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Relevant bibliographies by topics / Glomerulonephritis, IGA

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Academic literature on the topic 'Glomerulonephritis, IGA'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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Journal articles on the topic "Glomerulonephritis, IGA"

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Zhang, Minfang, Wenyan Zhou, Shaojun Liu, Liyin Zhang, Zhaohui Ni, and Chuanming Hao. "KM55 Monoclonal Antibody Staining in IgA-Dominant Infection-Related Glomerulonephritis." Nephron 145, no. 3 (2021): 225–37. http://dx.doi.org/10.1159/000513269.

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<b><i>Introduction:</i></b> IgA-dominant infection-related glomerulonephritis (IgA-IRGN) is a unique form of IRGN, which needs to be distinguished from IgA nephropathy (IgAN), due to overlapping clinical and pathological features. The key factor in the pathogenesis of IgAN is galactose-deficient IgA1 (Gd-IgA1). However, the mechanism of glomerular IgA deposition in patients with IgA-IRGN is unclear. Therefore, we evaluated whether Gd-IgA1 could be a useful biomarker to distinguish between these 2 diseases. <b><i>Methods:</i></b> A case-control study was conducted to analyze the clinical and pathological characteristics of 12 patients with IgA-IRGN. The intensity and distribution of glomerular Gd-IgA1 (KM55) staining in renal biopsies were assessed. The control group consisted of 15 patients diagnosed with IgAN and an additional 17 patients with glomerulopathy involving IgA deposition. <b><i>Results:</i></b> The main clinical manifestations of patients with IgA-IRGN were nephrotic-range proteinuria, hematuria, acute renal injury, and hypocomplementemia. Active lesions were the leading pathological feature, while focal segmental sclerosis was rare. Half of the patients exhibited hump-shaped subepithelial deposits. Glomerular KM55 staining was negative in 7 patients, trace in 4 patients, and 2+ in 1 patient. The median intensity of KM55 staining in IgA-IRGN patients was 0 (range 0∼2+), which was significantly lower than that of primary IgAN patients (median 2+, range 1+∼3+). The receiver operating characteristic analysis demonstrated that the optimal cutoff level to identify these 2 diseases was 0.5+. <b><i>Conclusions:</i></b> Glomerular KM55 staining intensity might be helpful to distinguish IgA-IRGN from primary IgAN. Weak or negative staining may favor IgA-IRGN. In addition, integrated analysis including clinical data, pathological findings, and prognostic information would further improve the differential diagnosis.

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Cassol, Clarissa A., Cherri Bott, Gyongyi M. Nadasdy, et al. "Immunostaining for galactose-deficient immunoglobulin A is not specific for primary immunoglobulin A nephropathy." Nephrology Dialysis Transplantation 35, no. 12 (2019): 2123–29. http://dx.doi.org/10.1093/ndt/gfz152.

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Abstract Background Primary immunoglobulin A nephropathy (IgAN) is characterized by IgA1-dominant or codominant glomerular deposits, postulated to be galactose deficient (Gd). However, glomerular IgA deposition can also occur in nonrenal diseases such as liver cirrhosis, psoriasis and inflammatory bowel disease (‘secondary IgAN’) or be an incidental finding in biopsies with other pathologies. A glomerulonephritis resembling IgAN can develop in patients with bacterial, mainly staphylococcal infections [staphylococcal infection-associated glomerulonephritis (SAGN)]. There are no specific histological features to distinguish between these, but differentiation is critical for appropriate management. The aim of this study was to investigate whether a recently described antibody to Gd-IgA1 (KM-55) could aid in differentiating primary IgAN from other conditions with glomerular IgA deposition, especially SAGN. Methods We performed a retrospective cohort study of patients who underwent kidney biopsy for clinical indications and were found to have glomerular IgA deposits. Results We evaluated 100 biopsies, including primary IgAN (n = 44), secondary IgAN (n = 27), SAGN (n = 13), incidental IgA deposition (n = 8) and lupus nephritis (n = 8). There was no difference in Gd-IgA staining intensity or the proportion of positive cases between primary and secondary IgAN. SAGN and cases with incidental IgA deposits had significantly lower Gd-IgA staining intensity than primary IgAN, but up to 69% of SAGN cases were positive (albeit weaker). Conclusions Gd-IgA staining is present not only in primary IgAN, but also in biopsies with secondary IgAN, SAGN and incidental IgA. Weak or negative staining may favor SAGN, especially in the setting of infection, or incidental IgA in the absence of nephritic symptoms or in the presence of other unrelated glomerular pathologies. However, positive staining for Gd-IgA alone is not specific enough for a diagnosis of primary IgAN.

