Membranous Nephropathy Associated with Thyroid Disorders

Grcevska, L; Polenakovič, Momir; Petruševska, Gordana

doi:10.1159/000045857

Cited by 17 publications

(12 citation statements)

References 7 publications

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“…One is anti-neutrophil cytoplasmic antibody (ANCA)-positive crescentic glomerulonephritis as a complication of treatment with propylthiouracil [4,5]. The other is MN associated with autoimmune thyroid diseases, such as Hashimoto's and Graves' diseases, in which a considerable proportion of patients have thyroid-associated antigens, such as thyroglobulin and TPO [6][7][8][9][10][11][12][13][14][15]. In the latter condition, the development of MN may be associated with administration of 131 I [8,14].…”

Section: Discussionmentioning

confidence: 99%

“…The release of thyroidassociated antigens, such as thyroglobulin, from the thyroid may ultimately lead to MN [6][7][8][9][10][11][12][13][14][15]. It is believed that 131 I therapy may cause MN as a result of antigens released from the ablated thyroid tissue [8,14].…”

Section: Discussionmentioning

confidence: 99%

“…In 1976, the first clinical case of MN related to autoimmune thyroiditis (Hashimoto's thyroiditis) was reported by O'Regan et al [6]. To our knowledge, there have been only seven Englishlanguage reports of MN associated with Graves' disease (total 11 cases) [8][9][10][11][13][14][15]. Immunofluorescence studies of thyroglobulin were carried out in five of the 11 cases [8,9,11,13,14], and deposits of thyroglobulin were proven in only four [8,9,11,13].…”

Section: Discussionmentioning

confidence: 99%

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Membranous nephropathy associated with thyroid-peroxidase antigen

et al. 2009

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A 6-year-old previously healthy Japanese girl was found to have dipstick 2+ proteinuria and a goiter based on the results of a routine school medical examination. Her serum free-thyroxine level was 4.98 ng/dL (normal range 0.95-1.74 ng/dL), thyroid-stimulating hormone (TSH) was less than 0.003 microU/mL (0.34-3.88 microU/mL), anti-microsomal (anti-thyroid-peroxidase) antibody was 1600 T (up to 100), anti-thyroglobulin antibody was 400 T (up to 100), and TSH-receptor antibody was 84% (up to +/-10%). These results are consistent with a diagnosis of Graves' disease. Electron microscopy examination of a renal biopsy specimen revealed electron-dense deposits located in the subepithelial spaces, and immunofluorescence microscopy examination demonstrated bright granular stainings of immunoglobulin G along the glomerular capillary walls. These findings are characteristic of membranous nephropathy. To investigate the relationship between the membranous nephropathy and Graves' disease, we carried out a second immunofluorescence study, which revealed that the immunoglobulin G granular deposits corresponded to glomerular granular staining of thyroid-peroxidase, whereas staining for thyroglobulin was absent. It was therefore assumed that the deposition of immune complexes mediated by thyroid-peroxidase had caused the membranous nephropathy in this patient. This is the first report of membranous nephropathy associated with Graves' disease in which deposits of thyroid-peroxidase, rather than thyroglobulin, have been confirmed in the kidney.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Membranous nephropathy associated with thyroid-peroxidase antigen

et al. 2009

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“…The more frequent form is membranous glomerulopathy associated with nephrotic syndrome (NS) (50,52,(55)(56)(57)59). Thyroid dysfunction has been reported to be associated with IgA glomerulonephritis (49,51,60), mesangiocapillary or membranoproliferative glomerulonephritis (47, 48,61), and minimal change glomerulonephritis (58,59,62,63).…”

