The Effect of Tonsillectomy and Its Postoperative Clinical Course in IgA Nephropathy with Chronic Tonsillitis

Masuda, Yu; Tamura, S.; Sugiyama, Nobuyoshi

doi:10.1159/000421745

Cited by 6 publications

(5 citation statements)

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“…However, on the basis of the recent works, the tonsils are thought to be a source organ of serum IgA in patients with IgAN. In patients with IgAN, serum IgA levels decrease after tonsillectomy and when the tonsillar lymphocytes are cultured under mitogenic stimulation, the production of polymeric IgA is enhanced…”

Section: Iga Overproduction In Tonsils Of Patients With Iganmentioning

confidence: 99%

“…In patients with IgAN, serum IgA levels decrease after tonsillectomy. 25 The number of multimeric IgA-producing cells with a J chain is increased in the tonsils with IgAN, 26,27 and when the tonsillar lymphocytes are cultured under mitogenic stimulation, the production of polymeric IgA is enhanced. 28 Furthermore, in the germinal centers of the tonsil tissues in patients with IgAN, the number of CD5-positive B cells involved in IgA1 production increase.…”

Section: Tonsils Of Patients With Iganmentioning

confidence: 99%

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Recent advances in the immunological understanding of association between tonsil and immunoglobulin A nephropathy as a tonsil‐induced autoimmune/inflammatory syndrome

Harabuchi

Takahara

2019

Immunity Inflam & Disease

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Introduction Immunoglobulin A nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide. It is well known that upper respiratory tract infections, particularly acute tonsillitis, often worsen IgAN. Recent many clinical studies clearly show that tonsillectomy with steroid pulse therapy is the effective treatments for IgAN patients. Recently, the immunological evidence of association between tonsil and IgAN has been reported. Methods In this review, the mechanism underlying the onset of IgAN, as a tonsil‐induced autoimmune/inflammatory syndrome (TIAS), is outlined with the main focus on the authors' research results. Results In the tonsils of patients with IgAN, hyperimmune response to the unmethylated deoxycytidyl‐deoxyguanosine oligodeoxynucleotides (CpG‐ODN) take place, resulting in hyperproduction of interferon‐γ. The hyperproduction is followed by both overproduction of mutated IgA via B‐cell activating factor (BAFF)/a proliferation‐inducing ligand (APRIL)‐mediated pathways and overexpression of T‐cell receptor Vβ6, CXCR3, and CX3CR1 on tonsillar T cells. These IgA and T cells home to the kidney via the systemic circulation, resulting in nephritis of IgAN. Conclusions Scientific evidence supporting the use of tonsillectomy has gradually accumulated. We hope that many additional researchers will publish new evidence linking the tonsils and kidneys in the future.

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Section: Iga Overproduction In Tonsils Of Patients With Iganmentioning

confidence: 99%

Section: Tonsils Of Patients With Iganmentioning

confidence: 99%

Recent advances in the immunological understanding of association between tonsil and immunoglobulin A nephropathy as a tonsil‐induced autoimmune/inflammatory syndrome

Harabuchi

Takahara

2019

Immunity Inflam & Disease

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“…). After tonsillectomy the episodes of macrohaematuria might have been reduced , but there was no clear benefit in reducing the disease progression . However, tonsillectomy affected only a part of the widespread MALT.…”

Section: Treatment In Non‐progressive Disease and Supportive Therapymentioning

confidence: 99%

“…1). After tonsillectomy the episodes of macrohaematuria might have been reduced [106][107][108], but there was no clear benefit in reducing the disease progression [77,90,109]. Table 2).…”

Section: Tonsillectomy and Mucosa-associated Lymphoid Tissue (Malt)mentioning

confidence: 99%

Why, when and how should immunosuppressive therapy considered in patients with immunoglobulin A nephropathy?

Rasche

Keller

Rasche³

et al. 2016

Clinical and Experimental Immunology

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SummaryIgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Lifelong mesangial deposition of IgA1 complexes subsist inflammation and nephron loss, but the complex pathogenesis in detail remains unclear. In regard to the heterogeneous course, classical immunosuppressive and specific therapeutic regimens adapted to the loss of renal function will here be discussed in addition to the essential common renal supportive therapy. Renal supportive therapy alleviates secondary, surrogate effects or sequelae on renal function and proteinuria of high intraglomerular pressure and subsequent nephrosclerosis by inhibition of the renin angiotensin system (RAASB). In patients with physiological (DGFR < 1Á5 ml/min/year) or mild (DGFR 1Á5-5 ml/min/year) decrease of renal function and proteinuric forms (> 1 g/day after RAASB), corticosteroids have shown a reduction of proteinuria and might protect further loss of renal function. In patients with progressive loss of renal function (DGFR > 3 ml/min within 3 months) or a rapidly progressive course with or without crescents in renal biopsy, cyclophosphamide with high-dose corticosteroids as induction therapy and azathioprine maintenance has proved effective in one randomized controlled study of a homogeneous cohort in loss of renal function (DGFR). Mycophenolic acid provided further maintenance in non-randomized trials. Differentiated, precise, larger, randomized, placebo-controlled studies focused on the loss of renal function in the heterogeneous forms of IgAN are still lacking. Prospectively, fewer toxic agents will be necessary in the treatment of IgAN.

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“…The contribution of tonsillar IgA1-producing cells to the total pool of IgA produced in the human body must be minimal considering the absolute number of cells in tonsils versus the mucosal tissues such as gut, bone marrow, lymph nodes, and spleen. However, most IgAN patients indeed showed a decrease in serum IgA after tonsillectomy, in association with improvement of clinical manifestations [89–91]. Moreover, tonsillar B cells in IgAN patients produced more GdIgA1 and pIgA than those of chronic tonsillitis or sleep apnea syndrome [52].…”

Section: Tonsillar B Cells In the Generation Of Nephritogenic Iga mentioning

confidence: 99%

Pathological Role of Tonsillar B Cells in IgA Nephropathy

Suzuki

Nakata

et al. 2011

Clinical and Developmental Immunology

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Although impaired immune regulation along the mucosa-bone marrow axis has been postulated to play an important role, the pathogenesis of IgA nephropathy (IgAN) is unknown; thus, no disease-specific therapy for this disease exists. The therapeutic efficacy of tonsillectomy or tonsillectomy in combination with steroid pulse therapy for IgAN has been discussed. Although randomized control trials for these therapies are ongoing in Japan, the scientific rationale for these therapies remains obscure. It is now widely accepted that abnormally glycosylated IgA1 and its related immune complex (IC) are probably key molecules for the pathogenesis, and are thus considered possible noninvasive biomarkers for this disease. Emerging evidence indicates that B cells in mucosal infections, particularly in tonsillitis, may produce the nephritogenic IgA. In this paper, we briefly summarize characteristics of the nephritogenic IgA/IgA IC, responsible B cells, and underlying mechanisms. This clinical and experimental information may provide important clues for a therapeutic rationale.

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The Effect of Tonsillectomy and Its Postoperative Clinical Course in IgA Nephropathy with Chronic Tonsillitis

Cited by 6 publications

References 0 publications

Recent advances in the immunological understanding of association between tonsil and immunoglobulin A nephropathy as a tonsil‐induced autoimmune/inflammatory syndrome

Recent advances in the immunological understanding of association between tonsil and immunoglobulin A nephropathy as a tonsil‐induced autoimmune/inflammatory syndrome

Why, when and how should immunosuppressive therapy considered in patients with immunoglobulin A nephropathy?

Pathological Role of Tonsillar B Cells in IgA Nephropathy

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