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Background: Immune check point inhibitors (ICPi) have become the first line treatment for most of the cancers and have shown promising results. However, they can provoke reactions, the most feared being immune related adverse events (irAE). Case presentation: We present a series of three cases, of patients recieving ICPi. All three patients developed AKI after administration of SARS-CoV-2 mRNA vaccine. Two patients had kidney-biopsy-proven acute interstitial nephritis (AIN) which responded to ICPi discontinuation and treatment with steroids. One had presumed AIN based on the high levels of CRP and urine retinol binding protein to creatinine ratio and responded to cessation of ICPi alone. Conclusion(s): These three cases demonstrate that a strong immune response from the SARS-CoV-2 mRNA vaccine combined with an uninhibited immune system under influence of ICPi led to an amplification of autoimmunity leading to AKI presenting as AIN.Copyright © The Author(s) 2022.
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Background: In early 2020, severe acute respiratory syndrome-corona virus 2 (SARS-CoV-2) pandemics caused previously unheard of health, social, and economic problems worldwide. The disease can affect different organs such as the lungs, heart, pancreas, kidney, and unusual symptoms can be seen. Information on the clinical impact of SARS-CoV-2 infection on renal function among pediatric age groups is scarce. Case Report: In this report, we presented a 13-year-old boy who was admitted to our hospital with the relapse of nephrotic syndrome caused by COVID-19. The patient had mild upper respiratory tract symptoms, eyelid edema and progressive swelling of the lower extremities. Clinical remission was achieved with oral prednisolone therapy without the use of any antiviral drugs. Conclusion(s): Patients with nephrotic syndrome presenting with relapse should be evaluated for potential COVID-19 infection during the pandemic. The use of routine doses of prednisolone appears to be safe in mild disease. Copyright © 2023 by Erciyes University Faculty of Medicine.
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Purpose: Vaccination against SARS-CoV-2 is essential. Complicating this effort are reports of a suboptimal response to the SARS-CoV-2 spike protein in patients on immunosuppressive medications and possible thrombotic microangiopathy (TMA) in renal transplant patients who receive the mRNA type vaccines. Method(s): 48 year old male with end stage renal disease who received a living unrelated transplant in 2015. Pre-operative creatinine was 10.42 mg/dL and decreased to 2.48 mg/dL within a week. Patient received Basiliximab induction and maintained on tacrolimus and mycophenolate (MMF). One month post-transplant patient was diagnosed with TMA. Tacrolimus was stopped and patient was switched to Sirolimus and continued on MMF. Patient was followed closely by transplant nephrology for the next 5 years with a baseline creatinine of 1.9 mg/dL, protein to creatinine ratio below 0.5 mg/mg and well controlled diabetes. No DSA Class I or II detected on regular testing. Patient was compliant with all prescribed medications. On January 25 2021 patient received Pfizer Vaccine. Second Pfizer vaccine administered on February 18 2021. A week later creatinine was noted to be 3.44 mg/dL. Repeat creatinine of 4.27 mg/dL. Biopsy revealed diffuse lymphocytic interstitial inflammation, peritubular capillaritis, and C4D negative. Findings consistent with chronic TMA. DSA testing revealed Class II DSA:DQ2 (SI-5933), Allosure 1.2 %. BK < 500 and CMV undetected. Patient received therapeutic plasma exchange, IV Ig infusion and steroids while on MMF and sirolimus. His creatinine decreased to 2.9 mg/dL on discharge. Over the next 6 months graft function deteriorated. He is now CKD stage 5 and under evaluation for a second transplant. Result(s): There are case reports of COVID-19 vaccine administration and transplant graft dysfunction. A possible mechanism involves the mRNA lipid nanoparticleencapsulated platform producing such a robust CD4 and CD8 T-cell response that pro-inflammatory cytokines are activated or that immune complex associated glomerular disease occurs resulting in the development of TMA in susceptible patients. Conclusion(s): A possible link between SARS CoV-2 vaccination and kidney transplant TMA warrants the implementation of close surveillance of vaccinated transplant patients, particularly susceptible individuals. More research is needed to determine if this link exists.
