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Journal articles on the topic 'Glomerulonephritis, IGA'

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Published: 4 June 2021

Last updated: 4 February 2022

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1

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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3

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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4

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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6

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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9

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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Shimamura, Yoshinosuke, Takuto Maeda, Yufu Gocho, Yayoi Ogawa, and Hideki Takizawa. "IgA-dominant infection-related glomerulonephritis." Nefrología 38, no. 6 (2018): 669–70. http://dx.doi.org/10.1016/j.nefro.2018.02.002.

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Shimamura, Yoshinosuke, Takuto Maeda, Yufu Gocho, Yayoi Ogawa, and Hideki Takizawa. "IgA-dominant infection-related glomerulonephritis." Nefrología (English Edition) 38, no. 6 (2018): 669–70. http://dx.doi.org/10.1016/j.nefroe.2018.11.003.

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13

Hewitson, Timothy D., and Gavin J. Becker. "Interstitial Myofibroblasts in IgA Glomerulonephritis." American Journal of Nephrology 15, no. 2 (1995): 111–17. http://dx.doi.org/10.1159/000168813.

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14

Kaartinen, Kati, Jaana Syrjänen, Ilkka Pörsti, Aimo Harmoinen, Heini Huhtala, and Jukka Mustonen. "Metabolic Syndrome in IgA Glomerulonephritis." Nephron Extra 4, no. 2 (2014): 138–45. http://dx.doi.org/10.1159/000365591.

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Schmekel, Birgitta, Christian Svalander, Härje Bucht, and N. Gunnar Westberg. "Mesangial IgA Glomerulonephritis in Adults." Acta Medica Scandinavica 210, no. 1-6 (2009): 363–72. http://dx.doi.org/10.1111/j.0954-6820.1981.tb09832.x.

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Watanabe, Toru. "IgA deficiency and membranous glomerulonephritis." Pediatric Nephrology 21, no. 1 (2005): 131. http://dx.doi.org/10.1007/s00467-005-2059-6.

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Vas, Tibor, Tibor Kovács, István Késői, et al. "Treatment of IgA nephropathy." Orvosi Hetilap 152, no. 51 (2011): 2039–46. http://dx.doi.org/10.1556/oh.2011.29278.

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IgA nephropathy is the most common primary glomerulonephritis worldwide. The clinical spectrum covers a wide range of features from minor urinary abnormalities (asymptomatic hematuria and mild proteinuria with normal renal function) to acute and chronic renal insufficiency. Ideally, the goal of treatment would be to correct any defects in IgA1 glycosylation and to modify mesangial deposition or removal of IgA1 deposits. There are only a few randomized controlled trials in IgA nephropathy; for this reason most treatment options are largely based on expert opinion. Authors discuss therapeutic options of different clinical pictures and the optimized renoprotective treatment of all IgA nephropathy patients. Orv. Hetil., 2011, 152, 2039–2046.

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Wehbi, Batoul, Virginie Pascal, Lina Zawil, Michel Cogné, and Jean-Claude Aldigier. "History of IgA Nephropathy Mouse Models." Journal of Clinical Medicine 10, no. 14 (2021): 3142. http://dx.doi.org/10.3390/jcm10143142.

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IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world. It was first described in 1968 by Jean Berger and Nicole Hinglais as the presence of intercapillary deposits of IgA. Despite this simple description, patients with IgAN may present very broad clinical features ranging from the isolated presence of IgA in the mesangium without clinical or biological manifestations to rapidly progressive kidney failure. These features are associated with a variety of histological lesions, from the discrete thickening of the mesangial matrix to diffuse cell proliferation. Immunofluorescence on IgAN kidney specimens shows the isolated presence of IgA or its inconsistent association with IgG and complement components. This clinical heterogeneity of IgAN clearly echoes its complex and multifactorial pathophysiology in humans, inviting further analyses of its various aspects through the use of experimental models. Small-animal models of IgAN provide the most pertinent strategies for studying the multifactorial aspects of IgAN pathogenesis and progression. Although only primates have the IgA1 subclass, several murine models have been developed in which various aspects of immune responses are deregulated and which are useful in the understanding of IgAN physiopathology as well as in the assessment of IgAN therapeutic approaches. In this manuscript, we review all murine IgAN models developed since 1968 and discuss their remarkable contribution to understanding the disease.

