scholarly journals A case of acute kidney injury associated with anti-glomerular basement membrane antibody disease and thrombotic microangiopathy

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


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 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.


2019 ◽  
Vol 13 (2) ◽  
pp. 261-262
Author(s):  
Martin E Durcan ◽  
Beena Nair ◽  
John G Anderton

Abstract We report a case of anti-glomerular basement membrane (GBM) disease in association with human leucocyte antigen (HLA) DRB1 15:01. A 71-year-old woman presented with oligoanuric acute kidney injury accompanied by high titre anti-GBM antibodies. Renal biopsy revealed a severe crescentic glomerulonephritis. Her brother had presented 6 years earlier with oligoanuric acute kidney injury. He was dual positive for MPO ANCA and anti-GBM antibodies. Renal biopsy was not performed. Both had an absence of pulmonary involvement. Tissue typing confirmed both were heterozygous for HLA DRB1 15:01 and DRB1 04:03.


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.


2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Keiko Oda ◽  
Kan Katayama ◽  
Akiko Tanoue ◽  
Tomohiro Murata ◽  
Yumi Hirota ◽  
...  

2020 ◽  
Vol 6 (6) ◽  
pp. 414-421
Author(s):  
Youlu Zhao ◽  
Junwen Huang ◽  
Tao Su ◽  
Zhikai Yang ◽  
Xizi Zheng ◽  
...  

<b><i>Background:</i></b> The syndrome of tubulointerstitial nephritis and uveitis (TINU) is an uncommon and multisystemic autoimmune disorder. This review reports a rare case of TINU being superimposed on thrombotic microangiopathy (TMA) and, by comparing with the available literature, also summarizes the clinical features, associated conditions, treatment, and outcome of patients with TINU. <b><i>Summary:</i></b> Herein, we report the case of a 37-year-old male patient with acute kidney injury (AKI) clinicopathologically identified as malignant hypertension-induced TMA superimposed by acute tubulointerstitial nephritis, which was suspected to be related to drug hypersensitivity. After treatment with oral prednisone combined with a renin-angiotensin system inhibitor, the patient achieved partial renal recovery and was withdrawn from hemodialysis. Recurrent AKI concomitant with new-onset asymptomatic uveitis was detected during routine clinical follow-up after cessation of prednisone. TINU was then diagnosed, and prednisone followed by cyclophosphamide was prescribed. The patient achieved better renal recovery than in the first round of treatment and maintained stable renal function afterward. By reviewing the literature, 36 cases were reported as TINU superimposed on other conditions, including thyroiditis, osteoarthropathy, and sarcoid-like noncaseating granulomas. <b><i>Key messages:</i></b> TINU could be complicated by many other conditions, among which TMA is very rare. When presented as AKI, kidney biopsy is important for differential diagnosis. The case also shows that recurrent AKI with concomitant uveitis after prednisone withdrawal strongly suggested the need for long-term follow-up and elongated prednisone therapy for TINU syndrome.


2020 ◽  
pp. 5027-5032
Author(s):  
Edwin K.S. Wong ◽  
David Kavanagh

Haemolytic uraemic syndrome (HUS) is a thrombotic microangiopathy characterized by the triad of thrombocytopenia, microangiopathic haemolytic anaemia, and acute kidney injury. It is most often caused by Shiga toxin-producing Escherichia coli (STEC-HUS), and any HUS not caused by this is often termed atypical HUS (aHUS). aHUS may be caused by an underlying complement system abnormality (primary aHUS) or by a range of precipitating events, such as infections or drugs (secondary aHUS). Management of STEC-HUS is supportive. In aHUS, plasma exchange is the initial treatment of choice until ADAMTS13 activity is available to exclude thrombotic thrombocytopenic purpura as a diagnosis. Once this has been done, eculizumab should be instigated as soon as possible.


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