Renal amyloidosis in common variable immunodeficiency
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Aghamohammadi, A. Shafiei, H. Abolhassani, R. Sherkat, F. Mahjoub, N. Rezaei" "autores" => array:6 [ 0 => array:4 [ "Iniciales" => "A." "apellidos" => "Aghamohammadi" "email" => array:1 [ 0 => "aghamohammadi@sina.tums.ac.ir" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 1 => array:3 [ "Iniciales" => "A." "apellidos" => "Shafiei" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 2 => array:3 [ "Iniciales" => "H." "apellidos" => "Abolhassani" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 3 => array:3 [ "Iniciales" => "R." "apellidos" => "Sherkat" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "affb" ] ] ] 4 => array:3 [ "Iniciales" => "F." 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"apellidos" => "Rezaei" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Research Group for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran, " "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] 1 => array:3 [ "entidad" => "Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, Isfahan, Iran, " "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "affb" ] ] ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig1" "etiqueta" => "Tab. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "10280_108_1593_en_10280_t1_copy1.jpg" "Alto" => 485 "Ancho" => 536 "Tamanyo" => 33959 ] ] "descripcion" => array:1 [ "en" => "Patients laboratory finding" ] ] ] "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Dear Editor:</span></p><p class="elsevierStylePara">Common variable immunodeficiency (CVID) is the most prevalent symptomatic primary antibody deficiency, characterized by hypogamaglobulinemia, normal or decreased B-cell numbers and impaired antibody response leading to chronic and recurrent infections, mostly in the respiratory and gastrointestinal tracts<span class="elsevierStyleSup">1,2</span>. However, a significant proportion of patients manifest features of immune dysregulation, including polyclonal lymphocytic infiltration, autoimmunity, enteropathy and malignancy<span class="elsevierStyleSup">3</span>.</p><p class="elsevierStylePara">Secondary amylodosis is an extremely rare complication of CVID<span class="elsevierStyleSup">4</span>, mostly reported in middle aged males<span class="elsevierStyleSup">5-7</span>. This manifestation refers to the extra-cellular tissue deposition of serum amyloid A (SAA) protein fibrils with β-sheet structure, which could be due to chronic and recurrent infections in this group of patients<span class="elsevierStyleSup">8</span>. The self-assembly by amyloid proteins cannot progress in the soluble condition of dissembled precursor proteins alone, while it is speeded up by seeding with preformed amyloid fibrils<span class="elsevierStyleSup">9</span> which described as «seeding mechanism». Also, enzyme inhibitory function against SAA proteins was confirmed in AA type of amyloid formation and deposition<span class="elsevierStyleSup">10</span>. All reported CVID cases with amyloidosis had a sever status of infectious disease or underling complications like cor pulmonale, congestive hepatomegaly, bilateral bronchiectasis, severe respiratory failure<span class="elsevierStyleSup">7</span> and tuberculosis<span class="elsevierStyleSup">6</span>. Recurrent infections could be considered as the main cause of the amyloidosis development; although recurrent infections could be as a consequence of inadequate IVIG therapy, long delay diagnosis can also prone patient to chronic and recurrent infections<span class="elsevierStyleSup">7</span>.