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SARS-COV-2 infection is often associated with exaggerated immune response, also referred to as a ‘cytokine storm’. There is growing concern that it may be linked to autoimmunity, with many cases of autoimmune diseases either triggered by or related to SARS-COV-2 having been reported, ranging from Guillain-Barre syndrome, Graves’ disease, multiple sclerosis, Kawasaki-like disease. Our patient was a 20-year-old female with a history of hidradenitis who presented with malaise, feet and ankle swelling, asthenia, anorexia, weight loss of 50 Ibs of 4 months. She had COVID pneumonia 7 months prior and was also seen in the ER thrice afterwards for ankle pain and fatigue managed with antibiotics and analgesics. Exam findings included tender bilateral lower extremity edema, diffuse hyperkeratotic and hyperpigmented purpuric rashes and bilateral suppurative axillary swellings. She was admitted for protein-energy malnutrition. Blood work showed WBC 13.5, low Hb 9.3, AST 509, ALT 104, BUN 29, Creatinine 0.9, Protein 7.5, albumin 1.5 (globulin gap of 6). Urine assay showed 3+ proteinuria Hb 3+ with RBC 3-10/hpf, absent nitrite, LE 1+, protein/creatinine ratio was 2949 mg/g. Blood cultures returned negative. US showed trace pericardial effusion and normal kidneys. Infectious workup returned negative for anti-streptolysin O, HIV, hepatitis B and C. Two days after, she developed AMS, fever, tachycardia and neck stiffness concerning for possible meningoencephalitis. CT head was normal. Lumbar puncture was performed. IV vancomycin and piperacillin-tazobactam was started. CSF fluid analysis revealed total protein of 125mg/dl, elevated IgG 79.8, concerning for an underlying inflammatory pathology. EEG was unremarkable. She became oliguric with creatinine and BUN both peaking at 2.6 and 58 respectively. Renal ultrasound revealed medical renal disease. Urine microscopy showed granular cast and no dysmorphic RBCs. ANA, anti-smith SSA, SSB, DS-DNA, RF, smooth muscle, anti-histone, anti-centromere, JO-1 and RNP antibodies were markedly elevated. She was unstable for CT trocar biopsy of the kidney. She subsequently went into cardiac arrest multiple times about a week into admission, before eventually expiring. Though causation was not established in our patient, SARS-COV-2 infection causing exaggerated immune response may unmask SLE or be associated with SLE.
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Vaccination against SARS-CoV-2 is essential. Complicating this effort are reports of a suboptimal response to the SARS-CoV-2 spike protein in patients on immunosuppressive medications and possible thrombotic microangiopathy (TMA) in renal transplant patients. 48-year-old male who received a living unrelated transplant in 2015. Pre-operative creatinine was 10.42 mg/dL and decreased to 2.48 mg/dL within a week. Patient received Basiliximab induction and maintained on tacrolimus and mycophenolate (MMF). One month post-transplant patient was diagnosed with TMA. Tacrolimus was stopped and patient was switched to Sirolimus and continued on MMF. Patient was followed closely by transplant nephrology for the next 5 years with a baseline creatinine of 1.9 mg/dL, protein to creatinine ratio below 0.5 mg/mg and well controlled diabetes. No DSA Class I or II detected on regular testing. Patient was compliant with all prescribed medications. On January 25 2021 patient received Pfizer Vaccine. Second Pfizer vaccine administered on February 18 2021. A week later creatinine was noted to be 3.44 mg/dL. Repeat creatinine of 4.27 mg/dL. Biopsy revealed diffuse lymphocytic interstitial inflammation, peritubular capillaritis, and C4D negative. Findings consistent with chronic TMA. DSA testing revealed Class II DSA:DQ2 (SI- 5933), Allosure 1.2 %. BK < 500 and CMV undetected. Patient received therapeutic plasma exchange, IV Ig infusion and steroids while on MMF and sirolimus. His creatinine decreased to 2.9 mg/dL on discharge. Over the next 6 months graft function deteriorated. He is now CKD stage 5 and under evaluation for a second transplant. There are case reports of COVID-19 vaccine administration and transplant graft dysfunction. A possible mechanism involves the mRNA lipid nanoparticle-encapsulated platform producing such a robust CD4 and CD8 T-cell response that pro-inflammatory cytokines are activated or that immune complex associated glomerular disease occurs resulting in the development of TMA in susceptible patients. A possible link between SARS CoV-2 vaccination and kidney transplant TMA warrants the implementation of close surveillance of vaccinated transplant patients, particularly susceptible individuals. More research is needed to determine if this link exists.