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Mascarenhas, Ryan, Agnes B. Fogo, Russell W. Steele, and Radhakrishna Baliga. "IgA-Dominant Postinfectious Glomerulonephritis." Clinical Pediatrics 55, no. 9 (2016): 873–76. http://dx.doi.org/10.1177/0009922815608279.

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Kimura, Shinya, Akeyo Horie, Yoshiyuki Hiki, et al. "Nephrotic syndrome with crescent formation and massive IgA deposition following allogeneic bone marrow transplantation for natural killer cell leukemia/lymphoma." Blood 101, no. 10 (2003): 4219–21. http://dx.doi.org/10.1182/blood-2002-07-2290.

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Abstract We describe herein a case of nephrotic syndrome (NS) following allogeneic bone marrow transplantation (allo-BMT) for natural killer cell leukemia/lymphoma. Histologic studies defined the diagnosis as crescentic glomerulonephritis with massive immunoglobulin A (IgA) deposition, which has never been reported in NS cases following allo-BMT. Most of the massive infiltrated cells in the interstice were CD3+CD4−CD8+ T cells derived from the donor. We observed mesangial deposition of Haemophilus parainfluenza outer membrane (OMHP) antigen and decreased glycosylation of the IgA1 hinge in the recipient's samples is consistent with the recently reported pathogenesis of IgA nephropathy. Further, the titer of IgA antibody against the donor serum was as high as other IgA nephropathy cases. These findings suggest that NS and crescentic glomerulonephritis in this case occurred as one of the forms of chronic graft-versus-host disease (GVHD), and that IgA deposition was associated with H parainfluenza and decreased glycosylation of the IgA1 hinge.

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Hiki, Y., A. Tanaka, T. Kokubo, et al. "Analyses of IgA1 hinge glycopeptides in IgA nephropathy by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry." Journal of the American Society of Nephrology 9, no. 4 (1998): 577–82. http://dx.doi.org/10.1681/asn.v94577.

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This study was performed to analyze the structural variety of O-glycans on the IgA1 hinge in IgA nephropathy (IgAN). The IgA1 fragments containing the hinge glycopeptide (33-mer hinge peptide core (HP) + O-glycans) were separated from 13 IgAN patients, eight healthy control subjects, and 11 patients with other primary glomerulonephritides by pyridylethylation, trypsin treatment, and Jacalin affinity chromatography. Because of the use of Jacalin, only the Gal beta 1-3GalNAc residue containing IgA was analyzed. The molecular weights (MW) of the IgA1 fragments treated by the following sequential treatment by exoglycosidases were estimated using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry: (1) Sialidase treatment: the MW of the two observed peaks A and B were compatible with (A) HP + 4GalNAc + 4Gal and (B) HP + 5GalNAc + 4Gal. (2) Sialidase and galactosidase: the MW of the two identified peaks a and b were consistent with (a) HP + 4GalNAc and (b) HP + 5GalNAc. (3) Sialidase, galactosidase, and alpha-N-acetylgalactosaminidase. All subjects revealed one peak, indicating the 33-mer IgA1 hinge peptide core. The intensity rate of peak B/A was significantly decreased in the IgAN group (mean +/- SD, 1.01 +/- 0.08) compared with the negative control subjects (healthy group, 1.15 +/- 0.06, P = 0.0048; other glomerulonephritis group, 1.13 +/- 0.10, P = 0.0049; Scheffe's F test). These results suggested the presence of a defect in the Gal and/or GalNAc residues in the IgA1 hinge glycopeptides in IgAN.

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Cho, Won-Hee, Seon-Hwa Park, Seul-Ki Choi, 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 (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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Ghasempoor Dabaghi, Ghazal, Mehrdad Rabiee Rad, Muhammed Mubarak, Romina Amir Sardari, Golnaz K. Holm, and Hamid Nasri. "Infection-related immunoglobulin A nephropathy or IgA-dominant postinfectious glomerulonephritis; what is in a name?" Journal of Preventive Epidemiology 6, no. 2 (2021): e30-e30. http://dx.doi.org/10.34172/jpe.2021.30.