</p><p class="elsevierStylePara">We report herein a 50-year old male with a history of recurrent respiratory tract infections and diarrhea from early childhood. The diagnosis of amyloidosis was made for this patient based on histopathological findings of renal biopsy, once he hospitalized due to edema and massive proteinuria at the age of 48 years. Renal fine needle aspiration biopsy revealed deposition of amorphous pink hyaline eosinophilic material in glomerulus, tubular basement membrane (TBM), interstitial area and vessel walls of arterioles; it was documented by green appearance fibrils under polarized light which stained and bind with Congo red (figure 1). As the patient experienced several episodes of infections, immunological studies were performed which showed significant decreased in all serum immunoglobulin levels, compatible with diagnosis of CVID (table 1). Regular hypo-osmolar intravenous immunoglobulin was started in addition to prophylactic antibiotics and cholchicin, which controlled his renal disease. Moreover, he has not experienced further episode of serious infection since last two years.</p><p class="elsevierStylePara">The clinical manifestations of amyloidosis are widely dependent to the type of deposited protein and amount of amyloid deposition. Variation in the clinical picture of amyloidosis is related to the type of precursor involved<span class="elsevierStyleSup">8,11</span>. Moreover, the clinical features of amyloidosis vary by the organ affected; the most common organ involvement in CVID patients, which are complicated with amyloidosis, is kidney<span class="elsevierStyleSup">5,12</span>. Gastrointestinal (malabsorption, perforation, hemorrhage and obstruction)<span class="elsevierStyleSup">6</span>, joints (arthropathy)<span class="elsevierStyleSup">13</span>, thyroid<span class="elsevierStyleSup">7</span>, and gum were other sites which could be affected by secondary amyloidosis in CVID. Kidney organ function does not change with small amounts of AA amyloid deposition, while the prognosis of excessive deposition of AA renal amyloidosis is generally poor and potentially fatal<span class="elsevierStyleSup">14</span>.</p><p class="elsevierStylePara">It is considerable that renal AA amyloidosis in CVID patients commonly presented with asymptomatic proteinuria, whilst nephrotic syndrome is present in more than one fourth of patients at the time of diagnosis<span class="elsevierStyleSup">15</span>. Also, red blood cells count in urinary sediments and microscopic haematuria may present in CVID patients with the AA type, which more prominent than primary amyloidosis (AL type)<span class="elsevierStyleSup">15</span>.</p><p class="elsevierStylePara">The incidence of AA amyloidosis could be increased with duration of the underlying disease condition and associated factors such as long delay diagnosis. The mean duration of inflammation before the diagnosis of amyloidosis is estimated about 8–14 years<span class="elsevierStyleSup">15</span>. CVID patients usually experience several episodes of infections since childhood; it is expected that the patients had a history of many years inflammation without appropriate treatment, which is enough for progression of AA amyloidosis. The average age of reported CVID patients with renal secondary amyloidosis was 40.7 ± 10.9 years<span class="elsevierStyleSup">5-7</span>, which is much lower than the age of other renal amyloidosis population (70.7 ± 12.0 years)<span class="elsevierStyleSup">15</span>.