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Okabayashi, Yusuke, Nobuo Tsuboi, Naoko Nakaosa та ін. "A Case of Hepatic Glomerulosclerosis with Monoclonal IgA1-κ Deposits". Case Reports in Nephrology 2018 (1 жовтня 2018): 1–5. http://dx.doi.org/10.1155/2018/4748357.

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Glomerular immunoglobulin A (IgA) deposition is a common finding in hepatic glomerulosclerosis; thus, this disease is also called hepatic IgA nephropathy. However, only a small number of patients with hepatic IgA nephropathy have active glomerular lesions, so functional decline is slow in most cases. In this report, we describe a 60-year-old man who developed nephrotic syndrome and progressive renal impairment during follow-up for alcoholic liver cirrhosis. A renal biopsy showed a membranoproliferative glomerulonephritis-like pattern; diffuse double-contours of the glomerular basement membrane and focal active glomerular lesions with moderate-to-severe endocapillary proliferation and fibrocellular crescents. Immunofluorescence findings revealed granular staining for monoclonal IgA1-κ and C3 on the peripheral capillary walls. Laboratory examinations did not reveal any definitive evidence of myeloproliferative disorders. Therefore, this case may represent a previously unrecognized etiology of renal injury in relation to liver cirrhosis that is characterized by monoclonal IgA1-κ deposits and proliferative glomerulonephritis.

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Lai, K. N., and A. Y. M. Wang. "IgA nephropathy: common nephritis leading to end-stage renal failure." International Journal of Artificial Organs 17, no. 9 (1994): 457–60. http://dx.doi.org/10.1177/039139889401700902.

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IgA nephropathy (IgAN) characterized by mesangial proliferative glomerulonephritis with predominant mesangial IgA deposition is the commonest glomerulonephritis worldwide. In contrast to the initial report indicated a favorable prognosis, subsequent reports have shown a highly variable outcome leading to end-stage renal failure (ESRF) in a significant proportion of patients. Many centers report a high incidence (ranging from 10-22%) of patients with idiopathic IgAN amongst the total population of patients on maintenance dialysis. Most of these patients develop ESRF at their middle-age and hence, will pose a significant and important workload in the dialysis and transplantation programme. Because IgAN is a disease with a variable rate of progression leading to chronic renal failure amongst younger patients and with neither effective nor specific treatment, identification of the clinical and pathologic prognostic indicators for these patients is of paramount importance in planning the long-term renal replacement program.

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Rodriguez-Soriano, J., A. Arrieta, A. Vallo, M. J. Sebastian, J. C. Vitoria, and M. D. Masdevall. "IgA ANTIGLIADIN ANTIBODIES IN CHILDREN WITH IgA MESANGIAL GLOMERULONEPHRITIS." Lancet 331, no. 8594 (1988): 1109–10. http://dx.doi.org/10.1016/s0140-6736(88)91928-9.

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Garces, Christopher Cantoria, Nora Hernandez Garcilazo, Akhil Sharma, and Georgette Nader. "Severe psoriasis presenting with rapidly progressive (crescentic) IgA-predominant glomerulonephritis." BMJ Case Reports 14, no. 5 (2021): e242627. http://dx.doi.org/10.1136/bcr-2021-242627.

