IgA et propriétés biologiques des facteurs liant les IgA : iga-bf." Lyon 1, 1988. http://www.theses.fr/1988LYO1T156.

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Books on the topic "IgAN"

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Igan to daichōgan. Tōkyō: Iwanami Shoten, 1999.

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(Japan), Tottori-ken. Igan shibō hangen taisaku ni kansuru hōkoku: Jushinritsu kōjō taisaku oyobi shūdan kenshin no kōka hantei. [Tottori-shi]: Tottori-ken, 1989.

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Ōtani, Katsuya. Pirorikin de wakatta i no atarashii byōkitachi: Ien kara igan made sono genʾin no nazo o toku. Tōkyō: Gendai Shorin, 2003.

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Ip e igŭn uri igŭn mal. Sŏul-si: Hakkojae, 2006.

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Engqvist, Hans Erik. Ge igen! Stockholm: Bonniers junior förlag, 1985.

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Onda, Riku. Shōsetsu igai. Tōkyō: Shinchōsha, 2005.

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Culukiże, Nika. Igav-arakebi. Tʻbilisi: Gamomcʻemloba "Universali", 2008.

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Hizazi, Nasim. Simanta igal. Dhaka: Priti Prakashan, 1987.

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Igav-arakebi. Tʻbilisi: Gamomcʻemloba "Universali", 2008.

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Development, Intergovernmental Authority on. IGAD strategy. Djibouti, Republic of Djibouti: IGAD Secretariat, 2005.

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Book chapters on the topic "IgAN"

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Gartler, Stanley M., R. Scott Hansen, Vinzenz Oji, Heiko Traupe, Julia Horn, Bodo Grimbacher, Srijita Sen-Chowdhry, et al. "IgAN." In Encyclopedia of Molecular Mechanisms of Disease, 1031. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8940.

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Narita, Ichiei, Yoshikatsu Kaneko, Yumi Itoh, Yuichi Sakamaki, Seitaro Iguchi, Suguru Yamamoto, Minako Wakasugi, Junichiro J. Kazama, and Shin Goto. "Is IgA Nephropathy (IgAN) a Familial or Sporadic Disease?" In Pathogenesis and Treatment in IgA Nephropathy, 43–51. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55588-9_3.

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Shah, Jui, and Maniklal Das. "IGAN: Intrusion Detection Using Anomaly-Based Generative Adversarial Network." In Advances in Intelligent Systems and Computing, 371–79. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-2008-9_36.

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Wold, Agnes E., Cecilia Motas, Catherina Svanborg, Lars Ake Hanson, and Jiri Mestecky. "Characterization of IgA1, IgA2 and Secretory IgA Carbohydrate Chains using Plant Lectins." In Advances in Experimental Medicine and Biology, 585–89. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1941-6_123.

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Novak, Jan, Kazuo Takahashi, Hitoshi Suzuki, Colin Reily, Tyler Stewart, Hiroyuki Ueda, Koshi Yamada, et al. "Heterogeneity of Aberrant O-Glycosylation of IgA1 in IgA Nephropathy." In Pathogenesis and Treatment in IgA Nephropathy, 53–68. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55588-9_4.

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Suzuki, Hitoshi, Zina Moldoveanu, Stacy Hall, Rhubell Brown, Bruce A. Julian, Robert J. Wyatt, Milan Tomana, Yasuhiko Tomino, Jan Novak, and Jiri Mestecky. "IgA Nephropathy: Characterization of IgG Antibodies Specific for Galactose-Deficient IgA1." In IgA Nephropathy Today, 129–33. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000102454.

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Hiki, Yoshiyuki, Akihiko Ito, Yoshihiro Yamamoto, Koichiro Yamamoto, and Hitoo Iwase. "IgA Nephropathy and Aberrant Glycosylation of Tonsillar, Serum and Glomerular IgA1." In Recent Advances in Tonsils and Mucosal Barriers of the Upper Airways, 68–70. Basel: KARGER, 2011. http://dx.doi.org/10.1159/000324609.