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Immunoglobulin A nephropathy (IgAN) is the most common glomerulonephritis worldwide. However, its incidence and prevalence vary depending on racial and geographical factors. IgAN is a highly heterogeneous disease with wide clinical and pathological variability. The defining and consistent feature of IgAN is the dominance or co-dominance of IgA deposits in the glomeruli on immunofluorescence (IF) microscopy. However, recent reports suggest that a number of post-infectious glomerulonephritis (PIGN) cases also exhibit dominance or co-dominance of IgA deposits on IF microscopy. Therefore, a debate has arisen on labeling these cases either as infection-related IgAN (a form of secondary IgAN) or IgA-dominant PIGN. Although the majority favors the later nosology, this issue has remained unresolved, as is the issue of labelling this condition as PIGN when, in fact, the infection is often intercurrent, and no latent period is found in this condition. This brief narrative review aims to discuss the salient features of this condition and issues related to its nomenclature.

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Yamaguchi, Hiroki, Shin Goto, Nao Takahashi, et al. "Aberrant mucosal immunoreaction to tonsillar microbiota in immunoglobulin A nephropathy." Nephrology Dialysis Transplantation 36, no. 1 (2020): 75–86. http://dx.doi.org/10.1093/ndt/gfaa223.

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Abstract Background Immunoglobulin A nephropathy (IgAN) is the most common glomerulonephritis worldwide, characterized by mesangial polymeric IgA1 deposition. IgAN is believed to develop owing to aberrant mucosal immunoreaction against commensals in the tonsils. However, the exact interrelation between pathogenic IgA and mucosal microbiota in IgAN patients is unclear. Methods Biopsy-proven IgAN or recurrent tonsillitis (RT) patients who had undergone tonsillectomy were enrolled. We used 16S ribosomal RNA gene amplicon sequencing with a flow cytometry-based bacterial cell sorting technique) and immunoglobulin repertoire sequencing of the IgA heavy chain to characterize IgA-coated bacteria of the tonsillar microbiota (IgA-SEQ) and their corresponding IgA repertoire. Furthermore, we fractionated patient serum using gel-filtration chromatography and performed flow cytometry-based analysis of IgA binding to bacteria cultured from incised tonsils. Results Tonsillar proliferation-inducing ligand and B-cell activating factor levels were significantly higher in IgAN than in RT patients. IgA-SEQ for tonsillar microbiota revealed the preferential binding ability of IgA to Bacteroidetes in IgAN tonsils compared with those from RT patients. Expression of immunoglobulin heavy (IGH) constant alpha 1 with IGH variable 3–30 was significantly higher in IgAN than that in RT, and positively correlated with the IgA-coated enrichment score of Bacteroidetes. Serum polymeric IgA, comprising high levels of GdIgA1, exhibited considerable binding to Bacteroidetes strains cultured from the tonsils of IgAN patients. Conclusions These findings provide evidence that aberrant mucosal immune responses to tonsillar anaerobic microbiota, primarily consisting of members of the phylum Bacteroidetes, are involved in IgAN pathophysiology.

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Savige, J. A., and M. Gallicchio. "IgA antimyeloperoxidase antibodies associated with crescentic IgA glomerulonephritis." Nephrology Dialysis Transplantation 7, no. 9 (1992): 952–55. http://dx.doi.org/10.1093/ndt/7.9.952.

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Suzuki, Yusuke, and Masahiro Muto. "Novel therapeutic approach targeting mucosal APRIL in IgA nephropathy." Impact 2019, no. 8 (2019): 62–64. http://dx.doi.org/10.21820/23987073.2019.8.62.

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Immunoglobulin A nephropathy (IgAN) is a form of glomerulonephritis. Also known as Berger's disease, it is the most common type of primary glomerulonephritis worldwide and is characterised by IgA deposits in the glomerulus. IgA nephropathy expert Prof. Yusuke Suzuki, who is based at Jutendo University Faculty of Medicine in Japan, explains that studies suggest that a number of factors, including aberrently-glycosylated IgA1, or its immune complex with glycan-specific IgG and IgA may play key roles in the pathogenesis of the condition. 'A proliferation-inducing ligand (APRIL) is one of protein froms the tumour necrosis factor (TNF) ligand superfamily. Research suggests a key role for this ligand in the long-term survival of plasma cells in the bone marrow and lymphoid tissues including mucosae and it is being explored as a potential target for the development of therapeutic options for autoimmune diseases and B cell malignancies. 'Recent studies into the pathological role of APRIL in IgAN, including our own recent findings, have led us to consider a new therapeutic approach,' he outlines. 'Our data using human samples from patients with IgAN and targeting APRIL in animal models has provided proof of concept (POC) of the beneficial effects of neutralising APRIL in IgAN.' Based on this work, clinical trials of new drugs that target APRIL have so far demonstrated exciting possibilities as one of the most promising new treatments for IgAN. A number of pharmaceutical companies are currently working on this and other, related drugs to treat the condition.

