scholarly journals Nodular glomerulosclerosis with anti-glomerular basement membrane-like glomerulonephritis; a distinct pattern of kidney injury observed in smokers

2014 ◽  
Vol 7 (4) ◽  
pp. 361-366 ◽  
Author(s):  
I. Batal ◽  
D. B. Reyes ◽  
S. Popham ◽  
V. Bijol
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Alexander Winkler ◽  
Emanuel Zitt ◽  
Hannelore Sprenger-Mähr ◽  
Afschin Soleiman ◽  
Manfred Cejna ◽  
...  

Abstract Background Anti-glomerular basement membrane disease (GBM) disease is a rare autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary haemorrhage. Recently, an association between COVID-19 and anti-glomerular basement membrane (anti-GBM) disease has been proposed. We report on a patient with recurrence of anti-GBM disease after SARS-CoV-2 infection. Case presentation The 31-year-old woman had a past medical history of anti-GBM disease, first diagnosed 11 years ago, and a first relapse 5 years ago. She was admitted with severe dyspnoea, haemoptysis, pulmonary infiltrates and acute on chronic kidney injury. A SARS-CoV-2 PCR was positive with a high cycle threshold. Anti-GBM autoantibodies were undetectable. A kidney biopsy revealed necrotising crescentic glomerulonephritis with linear deposits of IgG, IgM and C3 along the glomerular basement membrane, confirming a recurrence of anti-GBM disease. She was treated with steroids, plasma exchange and two doses of rituximab. Pulmonary disease resolved, but the patient remained dialysis-dependent. We propose that pulmonary involvement of COVID-19 caused exposure of alveolar basement membranes leading to the production of high avidity autoantibodies by long-lived plasma cells, resulting in severe pulmonary renal syndrome. Conclusion Our case supports the assumption of a possible association between COVID-19 and anti-GBM disease.


2012 ◽  
Vol 45 (10) ◽  
pp. 973-978
Author(s):  
Aiko Ookubo ◽  
Yuka Shimizu ◽  
Taisuke Irifuku ◽  
Takayuki Naito ◽  
Takahiko Ogawa ◽  
...  

2016 ◽  
Vol 59 (12) ◽  
pp. 1282-1289 ◽  
Author(s):  
Shui-Yi Hu ◽  
Xiao-Yu Jia ◽  
Jian-Nan Li ◽  
Xin Zheng ◽  
Jie Ao ◽  
...  

2020 ◽  
Author(s):  
Wenjing Wang ◽  
Xiao-yu Jia Jia ◽  
Zhao Cui ◽  
Yan Chen ◽  
Wei Wang ◽  
...  

Abstract Background: Anti-glomerular basement membrane disease (GBM) is a kind of chronic autoimmune disease caused by the deposition of circulating anti-GBM antibodies. Non-collagen region of α3 chain of type IV collagen (α3(IV)NC1) is one of the main target antigens. And on α3, EA and EB are the most classical antigen epitopes. It has been reported that anti-GBM antibodies can be detected in HIV patients, but its immunological characteristics are still unclear. In this study, the immunological characteristics of the target antigens were clarified. Methods: Total 93 HIV patients and 20 healthy volunteers were selected in Beijing Youan Hospital from 2017 to 2018. Recombinant human α1-α5(IV)NC1, chimeric protein EA and EB were used as solid phase antigens. Enzyme-linked immunosorbent assay was employed to measure concentrations and subtypes of serum IgG autoantibodies specifically against GBM.Results: Five out of the 93 patients with HIV had low to moderate levels of anti-GBM antibodies. However, these patients presented with no clinical manifestation of any kidney injury or pulmonary hemorrhages. Compared with HIV patients with negative antibodies, there were no significant differences in gender, age, CD4+T cell count and HIV viral load. All sera of five patients recognized non-collagenous domain1 (NC1) of alpha 3 chain of type IV collagen [(α3(IV)NC1] as classic anti-GBM patients, followed by α5(IV)NC1. The antibodies against α3(IV)NC1 were IgG3 predominant, but did not react with either of the classic epitopes on α3 (EA and EB).Conclusion: These data suggest a distinct immunological profile of anti-GBM antibodies in patients with HIV, and might explain the non-pathogenic features of HIV associated anti-GBM antibodies.


2021 ◽  
Vol 14 (4) ◽  
pp. e241265
Author(s):  
Sheikh Raza Shahzad ◽  
Faris Alfaris ◽  
Mustafa Erdem Arslan ◽  
Swati Mehta

Calciphylaxis is commonly associated with end-stage renal disease (ESRD) and renal transplant. We present a rare case of early onset calciphylaxis in a patient presenting with acute kidney injury (AKI) secondary to anti-glomerular basement membrane (anti-GBM) antibody disease. A 65-year-old obese Caucasian woman with type 2 diabetes mellitus and hypertension presented with a 1-month history of painless gross haematuria and worsening lower extremity oedema. Laboratory results indicated AKI and nephrotic-range proteinuria. Anti-glomerular antibodies were elevated. Renal biopsy revealed focal crescentic glomerulonephritis with linear capillary immunoglobulin G staining consistent with anti-GBM antibody disease. She was treated with haemodialysis, plasmapheresis, steroids, bumetanide and cyclophosphamide. Two months later, she developed necrotic lesions on bilateral thighs. Wound biopsy was consistent with calciphylaxis. This case highlights that calciphylaxis, usually seen in patients with chronic kidney disease or ESRD, can manifest in patients with AKI as well.