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BACKGROUND AND AIMS: During the time of the COVID-19 pandemic, multiple treatment options have been investigated, even though their efficacy and secondary effects remain insufficiently known. We report the case of a vitamin C induced oxalate nephropathy in a COVID-19 patient with preexisting chronic kidney disease (CKD) resulting in irreversible acute renal failure. Vitamin C, also known as ascorbic acid, has been used as an anti-inflammatory therapy for COVID-19, but review of the literature shows similar cases of acute kidney injury (AKI), raising concern. METHOD: We report the case of a 73-year-old Caucasian woman admitted for hyperthermia and digestive disorders. She had recently started a first-line chemotherapy for multiple myeloma with partial response. She also displayed preexisting stage 4 CKD (eGFR 18.50 mL/min/1.73 m2 using CKD-EPI) of unknown aetiology. She was tested positive for SARS-CoV2 by nasopharyngeal swab and soon transferred to the intensive care unit. She received intravenous corticosteroids using dexamethasone 6 g/24 h for 10 days and a piperacillin + tazobactam probabilistic antibiotherapy. She also received high doses (15 g/24 h) of vitamin C for three consecutive days. No monoclonal antibodies were prescribed due to a previous vaccination with a positive serology upon admission. Although the patient recovered from respiratory tract infection, her kidney function progressively deteriorated with serum creatinine levels rising up to 8.06 g/dL, leading to her admission in our nephrology department. The patient was initially treated with high doses of diuretics for anasarca and an abdominal CT excluded urinary tract obstruction with normal kidney size and aspect. Urinary analysis showed protein to creatinine (p/c) ratio of 1348 g/g, and presence of urinary light chains. Her monoclonal spike was measured at 2.3 g/L and her kappa/lambda fraction was 1.74. Intermittent haemodialysis was initiated, and a kidney biopsy was performed. RESULTS: Histology revealed hundreds of intratubular calcium oxalate crystals, with severe and diffuse acute tubular necrosis and interstitial edema. There was no amyloidosis, no sign of active glomerular disease and no interstitial fibrosis. Immunofluorescence (IgA, IgG, IgM, C1Q, C3, kappa and lambda) was negative. We concluded to oxalate nephropathy. After a 2-month follow-up, the patient remains dialysis dependent. Vitamin C is a precursor of oxalate and has been shown to cause secondary oxaluria, particularly with high-dose regimens in patients with altered renal function. Given the histological findings evocative of acute oxalate nephropathy, the accountability of high doses of vitamin C should be considered. No other cause of hyperoxaluria was identified in our patient beside broad spectrum antibiotic use, which could decrease intestinal bacterial oxalate degradation. In particular, there was no malabsorption The limitation of our report is the unknown cause of preexisting CKD;therefore, we cannot rule out preexisting hyperoxaluria. Also, no dosage of serum vitamin C and oxalate levels were performed during follow-up. Finally, our patient had other possible causes AKI, such as recent SARS-CoV2 infection, or linked to multiple myeloma, but these were considered unlikely given the proper haematological response to treatment and non-evocative biopsy. The rationale for vitamin C use in COVID-19 is based on in vitro studies showing its antioxidant, anti-inflammatory, anticoagulant and immune modulatory properties. There lack large clinical studies, and the literature shows conflicting results. Multiple cases of acute oxalate nephropathy were described. CONCLUSION: Vitamin C is an anti-inflammatory treatment used in COVID-19 that can lead to secondary hyperoxaluria with significant and irreversible AKI. Due to the severity of AKI in patients with preexisting CKD, we believe renal function should be considered before using high doses of vitamin C. Larger controlled trials are needed both to establish the clinical benefit of vitamin C and further describe its potential ephrotoxicity.