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IgA nephropathy (IgAN) is commonly associated with psoriasis; however, psoriasis presenting with crescentic IgAN is uncommon. A 49-year-old man with erythrodermic psoriasis with arthritis and stage 2 chronic kidney disease presented to the emergency department with worsening peripheral oedema and difficulty breathing. The patient had been hospitalised previously for a psoriasis flare. He was found to have an acute kidney injury on chronic kidney disease and was diagnosed with crescentic IgA glomerulonephritis on his first hospitalisation. He was treated with corticosteroids and was discharged stable with a plan to start cyclophosphamide in the outpatient setting. On his current hospitalisation, cyclophosphamide was added to his corticosteroids. Crescentic IgAN is rare. Its management has been based largely on observational studies. Our case highlights the importance of starting combined corticosteroids and cyclophosphamide early in crescentic IgAN and that corticosteroid monotherapy is insufficient in controlling disease progression.

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Launay, Pierre, Béatrice Grossetête, Michelle Arcos-Fajardo та ін. "Fcα Receptor (Cd89) Mediates the Development of Immunoglobulin a (Iga) Nephropathy (Berger's Disease)". Journal of Experimental Medicine 191, № 11 (1999): 1999–2010. http://dx.doi.org/10.1084/jem.191.11.1999.

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The pathogenesis of immunoglobulin A (IgA) nephropathy (IgAN), the most prevalent form of glomerulonephritis worldwide, involves circulating macromolecular IgA1 complexes. However, the molecular mechanism(s) of the disease remain poorly understood. We report here the presence of circulating soluble FcαR (CD89)-IgA complexes in patients with IgAN. Soluble CD89 was identified as a glycoprotein with a 24-kD backbone that corresponds to the expected size of CD89 extracellular domains. To demonstrate their pathogenic role, we generated transgenic (Tg) mice expressing human CD89 on macrophage/monocytes, as no CD89 homologue is found in mice. These mice spontaneously developed massive mesangial IgA deposition, glomerular and interstitial macrophage infiltration, mesangial matrix expansion, hematuria, and mild proteinuria. The molecular mechanism was shown to involve soluble CD89 released after interaction with IgA. This release was independent of CD89 association with the FcRγ chain. The disease was induced in recombination activating gene (RAG)2−/− mice by injection of serum from Tg mice, and in severe combined immunodeficiency (SCID)-Tg mice by injection of patients' IgA. Depletion of soluble CD89 from serum abolished this effect. These results reveal the key role of soluble CD89 in the pathogenesis of IgAN and provide an in vivo model that will be useful for developing new treatments.

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Sallustio, Fabio, Claudia Curci, Vincenzo Di Leo, Anna Gallone, Francesco Pesce, and Loreto Gesualdo. "A New Vision of IgA Nephropathy: The Missing Link." International Journal of Molecular Sciences 21, no. 1 (2019): 189. http://dx.doi.org/10.3390/ijms21010189.

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IgA Nephropathy (IgAN) is a primary glomerulonephritis problem worldwide that develops mainly in the 2nd and 3rd decade of life and reaches end-stage kidney disease after 20 years from the biopsy-proven diagnosis, implying a great socio-economic burden. IgAN may occur in a sporadic or familial form. Studies on familial IgAN have shown that 66% of asymptomatic relatives carry immunological defects such as high IgA serum levels, abnormal spontaneous in vitro production of IgA from peripheral blood mononuclear cells (PBMCs), high serum levels of aberrantly glycosylated IgA1, and an altered PBMC cytokine production profile. Recent findings led us to focus our attention on a new perspective to study the pathogenesis of this disease, and new studies showed the involvement of factors driven by environment, lifestyle or diet that could affect the disease. In this review, we describe the results of studies carried out in IgAN patients derived from genomic and epigenomic studies. Moreover, we discuss the role of the microbiome in the disease. Finally, we suggest a new vision to consider IgA Nephropathy as a disease that is not disconnected from the environment in which we live but influenced, in addition to the genetic background, also by other environmental and behavioral factors that could be useful for developing precision nephrology and personalized therapy.

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Esteve Cols, Clara, Freddzia-Amanda Graterol Torres, Bibiana Quirant Sánchez, et al. "Immunological Pattern in IgA Nephropathy." International Journal of Molecular Sciences 21, no. 4 (2020): 1389. http://dx.doi.org/10.3390/ijms21041389.