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Clarkson, Anthony R. "IgA Nephropathy: History, Classification, and Geographic Distribution." In IgA Nephropathy, 1–8. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2039-5_1.

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Allardyce, Randall A. "The Biology of IgA Mucosal Immunity." In IgA Nephropathy, 127–56. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2039-5_10.

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Egido, Jesus. "The Role of Polymeric IgA in the Pathogenesis of IgA Nephropathy." In IgA Nephropathy, 157–75. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2039-5_11.

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Conference papers on the topic "IgAN"

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Altun, Ilayda, Seha Saygılı, Nur Canpolat, Salim Çalışkan, and Lale Sever. "359 A novel COL4A4 mutation in the proband initially diagnosed as IgAN with autosomal recessive Alport syndrome." In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.359.

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Paixão, Vitória da, Tamaris Roseira, Jônatas Bussador Do Amaral, Juliana De Melo Batista Dos Santos, and André Luis Lacerda Bachi. "IDOSOS SUPLEMENTADOS COM L-GLUTAMINA TEM MELHOR RESPOSTA DE MUCOSA E NÃO SÉRICA À VACINA PARA O VIRUS INFLUENZA." In II Congresso Brasileiro de Saúde On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1448.

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Introdução: Embora a suplementação com glutamina tenha mostrado diversos benefícios na imunidade, à ação deste aminoácido na resposta imune das vias aéreas superiores, especialmente em idosos, ainda necessita de esclarecimentos. Em relação à resposta imune em idosos, é amplamente aceito que durante o envelhecimento há evidente diminuição das atividades imunológicas, um fenômeno denominado de imunossenescência, o qual leva os idosos a apresentarem uma menor capacidade de se protegerem contra infecções e também de responder à imunização. Objetivo: Diante destas informações, neste estudo objetivamos avaliar o efeito da suplementação de L-glutamina nos níveis da imunoglobulina A (IgA) tanto sérica quanto na mucosa das vias aéreas de idosos vacinados para o vírus Influenza. Métodos: Foram coletadas amostras de sangue e saliva de 83 idosos fisicamente ativos, em dois momentos, antes (pré) e 30 dias após a vacinação para o vírus Influenza e suplementação com L-glutamina (Gln, n = 42) ou placebo (PL, n = 41) para avaliação dos níveis da imunoglobulina A (IgA). Resultados: Maiores níveis séricos de IgA foram observados em ambos os grupos pós-vacinação quando comparado aos valores pré-vacinação. Em relação à reposta de mucosa, foi evidenciado níveis salivares mais altos de IgA secretora (IgAs), tanto total quanto específica para a vacina, foram encontrados pós-vacinação no grupo Gln em comparação aos valores observados pré-vacinação e no grupo PL pós-vacinação. Conclusão: Diante dos resultados obtidos, pode-se concluir que a suplementação de Gln é capaz de melhorar a resposta à vacinação contra o vírus Influenza em idosos através de uma modulação da resposta imune na mucosa, pois induz a produção e liberação de IgAs, o que confere maior proteção à mucosa.
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Svärd, A., K. Roos Ljungberg, A. Kastbom, T. Skogh, and K. Martinsson. "AB0110 Serum and salivary iga1 and iga2 acpa subclasses in established rheumatoid arthritis and associations to smoking." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4131.

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Hitoo, Iwase, Nakamura Ikuko, Kenji Arai, Yoko Nagai, Kazunori Toma, Tadashi Katsumata, Takashi Sano, and Yutaka Kobayashi. "GENDER DIFFERENCE AND EPITOPE SPECIFICITY OF IGG ANTIBODY AGAINST IGA1 HINGE PORTION IN IGA NEPHROPATHY PATIENTS." In XXIst International Carbohydrate Symposium 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.666.

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Quiroz, Juan C., Amit Banerjee, and Sushil J. Louis. "IGAP." In the 10th annual conference. New York, New York, USA: ACM Press, 2008. http://dx.doi.org/10.1145/1389095.1389426.