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Background/Aims There is a growing number of reports of new-onset autoimmune disease or complications of underlying autoimmune disorders following COVID-19 infection and vaccination. Methods We describe two cases of systemic lupus erythematosus (SLE) that developed De novo in two female patients shortly after receiving their COVID-19 vaccinations. Results The first case is a 29-year-old female with no prior medical history. One week following her COVID-19 Pfizer/BioNTech vaccination, she developed widespread pruritus, fatigue, myalgia, arthralgia, fever and night sweats. Blood tests showed pancytopenia and she was referred for an urgent haematology opinion due to lymphoma. Positron Emission Tomography/computed tomography (PET/CT) demonstrated widespread lymphadenopathy. Bone and lymph node biopsy showed reactive changes only. Her symptoms progressed with polyarticular inflammatory arthritis, oral ulceration, Raynaud's, pleuritic chest pain, palmar purpuric rash, and a widespread tender urticarial rash. Further investigations showed low complement C3/C4, anti-double stranded DNA antibody titre (dsDNA) >200 IU/mL, positive Anti-Ro antibody, positive Anti-La antibody, weakly positive anti-RNP antibody and an Anti-C1q antibody >400 units/ml with a urine protein/creatinine ratio (PCR) of 39 mg/mmol. A diagnosis of SLE with urticarial vasculitis was made and she commenced Hydroxychloroquine in addition to weaning prednisolone (60mg). A skin biopsy confirmed lupus vasculitis. Despite high dose prednisolone, urine PCR increased over 2 weeks from 39 to 84 mg/mmol. Renal biopsy demonstrated class 3 lupus nephritis. She was pulsed with 500mg IV methyl prednisolone over 3 days and commenced mycophenolate 1g BD. Within weeks she was in clinical remission. The second case is a 70-year-old female with a past medical history of diverticulosis, uterine fibroids and small hand joint osteoarthritis. She presented with a sudden onset, 6-week history of bilateral symmetrical small and large joint synovitis that developed 8 days following the first dose of the COVID-19 Oxford-AstraZeneca vaccine. Her investigations showed reduced lymphocyte counts (0.9 109/L), raised CRP 26 mg/L and ESR 32 mm/hr. Antinuclear antibodies were weakly positive with a homogenous pattern. DsDNA titre was raised at 175 IU/mL and C4 reduced at 0.14 g/L. There was no proteinuria or any evidence of major internal organ involvement. She was started on a short reducing course of oral prednisolone given the severity of her presenting clinical features. Her symptoms improved, with no recurrence on stopping steroids but she has continued elevation in DsDNA;a conservative management approach is being adopted. Conclusion Both cases met the EULAR/ACR and SLICC classification criteria for SLE. There was a clear temporal association between the onset of SLE symptoms and COVID-19 vaccination. Our cases raise the possible association/causation of SLE following COVID-19 vaccination. Potential mechanisms include immune responses elicited by the COVID-19 vaccination, triggering autoimmunity in genetically predisposed individuals. Further research and data from registries are required.
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Purpose of Study Initially detected in Wuhan, China, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which is responsible for coronavirus disease 2019 (COVID-19) rapidly became a global pandemic. Immunocompromised patients, including kidney transplant recipients, are at increased risk of morbidity and mortality but granular data from transplant centers such as ours serving a majority- minority and rural population are still scant. We aim to describe the impact of COVID-19 in our unique cohort of transplant patients. Methods Used During the pandemic, all transplant patients followed up at our center with reported COVID-19 were included in a registry. A case series of 136 patients drawn from this registry were included in this preliminary analysis spanning the period of March 2020 to March 2021. Statistical analysis was performed with R. Summary of Results The characteristics of our patients were: 54% male, 53% Black, 40% White, Median age 53 years, Median BMI 31, 47% were diabetic, 96% had hypertension, 16% had coronary artery disease. Median time after transplantation was 6.2 years (range 4 days to 37 years), 61% had thymoglobulin induction and almost uniformly were on tacrolimus, mycophenolate and prednisone. Baseline median creatinine 1.3 mg/dl and urine protein to creatinine ratio 0.18 g/g. The most commonly reported symptoms were fever (51%) dyspnea (48%), fatigue (46%) and myalgia (31%). 