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The current gold-standard diagnostic technique for IgA nephropathy (IgAN), the leading form of primary glomerulonephritis, is renal biopsy. CD89 (the main IgA receptor) is expressed on the surface of monocytes and plays a role in disease pathogenesis. Immunocomplexes formed by sCD89 (soluble form) and Gd-IgA1 are related to disease prognosis. We hypothesize that reduced CD89 surface expression on monocytes may be a marker of disease severity. We aimed to analyze leukocyte subpopulations in peripheral blood and CD89 surface expression on monocytes in a prospective study of 22 patients and 12 healthy subjects (HS). Leukocyte subpopulations and CD89 expression were analyzed by flow cytometry. IgAN patients had a higher percentage of activated and effector memory CD4+ and CD8+ T lymphocytes, a lower percentage of transitional B lymphocytes and plasmablasts, and a higher percentage of CD56dimCD16+ NK cells and myeloid dendritic cells compared with HS. Correlations between reduced CD89 expression levels on nonclassical monocytes, histological findings of a poor prognosis on renal biopsy and baseline renal function were observed. IgAN patients show a characteristic immunological pattern in peripheral blood. A reduced expression level of CD89 on nonclassical monocytes identifies patients with a worse renal prognosis.

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Chan, S. H., G. Ku, and R. Sinniah. "HLA and Chinese IgA Mesangial Glomerulonephritis." Tissue Antigens 17, no. 3 (2008): 351–52. http://dx.doi.org/10.1111/j.1399-0039.1981.tb00712.x.

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CHENG, Ignatius KP. "Non-immune therapy of IgA glomerulonephritis." Nephrology 3, no. 1 (1997): 109–11. http://dx.doi.org/10.1111/j.1440-1797.1997.tb00199.x.

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Katz, Allan, and Patricia Chan. "IgA Glomerulonephritis with Irregular IntramembranousDense Deposits." Nephron 80, no. 3 (1998): 340–43. http://dx.doi.org/10.1159/000045195.

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Altunkova, J. P., S. K. Bocheva, D. N. Terziivanov, and N. J. Belovezhdov. "Lymphocyte subpopulations in mesangial IgA glomerulonephritis." International Urology and Nephrology 20, no. 3 (1988): 307–11. http://dx.doi.org/10.1007/bf02549521.

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30

Steciwko, A., Z. Szewczyk, W. Letachowicz, and M. Steciwko. "Chronic glomerulonephritis with massive IgA deposits." International Urology and Nephrology 17, no. 3 (1985): 269–79. http://dx.doi.org/10.1007/bf02085414.

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31

Lhotta, K., H. P. Neumayer, M. Joannidis, D. Geissler, and P. KöNig. "Renal expression of intercellular adhesion molecule-1 in different forms of glomerulonephritis." Clinical Science 81, s25 (1991): 477–81. http://dx.doi.org/10.1042/cs0810477.

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1. Expression of intercellular adhesion molecule-1 was investigated in five normal kidneys and 47 renal biopsies with the use of monoclonal antibody 7F7 and immunoperoxidase staining. 2. In the normal kidney, intercellular adhesion molecule-1 was expressed on endothelial cells of glomerular and peritubular capillaries, on Bowman's capsule, on some interstitial cells and weakly in the mesangium. 3. Increased glomerular staining was detected in early cases of rapidly progressing glomerulonephritis (5/8) and in some cases of non-IgA mesangioproliferative glomerulonephritis (5/9), IgA nephropathy (3/5), Henoch-Schoenlein purpura (2/2), lupus nephritis (5/6) and focal segmental glomerulosclerosis (1/3). A decrease in intercellular adhesion molecule-1 expression was noted in advanced rapidly progressive glomerulonephritis (3/8), two cases of membraneous nephropathy, one severe mesangioproliferative glomerulonephritis biopsy, the two membranoproliferative glomerulonephritis biopsies and in sclerotic loops in focal segmental glomerulosclerosis. 4. Expression de novo on tubular epithelial cells occurred in rapidly progressive glomerulonephritis, in membranoproliferative glomerulonephritis, and to a lesser extent in some cases of membranous nephropathy, minimal change disease, IgA nephropathy, focal segmental glomerulosclerosis, a severe case of mesangioproliferative glomerulonephritis and in the mixed essential cryoglobulinaemia case. In 63% of positive tubuli, intraluminal cells which expressed CD18, the common β-chain of leucocyte-function-associated antigen-1, Mac-1 and p150,95, were present. 5. Intercellular adhesion molecule-1 was also found on the majority (59%) of infiltrating mononuclear cells in all forms of glomerulonephritis.