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Dissertations / Theses on the topic "Glomerulonephritis, IGA"

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Leung, Chi-kam Joseph, and 梁志錦. "The pathogenesis of IgA nephropathy: the roleof IgA molecule and the nature of IgA receptors." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29744908.

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Menahem, Solomon. "Apoptosis in the progression of IGA nephropathy." Monash University, Faculty of Medicine, Nursing and Health Sciences, 2003. http://arrow.monash.edu.au/hdl/1959.1/9449.

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Chan, Yuk-yee. "The role of angiotensin II and angiotensin receptors in the pathogenesis of IgA nephropathy." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36612248.

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Chan, Wai-long, and 陳慧朗. "The protective role of bone morphogenetic protein-7 against mesangial cell injury in IgA nephropathy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290872.

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Chan, Wai-long. "The protective role of bone morphogenetic protein-7 against mesangial cell injury in IgA nephropathy." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290872.

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Chan, Yuk-yee, and 陳玉儀. "The role of angiotensin II and angiotensin receptors in the pathogenesis of IgA nephropathy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B36612248.

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Sailer, Leif-Konradin. "Einfluss der sequentiellen Therapie mit Mycophenolsäure nach Induktionstherapie auf die Nierenfunktion bei progredienter IgA-Nephropathie." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-62294.

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Barday, Zibya. "Clinico-pathological correlation and outcome in patients with mesangioproliferative glomerulonephritis in Cape Town: A single centre study." Master's thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/29802.

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Background Glomerulonephritis is a major cause of end-stage kidney disease (ESRD) in Africa. There is scanty data on the clinico-pathological characteristics and outcome of the mesangioproliferative glomerulonephritides in Africa, despite the non-IgA subtype being reported as a common cause of nephrotic syndrome. This study will assess the outcome of patients with biopsy proven mesangioproliferative glomerulonephritis (MesPGN) from a single centre in Cape Town, South Africa. Methods The study is designed as 10-year retrospective analysis of patients with biopsy proven MesPGN. The MesPGN patterns were divided into non-IgA MesPGN and IgA nephropathy (IgAN), depending on the predominant type of immune deposit. Univariate cox regression analysis was used to determine factors associated with ESRD. Results Data of 109 patients with renal biopsy-proven MesPGN were included for the period between 2005-2014. The mean age at biopsy was 33.8 ±14.9 years, 53.2% were males, and 39.4% were black Africans. Clinically, 58.7% presented with nephrotic syndrome. On histology 79.8% had non-IgA MesPGN, and 20.2% had IgAN. Compared to the non-IgA group, most patients with IgAN were not treated with immunosuppression (72.7% vs. 40.2%; p=0.006). At the last visit, 10.1% reached ESRD (40.9% vs. 2.3%; p<0.0001) and 30.2% achieved complete remission (9.1% vs. 35.7%; p=0.015) for IgAN and non-IgA MesPGN respectively. The 5-year renal survival for IgAN and non-IgA MesPGN respectively, were: 63.3% vs. 97.6%, log rank p=0.001. Overall, hypertension (p=0.019), not receiving immunosuppression (p=0.046) and having IgAN (p=0.007) were independent predictors of progression to ESRD. Conclusion There is a significantly higher ESRD-free survival of patients with biopsy proven non-IgA MesPGN than IgAN. Whether this is related to the limited use of immunosuppressive therapy in IgAN patients or represents a true nature of the disease still requires further research.

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Jauhola, O. (Outi). "Henoch-Schönlein purpura in children." Doctoral thesis, Oulun yliopisto, 2012. http://urn.fi/urn:isbn:9789514297960.