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Pedrosa, Lara Alípio, ARIANA LACERDA GARCIA, and BEATRIZ RIBEIRO COUTINHO DE MENDONÇA FURTADO. "OS BENEFÍCIOS DO ALEITAMENTO MATERNO NO SISTEMA IMUNOLÓGICO." In II Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/ii-conbrai/6018.

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Introdução: A Organização Mundial de Saúde (OMS), o Fundo das Nações Unidas para a Infância (UNICEF) e o Ministério da Saúde (MS) preconizam o aleitamento materno exclusivo até os seis meses de idade. Ao nascimento, a criança apresenta baixos níveis de imunoglobulinas (IgM, IgA e IgE). No entanto, o leite materno apresenta uma importante função na transferência de imunidade passiva no período pós-natal, pois possui funções antimicrobianas, anti-inflamatórias e imunorreguladoras. Nos primeiros três anos de vida, o .aleitamento materno exerce efeito benéfico sobre a incidência de eczema, alergia alimentar, sensibilização atópica e “doença sibilante”. Objetivo: Destacar a importância do aleitamento materno e os seus benefícios no sistema imunológico do recém-nascido. Metodologia: Esta revisão bibliográfica trata-se de um estudo qualitativo de artigos seletivos publicados em sites específicos, como BVS, Scielo e Pubmed, acerca da reflexão do impacto imunológico benéfico pelo aleitamento materno. Resultados: : O aleitamento materno protege o lactente de infecções principalmente por meio dos anticorpos IgA secretores (IgAS), além de fatores bioativos. A proteção contra infecções tem sido bem evidenciada durante a lactação, combatendo infecções do trato respiratório, incluindo otite média, infecção do trato urinário, sepse neonatal e enterocolite necrosante, diarreia aguda e prolongada, ganhando relação com o sistema imunológico do lactente pelas propriedades do leite materno, que, em especial o colostro, apresenta elevadas concentrações de anticorpos (IgA, IgM, IgE e IgD), sendo um reforço natural imunológico de destaque. Outra característica imunizante do leite materno é a presença de células polimorfonucleares (macrófagos, neutrófilos e eosinófilos) que fagocitam microrganismos patogênicos. Há ainda a presença de substâncias com propriedades probióticas e antibióticas como a lisozima, lactoferrina e o fator bífido que combatem a instalação de agentes envolvidos na etiologia de doenças diarreicas. Conclusão: Entende-se, portanto, a necessidade de se estimular o aleitamento materno durante o primeiro semestre de vida, período em que a produção própria de IgA secretória é ainda pouco significativa. O baixo teor de alérgenos no leite materno, bem como as propriedades anti-inflamatórias e imunomoduladoras, devem prevenir alergias e promover o desenvolvimento de tolerância.
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Llorà, Xavier, Kumara Sastry, David E. Goldberg, Abhimanyu Gupta, and Lalitha Lakshmi. "Combating user fatigue in iGAs." In the 2005 conference. New York, New York, USA: ACM Press, 2005. http://dx.doi.org/10.1145/1068009.1068228.

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Szmurło, Agnieszka, Marek Wiewiórka, and Tomasz Gambin. "iGAP: Interactive Genomic Analysis Platform." In Photonics Applications in Astronomy, Communications, Industry, and High-Energy Physics Experiments 2018, edited by Ryszard S. Romaniuk and Maciej Linczuk. SPIE, 2018. http://dx.doi.org/10.1117/12.2502040.

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Llorà, Xavier, Noriko Imafuji Yasui, and David E. Goldberg. "Graph-theoretic measure for active iGAs." In the 10th annual conference. New York, New York, USA: ACM Press, 2008. http://dx.doi.org/10.1145/1389095.1389281.

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LI, WILFRED W., PETER W. ARZBERGER, CHANG LIM YEO, LARRY ANG, OSAMU TATEBE, SATOSHI SEKIGUCHI, KARPJOO JEONG, SUNTAE HWANG, SUSUMU DATE, and JAE-HYUCK KWAK. "PROTEOME ANALYSIS USING IGAP IN GFARM." In Proceedings of the 2nd International Life Science Grid Workshop, LSGRID 2005. WORLD SCIENTIFIC, 2006. http://dx.doi.org/10.1142/9789812772503_0013.