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Novak, Jan. "Induction of IgA Deposits and Glomerulonephritis by IgA Rheumatoid Factor." Journal of the American Society of Nephrology 23, no. 3 (2012): 371–73. http://dx.doi.org/10.1681/asn.2012010076.

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Otani, Masako, Junichiro Nakata, Masao Kihara, et al. "O-Glycosylated IgA Rheumatoid Factor Induces IgA Deposits and Glomerulonephritis." Journal of the American Society of Nephrology 23, no. 3 (2011): 438–46. http://dx.doi.org/10.1681/asn.2011070701.

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Wen, Yao-Ko, and Mei-Ling Chen. "Discrimination between postinfectious IgA-dominant glomerulonephritis and idiopathic IgA nephropathy." Renal Failure 32, no. 5 (2010): 572–77. http://dx.doi.org/10.3109/08860221003753331.

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Brodsky, Sergey V., Tibor Nadasdy, Clarissa Cassol, and Anjali Satoskar. "IgA Staining Patterns Differentiate Between IgA Nephropathy and IgA-Dominant Infection-Associated Glomerulonephritis." Kidney International Reports 5, no. 6 (2020): 909–11. http://dx.doi.org/10.1016/j.ekir.2020.03.029.

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Al Harash, Abdalhamid, Stephanie Saeli, Michael Lucke, and Swati Arora. "IgA Vasculitis Nephritis: A Case Series and Comparison of Treatment Guidelines." Case Reports in Rheumatology 2020 (December 2, 2020): 1–5. http://dx.doi.org/10.1155/2020/8863858.

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Immunoglobulin A (IgA) vasculitis nephritis (IgAVN) and IgA nephropathy (IgAN) share many pathological parallels and are viewed as related diseases by many groups. Current treatment guidelines remain vague, controversial, and without consensus, especially regarding the role of immunosuppressive medications. We present five cases of IgAVN encountered at our tertiary care center between 2016 and 2020, which were treated with different immunosuppression regimens. Infection was the leading cause of death in this series. These cases provide evidence that IgAVN should be distinguished from IgAN on a spectrum of IgA-associated glomerulonephritis. The outcomes presented herein suggest that the morbidity and systematic involvement IgAVN is greater than previously believed and that these substantial risks should be reflected in contemporary treatment guidelines.

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Zhang, Xuecheng, Ning Su, and Dong Chen. "Expressions of CD3 and CD4 T Cells in Peripheral Blood of Patients with Immunoglobulin A Nephropathy and Their Clinical Significance." Journal of Biomaterials and Tissue Engineering 9, no. 6 (2019): 865–69. http://dx.doi.org/10.1166/jbt.2019.2050.

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Immunoglobulin A nephropathy (IgAN) is a primary glomerulonephritis characterized by abnormal immune response-mediated deposition of polymeric IgA (pIgA) in mesangium. As a type of important immune cells, the relationship of CD3 or CD4 with the pathogenesis of IgAN remains poorly understood. In this study, 38 patients with IgAN, 7 patients with idiopathic membranous nephropathy (MN) and 46 healthy adults without history of kidney disease were enrolled. Peripheral blood was collected for further evaluation of the expressions of CD3 and CD4 and IgA by flow cytometry, quantitative polymerase chain reaction (qPCR) and Western blot. Meanwhile, the expression of IgA was detected by ELISA. The result showed that expression of CD3 T cells was down-regulated in patients with IgAN, while amounts of CD4 T cells and IgA level were significantly increased compared to normal control (P < 0.05). However, no signficant changes in CD3, CD4 T cells were found in patients with MN. Our study demonstrates that CD3 and CD4 T cells as well as IgA are involved in the pathogenesis of IgAN and these targets might be beneficial for the treatment of IgAN.