</p><p class="elsevierStylePara">Glomerular deposition of amyloid substances in CVID patients had a significant differentiation from other individuals with renal amyloidosis. In these patients, immunoglobulins are not accompanied in intraglomerular deposition, while in other diseases associated with renal amyloidosis, deposition of IgG and C3 occurred at a rate of 60% and 45%, respectively. Furthermore, IgA deposition can be seen in 50-60% of cases with AA type<span class="elsevierStyleSup">9</span>.</p><p class="elsevierStylePara">Control of the underlying inflammatory disease is the preferred therapy of AA amyloid, but patients who have diagnostic criteria of CVID should receive immunoglobulin replacement therapy. Administration of IVIG could dramatically reduce recurrent infections and subsequent complications in the patients with antibody deficiency<span class="elsevierStyleSup">1,2</span>. Although the usual initial dosage for IVIG therapy is 300-400 mg/kg per month, higher doses of 600-800 mg/kg may be needed in subgroup of patients, especially in patients with bronchiectasis or chronic sinusitis. Nonetheless, IVIG may induce renal damage, especially in patients with preexisting renal insufficiency. Increased level of sucrose, blood viscosity and deposition of immune complex in renal tissue are the main causes of renal damage due to IVIG. Therefore treatment of CVID patients with amyloidosis is a subject of debate. However, high dosage of hypo-osmolar IVIG without sucrose (such as Gummunex or Octagam) is recommended for prevention of renal damage in addition with adjustment of dosage of antibiotics and colchicines. It is expected that new therapeutic strategies in addition to IVIG should be commenced in CVID-amyloidosis patients<span class="elsevierStyleSup">15</span>. The biological agents such as tumor necrosis factor alpha (TNF-α) blocker, Etanercept, Iododoxorubicin and low-molecular-weight sulfates (Fbrilex) have been shown to be effective in treatment of AA-type renal amyloidosis<span class="elsevierStyleSup">9</span>, which should be tried in CVID-amyloidosis patients as well.</p><p class="elsevierStylePara"><a href="grande/10280_108_1593_en_10280_t1_copy1.jpg" class="elsevierStyleCrossRefs"><img src="10280_108_1593_en_10280_t1_copy1.jpg" alt="Patients laboratory finding"></img></a></p><p class="elsevierStylePara">Table 1. Patients laboratory finding</p><p class="elsevierStylePara"><a href="grande/10280_108_1594_en_10280_new_f1.jpg" class="elsevierStyleCrossRefs"><img src="10280_108_1594_en_10280_new_f1.jpg" alt="Renal glomerule with deposition of amorphous pink material proved to be amyloid by Hematoxyline, Eosin staining (A. X400) and special reacting to Congo-red stain (B. X400)."></img></a></p><p class="elsevierStylePara">Figure 1. Renal glomerule with deposition of amorphous pink material proved to be amyloid by Hematoxyline, Eosin staining (A. X400) and special reacting to Congo-red stain (B. X400).</p>" "pdfFichero" => "P1-E501-S2459-A10280-EN.pdf" "tienePdf" => true "multimedia" => array:2 [ 0 => array:8 [ "identificador" => "fig1" "etiqueta" => "Tab. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "10280_108_1593_en_10280_t1_copy1.jpg" "Alto" => 485 "Ancho" => 536 "Tamanyo" => 33959 ] ] "descripcion" => array:1 [ "en" => "Patients laboratory finding" ] ] 1 => array:8 [ "identificador" => "fig2" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "10280_108_1594_en_10280_new_f1.jpg" "Alto" => 500 "Ancho" => 316 "Tamanyo" => 31891 ] ] "descripcion" => array:1 [ "en" => "Renal glomerule with deposition of amorphous pink material proved to be amyloid by Hematoxyline, Eosin staining (A. 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| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 7 | 3 | 10 |