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Abstract The aim of this work was to describe the clinical features and clinical course of Henoch-Schönlein purpura (HSP) in a prospective setting, to compare the efficacy of cyclosporine A (CyA) and methylprednisolone (MP) pulses for the treatment of severe HSP nephritis (HSN) and to study the effect of prophylactic prednisone treatment given at disease onset on the long-term outcome. A total of 223 children with newly diagnosed HSP were followed up prospectively for 6 months. Patients with severe HSN also had extrarenal symptoms more frequently during this time. Protein loss via the intestine was more common than previously described, occurring in 3% of the patients. HSN developed in the early course of the disease. The results suggest that weekly urine dipstick tests are indicated for 2 months after HSP onset and individually for over 6 months in cases of HSN or HSP recurrences. Prednisone did not affect the frequency or timing of the appearance of HSN. The efficacy of CyA and MP treatments was evaluated in a trial with a mean follow-up time of 6 years involving 24 paediatric patients (11 CyA, 13 MP), 15 of whom were randomized and 9 were treated according to the given protocol without randomization. Oral CyA was not inferior to intravenous MP pulses and proved to be an efficient, safe steroid-sparing treatment for severe HSN. All the CyA-treated patients achieved remission of nephrotic-range proteinuria within 3 months, while remission was achieved more slowly in the MP group and only in 6/13 (46%) with the initial treatment. There was no difference in the renal biopsy findings two years after initiation of the therapy. The 8-year outcome of HSP was assessed by means of a health questionnaire in 160 (94%) of the 171 former patients in the randomized placebo-controlled prednisone trial and in 138 (81%) with urine analysis and measurement of blood pressure. HSP carried a good prognosis, although skin relapses occurred up to a decade after the initial onset and could be accompanied by late-onset nephritis. Hypertension and/or renal abnormalities were recorded in 13% of the patients, being more frequent in those with an initial occurrence of HSN (OR 4.3, p=0.009, 95% CI 1.4–14.0) and warranting long-term follow-up of HSN patients. Early prednisone treatment did not affect the long-term outcome of HSP and should not be routinely used<br>Tiivistelmä Väitöskirjan tarkoituksena oli kuvata Henoch-Schönleinin purppuran (HSP) oireita ja taudinkulkua, verrata siklosporiini A:n (CyA) ja metyyliprednisolonipulssihoidon (MP-pulssihoidon) tehoa vaikean HSP-nefriitin (HSN) hoidossa ja selvittää taudin alussa annetun prednisonihoidon vaikutusta pitkäaikaisennusteeseen. Taudinkulkua seurattiin prospektiivisesti 6 kuukauden ajan diagnoosista 223 lapsipotilaan aineistossa. Potilailla, joilla oli vaikea HSN, esiintyi myös muita oireita pitempään. Proteiinin menetystä suolistoon esiintyi 3 %:lla, mikä on aiemmin kuvattua yleisempää. HSN ilmaantui taudin alkuvaiheessa. Tutkimustulosten perusteella viikoittainen virtsanäytteiden seuranta riittää 2 kuukauden ajan taudin alusta. Seuranta-aikaa tulee pidentää yksilöllisesti yli 6 kuukauden, jos potilaalla todetaan HSN tai HSP uusiutuu. Prednisonilla ei todettu olevan vaikutusta HSN:n yleisyyteen tai ilmaantumisaikaan. CyA- ja MP-hoitojen tehoa vaikeaan HSN:n seurattiin 24 lapsipotilaan aineistossa (11 CyA, 13 MP) 6 vuoden ajan. Potilaista 15 satunnaistettiin hoitoryhmiin ja 9 hoidettiin tutkimussuunnitelman mukaan ilman satunnaistamista. Suun kautta otettu CyA vaikutti hoidoista tehokkaammalta, sillä kaikilla potilailla nefroottistasoinen valkuaisvirtsaisuus hävisi kolmessa kuukaudessa. MP-hoitoa saaneista vain 6/13 (46 %) pääsi remissioon MP-hoidolla ja hekin CyA-hoidettuja hitaammin. Kaksi vuotta tutkimuksen alusta otettujen munuaisbiopsioiden histologisissa löydöksissä ei ollut eroa ryhmien välillä. Varhaisen kortisonihoidon pitkäaikaisvaikutuksia arvioitiin 8 vuotta lumekontrolloidun prednisonihoitotutkimuksen jälkeen, jolloin aiemman tutkimuksen 171 potilaasta 160 (94 %) vastasi terveyskyselyyn ja 138 (81 %) osallistui virtsa-analyysin ja verenpaineen mittauksen sisältäneeseen seurantatutkimukseen. HSP:n ennuste oli hyvä, vaikka taudin iho-oireet saattoivat uusia jopa 10 vuoden ajan ja taudin uusiutumisen yhteydessä saattoi ilmaantua myöhäinen HSN. Kohonnut verenpaine ja/tai valkuais-/verivirtsaisuus todettiin 13 %:lla. Ne olivat yleisempiä potilailla, joilla oli ollut HSN taudin alkuvaiheessa (OR 4.3, p=0.009, 95 % CI 1.4–14.0). Siten HSN-potilaiden pitkäaikaisseuranta on tarpeen. Varhaisella kortisonihoidolla ei ollut vaikutusta taudin ennusteeseen, minkä vuoksi kortisonia tulee käyttää HSP-potilaiden hoidossa vain harkiten