49% were hospitalized of whom half required ICU care. 82% of ICU patients were on ventilator support. 45% of patients had AKI, 7% required dialysis. 35% of patients required oxygen. There were 6 graft losses (4%) and 26 deaths (19%). Immunosuppression was reduced in most patients with antimetabolite reduction in 54%, and calcineurin inhibitor reduction in 44%. Treatments included dexamethasone (31%), and remdesivir (21%, convalescent plasma (6%), and monoclonal antibodies (4%). Creatinine and proteinuria post-COVID remained stable (1.4 mg/dl and 0.17 g/g respectively). 118 patients were followed up in clinic post-COVID and of these 15% reported continued severe COVID symptoms. On univariate analysis, age, race, gender, ABO blood type, diabetes status, cardiovascular disease, induction, time from transplant, baseline creatinine, proteinuria, baseline immunosuppression regimen, ACEi or ARB use, and reported symptoms (except for dyspnea) were not associated with risk of death. On multivariate analysis, ICU admission and need for dialysis were strongly predictive of death. Conclusions Despite serving a large rural population with a high burden of comorbidities, patient outcomes following COVID infection from our study are similar to other singlecenter and multi-center reports. As expected, the mortality rate in our cohort is much higher than the general population with high rates of hospitalization and need for ICU care. Aside from a significant minority, most patients recovered well and had stable renal allograft function. Our study is limited by its retrospective nature and risk of reporting bias.
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Background: Covid 19 infection associated glomerulopathy has most often been described as collapsing FSGS and occurs almost exclusively in black patients carrying APOL1 risk genotypes. Methods: We report an acute, COVID19-associated nephrotic glome-rulonephritis in a caucasian transplant recipient which led to terminal graft failure. Results: This 67 y old white female had received a living donor kidney 31 years ago for medullary cystic disease. Her clinical course on cyclos-porin/MMF had been stable with an eGFR around 20 ml/min/1.73 m in the last years. On her 31st annual checkup, she presented with an unusually high blood pressure (171/108), but afebrile (36.9°C), with an eGFR or 21 ml/min/1.73 m, a protein/creatinine ratio (PCR) of 503 mg/mmol and normal serum albumin. Physical examination was unremarkable except for some pain from thoracic herpes zoster 2 months previously. Her husband had tested positive for Covid19 on the same morning. She developed fever (38.9 °C) and cough on the same evening and tested positive for Covid19 the next day. MMF was paused and low dose steroids were instituted. In the following weeks, full nephrotic syndrome developed (edema, PCR of 1350 mg/mmol, serum albumin ↓ to 28 g/l). eGFR decreased to 8-10 ml/min/1.73 m. Renal biopsy on day 42 showed several instances of focal segmental sclerosis with collapsing morphology (Figure 1, consistent with "collapsing glomerulopathy"). In addition there were signs of capsular proliferation and electron dense deposits in the GBM, consistent with glome-rulonephritis. Sequencing of Exon 6 of the APOL1 gene was negative for G1 and G2 risk alleles in the patient and her kidney donor. Nephrotic syndrome never remitted, and renal function did not recover. Peritoneal dialysis was initiated 9 months after the Covid 19 infection. Figure 2: Self-rated health status over time Conclusions: Higher mortality in older recipients complies with data from the general population. The non-linear relationship between age and graft loss and the higher scored self-rated health status at all follow-up time-points compared to the pre-transplant status-regardless of age-highlight that age alone might not be an accurate measure for risk prediction and clinical decision making in kidney transplantation. Exploring other independent predictors, such as frailty as an indicator for biological age should be considered. Conclusions: This case documents an unusal Covid19-associated glo-merulonephritis with "collapsing features" which led to the loss of a 31 years functioning living donor kidney.