| 2024 October | 67 | 33 | 100 |
| 2024 September | 71 | 30 | 101 |
| 2024 August | 65 | 56 | 121 |
| 2024 July | 61 | 21 | 82 |
| 2024 June | 70 | 37 | 107 |
| 2024 May | 61 | 29 | 90 |
| 2024 April | 59 | 37 | 96 |
| 2024 March | 40 | 26 | 66 |
| 2024 February | 45 | 37 | 82 |
| 2024 January | 40 | 29 | 69 |
| 2023 December | 40 | 28 | 68 |
| 2023 November | 68 | 32 | 100 |
| 2023 October | 64 | 43 | 107 |
| 2023 September | 43 | 31 | 74 |
| 2023 August | 48 | 31 | 79 |
| 2023 July | 56 | 32 | 88 |
| 2023 June | 50 | 27 | 77 |
| 2023 May | 55 | 34 | 89 |
| 2023 April | 38 | 16 | 54 |
| 2023 March | 46 | 20 | 66 |
| 2023 February | 43 | 17 | 60 |
| 2023 January | 60 | 21 | 81 |
| 2022 December | 73 | 24 | 97 |
| 2022 November | 60 | 30 | 90 |
| 2022 October | 77 | 49 | 126 |
| 2022 September | 54 | 32 | 86 |
| 2022 August | 47 | 50 | 97 |
| 2022 July | 81 | 51 | 132 |
| 2022 June | 74 | 40 | 114 |
| 2022 May | 58 | 22 | 80 |
| 2022 April | 102 | 55 | 157 |
| 2022 March | 84 | 51 | 135 |
| 2022 February | 70 | 38 | 108 |
| 2022 January | 91 | 37 | 128 |
| 2021 December | 66 | 33 | 99 |
| 2021 November | 74 | 33 | 107 |
| 2021 October | 88 | 43 | 131 |
| 2021 September | 75 | 38 | 113 |
| 2021 August | 69 | 30 | 99 |
| 2021 July | 103 | 28 | 131 |
| 2021 June | 71 | 27 | 98 |
| 2021 May | 90 | 28 | 118 |
| 2021 April | 189 | 91 | 280 |
| 2021 March | 84 | 14 | 98 |
| 2021 February | 82 | 22 | 104 |
| 2021 January | 40 | 15 | 55 |
| 2020 December | 60 | 11 | 71 |
| 2020 November | 50 | 19 | 69 |
| 2020 October | 36 | 17 | 53 |
| 2020 September | 29 | 12 | 41 |
| 2020 August | 40 | 10 | 50 |
| 2020 July | 65 | 10 | 75 |
| 2020 June | 38 | 9 | 47 |
| 2020 May | 75 | 15 | 90 |
| 2020 April | 84 | 21 | 105 |
| 2020 March | 34 | 14 | 48 |
| 2020 February | 55 | 15 | 70 |
| 2020 January | 41 | 15 | 56 |
| 2019 December | 67 | 22 | 89 |
| 2019 November | 33 | 23 | 56 |
| 2019 October | 22 | 8 | 30 |
| 2019 September | 38 | 18 | 56 |
| 2019 August | 20 | 14 | 34 |
| 2019 July | 39 | 23 | 62 |
| 2019 June | 24 | 8 | 32 |
| 2019 May | 30 | 13 | 43 |
| 2019 April | 100 | 33 | 133 |
| 2019 March | 53 | 21 | 74 |
| 2019 February | 35 | 14 | 49 |
| 2019 January | 31 | 15 | 46 |
| 2018 December | 75 | 36 | 111 |
| 2018 November | 67 | 11 | 78 |
| 2018 October | 71 | 10 | 81 |
| 2018 September | 59 | 15 | 74 |
| 2018 August | 51 | 17 | 68 |
| 2018 July | 51 | 12 | 63 |
| 2018 June | 51 | 12 | 63 |
| 2018 May | 44 | 15 | 59 |
| 2018 April | 52 | 10 | 62 |
| 2018 March | 42 | 9 | 51 |
| 2018 February | 31 | 6 | 37 |
| 2018 January | 23 | 9 | 32 |
| 2017 December | 45 | 8 | 53 |
| 2017 November | 46 | 17 | 63 |
| 2017 October | 31 | 11 | 42 |
| 2017 September | 33 | 21 | 54 |
| 2017 August | 27 | 17 | 44 |
| 2017 July | 35 | 17 | 52 |
| 2017 June | 28 | 10 | 38 |
| 2017 May | 38 | 8 | 46 |
| 2017 April | 43 | 7 | 50 |
| 2017 March | 34 | 20 | 54 |
| 2017 February | 25 | 10 | 35 |
| 2017 January | 27 | 6 | 33 |
| 2016 December | 62 | 3 | 65 |
| 2016 November | 72 | 4 | 76 |
| 2016 October | 103 | 12 | 115 |
| 2016 September | 133 | 1 | 134 |
| 2016 August | 170 | 3 | 173 |
| 2016 July | 105 | 3 | 108 |
| 2016 June | 115 | 0 | 115 |
| 2016 May | 124 | 0 | 124 |
| 2016 April | 64 | 0 | 64 |
| 2016 March | 67 | 0 | 67 |
| 2016 February | 63 | 0 | 63 |
| 2016 January | 96 | 0 | 96 |
| 2015 December | 85 | 0 | 85 |
| 2015 November | 80 | 0 | 80 |
| 2015 October | 72 | 0 | 72 |
| 2015 September | 76 | 0 | 76 |
| 2015 August | 66 | 0 | 66 |
| 2015 July | 58 | 0 | 58 |
| 2015 June | 26 | 0 | 26 |
| 2015 May | 50 | 0 | 50 |
| 2015 April | 6 | 0 | 6 |
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