2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Wen-jing Wang ◽  
Xiao-yu Jia ◽  
Zhao Cui ◽  
Yan Chen ◽  
Wei Wang ◽  
...  

Abstract Background Anti-glomerular basement membrane disease (GBM) is an autoimmune disease caused by the deposition of circulating anti-GBM antibodies. Non-collagen region of α3 chain of type IV collagen (α3(IV)NC1) is one of the main target antigens, in which EA and EB are the most classical antigen epitopes. It has been reported that anti-GBM antibodies can be detected in HIV patients; however, its immunological characteristics are still unclear. Objectives In this study, the positive rate of the anti-GBM antibodies in HIV and the immunological characteristics of the target antigens were clarified. Methods A total of 93 HIV patients diagnosed in Beijing Youan Hospital from November 2017 to January 2018 were included. Enzyme-linked immunosorbent assay was used to measure the serum IgG autoantibodies specifically against GBM in these patients, as well as their subtypes and antigen spectra. Results It was found that five out of the 93 patients with HIV had low to moderate levels of anti-GBM antibodies. However, these patients presented with no clinical manifestation of any kidney injury or pulmonary hemorrhages. Compared with HIV patients with negative antibodies, there were no significant differences in gender, age, CD4+T cell count and HIV viral load. All sera of five patients recognized non-collagenous domain1 (NC1) of alpha 3 chain of type IV collagen [(α3(IV)NC1] as classic anti-GBM patients, followed by α5(IV)NC1. The antibodies against α3(IV)NC1 were IgG3 predominant, while these antibodies did not react with either of the classic epitopes on α3 (EA and EB). Conclusion These data suggest a distinct immunological profile of anti-GBM antibodies in patients with HIV, and might explain the non-pathogenic features of HIV associated anti-GBM antibodies.


2019 ◽  
Vol 12 (6) ◽  
pp. 801-802
Author(s):  
Arnaud Le Flecher ◽  
Nicolas Viallet ◽  
Delphine Hebmann ◽  
Bertrand Chauveau ◽  
Henri Vacher Coponat

Abstract We report a 35-year-old man who suffered from recurrent macroscopic haematuria after intensive exercise. One episode was associated with bilateral loin (flank) pain and severe acute kidney injury. His kidney biopsy revealed an atypical anti-glomerular basement membrane (GBM) disease typified by bright linear GBM staining for monotypic immunoglobulin G but without a diffuse crescentic phenotype and no circulating anti-GBM antibody. Outcome was spontaneously favourable. The patient had no recurrence or urine abnormality without running. The original presentation emphasized that exercise could reveal an underlying glomerulopathy.


2019 ◽  
Vol 20 (3) ◽  
pp. 519 ◽  
Author(s):  
Jenny Frese ◽  
Matthias Kettwig ◽  
Hildegard Zappel ◽  
Johannes Hofer ◽  
Hermann-Josef Gröne ◽  
...  

Kidney injury due to focal segmental glomerulosclerosis (FSGS) is the most common primary glomerular disorder causing end-stage renal disease. Homozygous mutations in either glomerular basement membrane or slit diaphragm genes cause early renal failure. Heterozygous carriers develop renal symptoms late, if at all. In contrast to mutations in slit diaphragm genes, hetero- or hemizygous mutations in the X-chromosomal COL4A5 Alport gene have not yet been recognized as a major cause of kidney injury by FSGS. We identified cases of FSGS that were unexpectedly diagnosed: In addition to mutations in the X-chromosomal COL4A5 type IV collagen gene, nephrin and podocin polymorphisms aggravated kidney damage, leading to FSGS with ruptures of the basement membrane in a toddler and early renal failure in heterozygous girls. The results of our case series study suggest a synergistic role for genes encoding basement membrane and slit diaphragm proteins as a cause of kidney injury due to FSGS. Our results demonstrate that the molecular genetics of different players in the glomerular filtration barrier can be used to evaluate causes of kidney injury. Given the high frequency of X-chromosomal carriers of Alport genes, the analysis of genes involved in the organization of podocyte architecture, the glomerular basement membrane, and the slit diaphragm will further improve our understanding of the pathogenesis of FSGS and guide prognosis of and therapy for hereditary glomerular kidney diseases.


2019 ◽  
Vol 48 (3) ◽  
pp. 030006051989239 ◽  
Author(s):  
Chenni Gao ◽  
Jingyuan Xie ◽  
Xiaoxia Pan ◽  
Xiaonong Chen

Renal insufficiency is common among patients with various types of malignant tumors. However, the occurrence of anti-glomerular basement membrane (GBM) nephritis in a patient with a malignant tumor is relatively rare. Here, we describe a patient with bronchial carcinoma who exhibited acute kidney injury, hematuria, and non-nephrotic-range proteinuria. The patient had positive serum anti-GBM antibody findings and biopsy-proven anti-GBM nephritis. This is a rare instance of anti-GBM nephritis in a patient with a malignant solid tumor. Neoplasia was presumed to contribute to the development of anti-GBM nephritis through secretion of tumor-related antigens or unusual exposure to GBM.


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