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Schena, F. P., L. Gesualdo, and V. Montinaro. "Immunopathological aspects of immunoglobulin A nephropathy and other mesangial proliferative glomerulonephritides." Journal of the American Society of Nephrology 2, no. 10 (1992): S167. http://dx.doi.org/10.1681/asn.v210s167.

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Immunoglobulin A nephropathy (IgAN) is an immune complex (IC) glomerulonephritis (GN) that represents one of the most common forms of primary glomerular disease. Proliferation of mesangial cells and the increase of mesangial matrix are histological hallmarks of mesangioproliferative GN. Increased serum levels of IgA, polymeric IgA, IgA rheumatoid factor, IgA-IC, and spontaneous or pokeweed mitogen-induced production of IgA by peripheral blood mononuclear cells are major humoral immune alterations reported in IgAN. Recently, we focused on the role of cytokines and growth factors in the mediation of glomerular injury. Platelet-derived growth factor, transforming growth factor beta, interleukin (IL)-1 and IL-6 are expressed by and act on mesangial cells. Increased expression of platelet-derived growth factor was found in both an active model of IgAN and in renal biopsies of patients with proliferative GN. A strict correlation between increased expression of B-chain mRNA and mesangial proliferation was found. Cytokines such as IL-1, interferon gamma, and IL-6, released by infiltrating mononuclear cells or produced locally by mesangial cells, affect the glomerular response to IgA-IC. In a passive murine experimental model of IgAN, IL-1 and interferon gamma increased mesangial hypercellularity, whereas IL-6 was highly pathogenic when associated to IL-1. In conclusion, classical immunological mechanisms in mesangial GN could interact with other pathways involving cytokines and growth factors in the progression of glomerular injury.

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Chung, Hyun Chul, Jongha Park, and Jong Soo Lee. "Treatment of Posttransplantation Recurrent Glomerulonephritis: IgA Nephropathy, Membranous Nephropathy, Membranoproliferative Glomerulonephritis." Journal of the Korean Society for Transplantation 25, no. 2 (2011): 81. http://dx.doi.org/10.4285/jkstn.2011.25.2.81.

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Iitaka, Kikuo, Asako Yamamoto, Natsuko Ogawa, Toru Sekine, Shinya Tamai, and Osamu Motoyama. "IgA-associated glomerulonephritis with membranoproliferative glomerulonephritis-like pattern in two children." Clinical and Experimental Nephrology 7, no. 4 (2003): 284–89. http://dx.doi.org/10.1007/s10157-003-0253-z.

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Reily, Colin, Hiroyuki Ueda, Zhi-Qiang Huang, et al. "Cellular Signaling and Production of Galactose-Deficient IgA1 in IgA Nephropathy, an Autoimmune Disease." Journal of Immunology Research 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/197548.