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Reports on the topic "IgAN"

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Zachary, Wayne, Thomas Santarelli, Joan Ryder, and James Stokes. Developing a Multi-Tasking Cognitive Agent Using the COGNET/iGEN Integrative Architecture. Fort Belvoir, VA: Defense Technical Information Center, December 2000. http://dx.doi.org/10.21236/ada416891.

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Ivy, John M. Production of Anti-Ferret IgA Antibodies; and production of monoclonal antibodies. Fort Belvoir, VA: Defense Technical Information Center, April 1994. http://dx.doi.org/10.21236/ada279534.

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Schmidt-Sane, Megan, Tabitha Hrynick, Erica Nelson, and Tom Barker. Mutual Learning for Policy Impact: Insights from CORE. Adapting research methods in the context of Covid-19. Institute of Development Studies (IDS), December 2021. http://dx.doi.org/10.19088/core.2021.008.

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On 25 November 2021, the CORE Knowledge Translation Services team at the Institute of Development Studies, UK, hosted an online clinic session to facilitate the sharing of experiences and mutual learning on how CORE projects have or can adapt their research activities in the context of the Covid-19 pandemic. The clinic was attended by 22 CORE members from 12 projects and featured contributions from two CORE projects: The Youth Question in Africa: Impact, Response and Protection Measures in the IGAD Region and A New Digital Deal for an Inclusive Post-Covid-19 Social Compact: Developing Digital Strategies for Social and Economic Reconstruction. This learning guide captures the practical insights and advice from the event, to help inform the practice of participants and other projects across the portfolio.
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Kløcker Larsen, Rasmus, and Maria Boström. “Låt renen få igen landet som det var”: Konsekvenser av gruvan och vägen på Stihken för Vilhelmina Södra sameby. Stockholm Environment Institute, June 2021. http://dx.doi.org/10.51414/sei2021.007.