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WEINBERG, ISABELLE. "La nephropathie primitive a iga en 1994 (maladie de berger)." Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20095.

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Books on the topic "Glomerulonephritis, IGA"

1

IgA nephropathy: From molecules to men. Karger, 1999.

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International Symposium on IgA Nephropathy (11th 2006 Tokyo, Japan). IgA nephropathy today. Edited by Tomino Yasuhiko 1949-. Karger, 2007.

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Dixhoorn, Mieneke G. A. van. IgA in experimental kidney disease. University of Leiden, 1998.

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R, Clarkson A., and Woodroffe A. J, eds. IgA nephropathy: Pathogenesis and treatment. Karger, 1995.

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Fijter, Johan Willem de. The mucosal immune response in primary IgA nephropathy. University of Leiden, 1998.

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R, Clarkson A., ed. IgA nephropathy. Nijhoff, 1987.

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Recent Advances in IGA Nephropathy. World Scientific Publishing Company, 2009.

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Tomino, Y. IgA Nephropathy Today. S. Karger AG (Switzerland), 2007.

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Iga Nephropathy: The 25th Year (Contributions to Nephrology). S. Karger Publishers (USA), 1993.

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(Editor), Rosanna Coppo, and Licia Peruzzi (Editor), eds. Moderately Proteinuric IgA Nephropathy in the Young (Biomedical and Health Research, V. 44). Ios Pr Inc, 2000.

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Book chapters on the topic "Glomerulonephritis, IGA"

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Power, D. A., and J. G. Simpson. "IgA Nephropathy." In Glomerulonephritis. Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-2225-9_4.

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Michalk, D. "IgA-Glomerulonephritis." In Pädiatrische Nephrologie. Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56378-2_24.

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Appel, Gerald B. "IgA Nephropathy - Clinical Features, Pathogenesis, and Treatment." In Glomerulonephritis. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-27334-1_20-1.

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Kakajiwala, Aadil, and Kevin E. Meyers. "IgA Nephropathy and Henoch Schönlein Nephritis, Pediatric." In Glomerulonephritis. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-27334-1_21-1.

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Appel, Gerald B. "IgA Nephropathy: Clinical Features, Pathogenesis, and Treatment." In Glomerulonephritis. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_20.

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Kakajiwala, Aadil, and Kevin E. Meyers. "IgA Nephropathy and Henoch Schönlein Nephritis, Pediatric." In Glomerulonephritis. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_21.

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Floege, Jürgen, Claudia van Roeyen, Peter Boor, and Tammo Ostendorf. "The Role of PDGF-D in Mesangioproliferative Glomerulonephritis." In IgA Nephropathy Today. KARGER, 2007. http://dx.doi.org/10.1159/000102460.

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Rifai, Abdalla. "Pathogenesis of IgA Immune Complex-Mediated Glomerulonephritis." In Nephrology. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-35158-1_99.

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Maringhini, S., L. Belvedere, F. Lunetta, I. Cutaja, P. Carmina, and D. Natoli. "Serum IgA in Children with Acute Post-Infectious Glomerulonephritis." In Current Therapy in Nephrology. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0865-2_33.

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Emancipator, Steven N., and Michael E. Lamm. "IgA Nephropathy: Pathogenesis of the Most Common Form of Glomerulonephritis." In Pathology Reviews • 1990. Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-0485-5_8.

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