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Immunoglobulin A (IgA) nephropathy (IgAN), the leading cause of primary glomerulonephritis, is characterized by IgA1-containing immunodeposits in the glomeruli. IgAN is a chronic disease, with up to 40% of patients progressing to end-stage renal disease, with no disease-specific treatment. Multiple studies of the origin of the glomerular immunodeposits have linked elevated circulating levels of aberrantly glycosylated IgA1 (galactose-deficient in someO-glycans; Gd-IgA1) with formation of nephritogenic Gd-IgA1-containing immune complexes. Gd-IgA1 is recognized as an autoantigen in susceptible individuals by anti-glycan autoantibodies, resulting in immune complexes that may ultimately deposit in the kidney and induce glomerular injury. Genetic studies have revealed that an elevated level of Gd-IgA1 in the circulation of IgAN patients is a hereditable trait. Moreover, recent genome-wide association studies have identified several immunity-related loci that associated with IgAN. Production of Gd-IgA1 by IgA1-secreting cells of IgAN patients has been attributed to abnormal expression and activity of several key glycosyltransferases. Substantial evidence is emerging that abnormal signaling in IgA1-producing cells is related to the production of Gd-IgA1. As Gd-IgA1 is the key autoantigen in IgAN, understanding the genetic, biochemical, and environmental aspects of the abnormal signaling in IgA1-producing cells will provide insight into possible targets for future disease-specific therapy.

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Lai, Kar Neng, Joseph C. K. Leung, and Sydney C. W. Tang. "The Treatment of IgA Nephropathy." Kidney Diseases 1, no. 1 (2015): 19–26. http://dx.doi.org/10.1159/000381508.

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Background: IgA nephropathy (IgAN) is a very common glomerulonephritis worldwide. Nevertheless, treatment options for primary IgAN are still largely based on opinion or weak evidence. There is a lack of large randomized controlled trials (RCT) that provide a definitive immunosuppressive protocol for IgAN. The recent KDIGO Clinical Practice Guidelines for Glomerulonephritis have assigned low levels of evidence for almost all recommendations and suggestions related to this nephropathy. Summary: In this article, we review different treatment options and emphasize that the key to therapeutic decision-making is the assessment of an individual's prognosis. The risk of disease progression is closely related to clinical parameters such as proteinuria, hypertension, and impaired glomerular filtration rate. For patients with minor urinary abnormalities, the mainstay of treatment is long-term regular follow-up to detect renal progression and hypertension. Optimized supportive care aiming to maintain proteinuria <1 g/day is preferred in the typical patient presenting with microhematuria, significant but nonnephrotic proteinuria, hypertension, and variable degrees of renal failure. The atypical patient with overt nephritic syndrome or rapidly progressive kidney injury that represents a vasculitic form of IgAN should be treated with immunosuppression. Finally, the variant of overlapping syndrome of IgAN and lipoid nephrosis that runs a good prognosis should be treated as lipoid nephrosis. Key Message: The treatment of IgAN should be structured according to the clinical scenario.

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Di Leo, Vincenzo, Patrick J. Gleeson, Fabio Sallustio, et al. "Rifaximin as a Potential Treatment for IgA Nephropathy in a Humanized Mice Model." Journal of Personalized Medicine 11, no. 4 (2021): 309. http://dx.doi.org/10.3390/jpm11040309.

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IgA Nephropathy (IgAN) is the most common glomerulonephritis worldwide, characterized by the mesangial deposition of abnormally glycosylated IgA1 (Gd-IgA). The production of Gd-IgA occurs in mucose-associated lymphoid tissue (MALT). The microbiota plays a role in MALT modulation. Rifaximin (NORMIX®), a non-absorbable oral antibiotic, induces positive modulation of the gut microbiota, favoring the growth of bacteria beneficial to the host. Here, we evaluate the effect of rifaximin on a humanized mice model of IgAN (α1KI-CD89Tg). Methods: The α1KI-CD89Tg mice were treated by the vehicle (olive oil) or rifaximin (NORMIX®). Serum levels of hIgA, hIgA1–sCD89, and mIgG–hIgA1 immune complexes were determined. Glomerular hIgA1 deposit and CD11b+ cells recruitment were revealed using confocal microscopy. Furthermore, the mRNA of the B-Cell Activating Factor (BAFF), polymeric immunoglobulin receptor (pIgR), and Tumor Necrosing Factor-α (TNF-α) in gut samples were detected by qPCR. Results: Rifaximin treatment decreased the urinary protein-to-creatinine ratio, serum levels of hIgA1–sCD89 and mIgG–hIgA1 complexes, hIgA1 glomerular deposition, and CD11b+ cell infiltration. Moreover, rifaximin treatment decreased significantly BAFF, pIgR, and TNF-α mRNA expression. Conclusions: Rifaximin decreased the IgAN symptoms observed in α1KI-CD89Tg mice, suggesting a possible role for it in the treatment of the disease.