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Denna rapport presenterar en studie av Vilhelmina Södra samebys erfarenheter av de konsekvenser som gruvan på Stihken fört med sig, en gruva som drevs av Boliden Mineral AB 1976–1988. Det finns i dag ett stort kunskapsglapp angående vilka de faktiska konsekvenserna är av gruvindustri på samisk markanvändning, inklusive renskötseln. Detta är så vitt vi vet första gången som forskningen empiriskt belyser konsekvenserna av gruvindustrin, och de faktiska utfallen av försöken till efterbehandling, utifrån en samebys egna erfarenheter och kunskap. Studien genomfördes 2019–2020 i ett samarbete mellan samebyn, Svenska Samernas Riksförbund och Stockholm Environment Institute. Datainsamlingen har bestått av arbetsmöten, intervjuer, workshops, dokumentanalys och kartering med stöd av RenGIS och forskning om störningszoner. Fokus i denna rapport ligger på just Vilhelmina Södra samebys erfarenheter och gruvans konsekvenser för andra samebyar eller icke-renskötande samer i området har därför inte inkluderats. Resultaten visar den omfattande påverkan som gruvan haft på samebyn, dels under driftperioden men i högsta grad också efteråt. Under drifttiden förorsakade gruvan stora direkta och indirekta markförluster, med störningar från brytningen och trafiken, damning på betet, blockering av det naturliga flyttstråket och förlust av stora delar av samebyns renar in i Norge eller in på grannbyarnas mark på svensk sida. I nutid handlar de största konsekvenserna om en omfattande störning från besöksnäringen på grund av vägen som drogs i tidigare väglöst land. Detta föranleder i sin tur stort betesbortfall; försämrad djurhälsa och kondition för renen; förhöjd arbetsbelastning, fysiska påfrestningar, och arbetsmiljörisker för renskötarna; ökade kostnader för renskötselaktiviteter; samt förlust av samiska kulturminnen, ökad psykisk påfrestning, försämrade möjligheter för samebyns unga att satsa på renskötseln, och förlust av traditionell kunskap. Dessa forskningsresultat är viktiga för att korrigera vanligt förekommande missuppfattningar i den politiska och offentliga debatten kring gruvindustrin: nämligen att gruvindustrin och renskötseln kan samexistera utan någon större påverkan på renskötseln. De visar också tydligt vem som har bäst kunskap att bedöma riskerna vid en gruvetablering: samebyn identifierade redan på 1960-talet, och det ganska så exakt, de risker som denna studie nu kunnat visa blivit verklighet medan försöken från statens representanter var långt mindre precisa. Exempelvis antog statens experter en total störningszon på 500 meter runt gruvområdet och 100 meter på bägge sidor om vägen. Detta står i stark kontrast till de störningszoner som samebyn faktiskt har upplevt, nämligen upp mot 10 kilometer för gruvan och 1,5 kilometer för vägen. Problemen härrör främst från det faktum att svensk lagstiftning inte ger tillräckligt skydd för samiska rättigheter. De hänger även ihop med statens tvetydiga roll i hanteringen av de intressekonflikter som uppstår när man både har en skyldighet att skydda samiska rättigheter och ska tillgodose olika samhälls- och företagsekonomiska intressen i utvinningen av mineraler. Denna brist på ansvarstagande, som samebyn upplever från statens sida, visar med all tydlighet att den koloniala exploateringen av naturresurserna i Sápmi inte är ett historiskt fenomen utan något som i allra högsta grad fortgår än i dag. Som ett exempel har inga ansträngningar som helst gjorts för att se över huruvida den begränsade ekonomiska ersättningen som staten genomförde under 1960–70 talet verkligen motsvarar de faktiska skador som samebyn fått uthärda. Det finns flera sätt att åtgärda problemen i området vid Stihken. Exempelvis skulle regeringen kunna ge SGU i uppdrag att återställa området från tidigare prospekteringsverksamhet och kommun och länsstyrelse skulle i sin tur kunna ingripa för att hantera besöksnäringen och friluftslivet. Vad denna studie främst belyser är dock behovet av en genomgripande strategi från statens sida för att komma till rätta med konsekvenserna av Bolidens gruvprojekt och dess följdeffekter. Utifrån senaste årens rättsutveckling torde det numera finnas goda möjligheter för staten att se över sitt ansvar för de skador som framkommit på området vid Stihken.
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He, Mingyu, Tianying Chang, and Shoulin Zhang. Efficacy and safety of Tripterygium wilfordii glycosides in treatment of IgA nephropathy：A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0037.

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Zachary, Wayne, Joan Ryder, James Stokes, Floyd Glenn, Jean-Christophe Le Mentec, and Thomas Santarelli. Developing Concept Learning Capabilities in the COGNET/IGEN Integrative architecture and Associated Agent-based Modeling and Behavioral Representation (AMBR) Air Traffic Control. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada439347.

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Lumsden, Jessee. An Investigation of the Mechanism of IGA/SCC of Alloy 600 in Corrosion Accelerating Heated Crevice Environments. Technical Progress Report. Office of Scientific and Technical Information (OSTI), November 1999. http://dx.doi.org/10.2172/761827.

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Lumsden, Jesse. An Investigation of the Mechanism of IGA/SCC of Alloy 500 in Corrosion Accelerating Heated Crevice Environments. Technical progress report. Office of Scientific and Technical Information (OSTI), March 2000. http://dx.doi.org/10.2172/762168.

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Lumsden, Jesse. An Investigation of the Mechanism of IGA/SCC of Alloy 600 in Corrosion Accelerating Heated Crevice Environments. Technical Progress Report. Office of Scientific and Technical Information (OSTI), January 1999. http://dx.doi.org/10.2172/762745.

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Lv, Guangxin, and Chengyuan Ming. Efficacy and safety of leflunomide combined with corticosteroids for the treatment of IgA nephropathy: a meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0158.

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