Section: Glomerular Diseasementioning

confidence: 99%

Thyroid dysfunction and kidney disease

Iglesias

Díez

2009

European Journal of Endocrinology

360

335

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Thyroid hormones (TH) are essential for an adequate growth and development of the kidney. Conversely, the kidney is not only an organ for metabolism and elimination of TH, but also a target organ of some of the iodothyronines' actions. Thyroid dysfunction causes remarkable changes in glomerular and tubular functions and electrolyte and water homeostasis. Hypothyroidism is accompanied by a decrease in glomerular filtration, hyponatremia, and an alteration of the ability for water excretion. Excessive levels of TH generate an increase in glomerular filtration rate and renal plasma flow. Renal disease, in turn, leads to significant changes in thyroid function. The association of different types of glomerulopathies with both hyper-and hypofunction of the thyroid has been reported. Less frequently, tubulointerstitial disease has been associated with functional thyroid disorders. Nephrotic syndrome is accompanied by changes in the concentrations of TH due primarily to loss of protein in the urine. Acute kidney injury and chronic kidney disease are accompanied by notable effects on the hypothalamus-pituitary-thyroid axis. The secretion of pituitary thyrotropin (TSH) is impaired in uremia. Contrary to other non-thyroidal chronic disease, in uraemic patients it is not unusual to observe the sick euthyroid syndrome with low serum triodothyronine (T 3 ) without elevation of reverse T 3 (rT 3 ). Some authors have reported associations between thyroid cancer and kidney tumors and each of these organs can develop metastases into the other. Finally, data from recent research suggest that TH, especially T 3 , can be considered as a marker for survival in patients with kidney disease.

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“…10 Tissue lysis by membrane attack complex, the terminal pathway of complement activation, has been demonstrated 18,19 as well as nephropathies associated with IgG and C3 deposition in capillary glomeruli walls. 20,21 The complement-opsonized IC interaction with neutrophils is mediated by FcRs (Fc RII (CD32) and FcRIII (CD 16)) and by receptors for C3 complement fragments (CR1 (CD35) and CR3 (CD11b/ CD18; Mac-1)). Neutrophils of GD patients and healthy controls were stimulated by ICs containing IgG whether opsonized or not by serum complement.…”

Section: Discussionmentioning

confidence: 99%

Neutrophils from Brazilian patients with Graves' disease: some biochemical and functional aspects

Russo¹,

Polizzelo²,

Azzolini³

et al. 2004

Cell Biochemistry & Function

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Graves' disease shows important systemic inflammatory complications and has been considered to be systemic autoimmune thyroid, skeletal muscle and connective tissue syndrome. Neutrophils participate in the pathophysiology of the two major immune and inflammatory manifestations of the disease, ophthalmopathy and myxedema, and may worsen the inflammatory picture. In this study we analysed some biochemical and functional aspects of neutrophils in Graves' disease patients to assess their participation in these processes. The results show that the complement and/or Fcgamma receptor-mediated oxygen radical production by neutrophils was increased when patient cells were compared with controls. However the percentage of cells expressing complement and IgG receptors and the per-cell fluorescence, were similar, indicating that the increased oxidative burst was not due to an abnormal expression of mediating receptors. The production of hydrogen peroxide was also increased in hyperthyroid patient neutrophils as compared to controls. Conversely, antioxidant defences (superoxide dismutase activity and reduced glutathione content) in neutrophils from patients were not significantly different from healthy controls. The liberation of potent oxidative compounds together with the absence of adequate quenching of them by antioxidant mechanisms could be responsible for greater tissue damage in inflammatory conditions, as is the case in ophthalmopathy and myxedema patients. Considering our results and those of other workers, we encourage and suggest an associated antioxidant therapy to complement the conventional anti-thyroid therapy, especially in obvious inflammatory cases and in individuals who smoke.

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Membranous Nephropathy Associated with Thyroid Disorders

Cited by 17 publications

References 7 publications

Membranous nephropathy associated with thyroid-peroxidase antigen

Membranous nephropathy associated with thyroid-peroxidase antigen

Thyroid dysfunction and kidney disease

Neutrophils from Brazilian patients with Graves' disease: some biochemical and functional aspects

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