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Liu, Youxia, Jie Zheng, Na Zhao, Junya Jia, and Tiekun Yan. "ELL2 Is Downregulated and Associated with Galactose-Deficient IgA1 in IgA Nephropathy." Disease Markers 2019 (June 4, 2019): 1–7. http://dx.doi.org/10.1155/2019/2407067.

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Background. Galactose-deficient IgA1 (Gd-IgA1) is an important causal factor in IgA nephropathy; however, the underlying mechanism for the production of Gd-IgA1 is unknown. The elongation factor for RNA polymerase II (ELL2), which encoded a key component of the superelongation complex (SEC), drives secretory-specific Ig mRNA production. Methods. We enrolled 21 patients with IgAN, 18 healthy controls, and 20 patients with non-IgAN glomerulonephritis. The differential expression of ELL2 was compared using publically available data from Gene Expression Omnibus (GEO) datasets. The relationship between ELL2 expressions and galactose-deficient IgA1 (Gd-IgA1) levels in serum were also studied. At last, the results were validated by shELL2 treatment experiment. Results. We found that the number of CD19+ B cells was increased in IgAN patients compared to healthy controls. The expression level of ELL2 in patients with IgAN was significantly lower than that of healthy control and disease control. Consistent with present results, the lower ELL2 expression in IgAN patients was observed in microarray expression profiles from GEO datasets. Pearson correlation analysis showed that ELL2 expression negatively correlated with Gd-IgA1 levels. Furthermore, in an in vitro experiment, we found that loss of ELL2 function in human B lymphoma DAKIKI cells, an IgA1-producing cell line, increased the levels of Gd-IgA1, which confirmed that ELL2 modulated the levels of Gd-IgA1. Conclusion. Our findings implied that decreased ELL2 expression was negatively correlated with the numbers of B cells and aberrant glycosylation of IgA1 in IgAN.

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Satoskar, Anjali A., Gyongyi Nadasdy, Jose Antonio Plaza, et al. "Staphylococcus Infection-Associated Glomerulonephritis Mimicking IgA Nephropathy." Clinical Journal of the American Society of Nephrology 1, no. 6 (2006): 1179–86. http://dx.doi.org/10.2215/cjn.01030306.

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Longano, Anthony. "Concurrent anti-GBM disease and IgA glomerulonephritis." Pathology 51, no. 3 (2019): 336–38. http://dx.doi.org/10.1016/j.pathol.2018.09.065.

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Locatelli, Francesco, Lucia Del Vecchio, and Claudio Pozzi. "IgA glomerulonephritis: beyond angiotensin-converting enzyme inhibitors." Nature Clinical Practice Nephrology 2, no. 1 (2006): 24–31. http://dx.doi.org/10.1038/ncpneph0055.

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Kincaid-Smith, Priscilla, Kathy Nicholls, and Ian Birchall. "Polymorphs infiltrate glomeruli in mesangial IgA glomerulonephritis." Kidney International 36, no. 6 (1989): 1108–11. http://dx.doi.org/10.1038/ki.1989.308.

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Koo, Tai Yeon, Gheun-Ho Kim, and Hyang Park. "Clinicopathologic Features of IgA-Dominant Postinfectious Glomerulonephritis." Korean Journal of Pathology 46, no. 2 (2012): 105. http://dx.doi.org/10.4132/koreanjpathol.2012.46.2.105.

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Waikhom, R., D. Sarkar, K. Patil, et al. "Non-IgA mesangioproliferative glomerulonephritis: a benign entity?" Nephrology Dialysis Transplantation 27, no. 6 (2011): 2322–27. http://dx.doi.org/10.1093/ndt/gfr653.

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