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Case report-IntroductionGranulomatosis with Polyangiitis (GPA) is a rare small-to medium-vessel vasculitis associated with anti-neutrophil cytoplasmic autoantibody (ANCA). Its multi-systemic features include pulmonary, ear, nose, and throat (ENT), renal, and neurological manifestations. Its incidence is estimated to be 10.2 cases per million population. It is challenging to diagnose when its symptoms are treated in isolation from one another. This case highlights the difficulty in diagnosing GPA in a patient with respiratory symptoms during the Coronavirus Disease 2019 (COVID-19) pandemic and describes the challenges of managing it in the context of a subsequent COVID-19 infection as the mainstay of treatment remains immunosuppression.Case report-Case descriptionA 78-year-old female non-smoker with a history of leg ulcers developed a 3-month history of cough and haemoptysis and was treated in primary care for suspected sinus and chest infections. She then presented to Accident and Emergency twice for the same symptoms and was discharged after having her antibiotics changed.2 weeks later, she presented for the third time with cough, ongoing haemoptysis, conjunctivitis in the right eye, pain over the right side of her head, and discharge from her right ear. She was admitted as she was pyrexical, tachycardic and her CRP was 60. COVID-19 swabs were negative. ENT team recommended IV ceftriaxone and metronidazole for suspected orbital cellulitis. Blood cultures remained negative. CT sinuses with contrast showed right sided thrombosis of transverse sinus and bilateral mastoid effusion of the middle ear. Following neurology review, she was anticoagulated with dalteparin. A day later, she was transferred to the Respiratory ward and dropped her Haemoglobin level to 70. Her chest radiograph showed diffuse alveolar haemorrhage and CT images showed widespread bilateral peri-hilar consolidation.A rheumatology opinion was sought and vasculitic screen showed ANCA 268, and PR3 >177. Her urinary protein/creatinine ratio was elevated at 90. Rheumatology team confirmed multi-systemic GPA and recommended starting oral Prednisolone 60 mg daily. After the renal team was consulted, she was moved to a side-room and started on IV Methylprednisolone (pulsed with three doses), along with cyclophosphamide and rituximab. Dalteparin was discontinued.2 days later, she desaturated, and became pyrexical. Repeat COVID-19 swabs were positive.Three Consultants agreed that Plasma Exchange and Non-Invasive Ventilation (NIV) would be inappropriate. A Do Not Attempt Resuscitation form was signed, and prognosis was discussed with the patient and her 78-year-old husband who requested to visit. Patient deteriorated and unfortunately died 6 days later.Case report-DiscussionThis case is interesting because it highlights the diagnostic challenge of GPA. Retrospectively, it may be noted that doctors persisted in treating suspected infection although the patient continued to deteriorate. However, a diagnosis should be re-considered if the patient does not respond to treatment and it is important to consider vasculitis as a cause of haemoptysis.Anticoagulation was started since the benefits were considered to outweigh the risks as her haemoptysis was of small volume. The patient soon developed pulmonary haemorrhage, so the risks of anticoagulation should not be underestimated in vasculitis.The Rheumatology team's cautious approach to immunosuppression was in stark contrast to the renal team's aggressive approach. The Renal team believed that concerns about protecting the patient from COVID-19 when she was negative from this infection should not take precedence over appropriate immunosuppression from a potentially fatal vasculitis.The patient was admitted at the start of the COVID-19 pandemic and was negative for COVID-19 on admission. She was nursed in a bay on the Respiratory ward where she later became COVID-19 positive. This raises questions about whether the earlier test was a false negative result or whether her infection was hospital-acquired. Infection cont ol guidelines were changing rapidly at the start of the COVID-19 pandemic.The decision to avoid plasma exchange was based on the findings of the PEXIVAS trial. NIV was avoided as it required a full-face mask to minimize particle dispersion but would pose an asphyxiation risk as patient was coughing up blood.Finally, the team learnt to be flexible in these extraordinary circumstances when dealing with the end-of-life decisions of the COVID-19 positive patient. Although her husband was a vulnerable person because of his age, he was given the opportunity to visit while wearing Personal Protective Equipment and agreed to self-isolate for two weeks.Case report-Key learning pointsThis case helped me appreciate the complexity of deciding to immunosuppress an already severely ill patient in the context of the COVID-19 pandemic. I recognised that the patient had a poor prognosis with or without immunosuppression and our role as healthcare professionals was to give her the best chance of recovery. The conference will allow me to interact with other colleagues and discuss what they would do in this situation as our Rheumatology and Renal teams had different approaches.After further reading on false negative results, we found that Johns Hopkins researchers found that testing people for SARS-CoV2 too early in the course of infection is likely to result in a false negative test even though they may eventually test positive for the virus.I have also learnt about the PEXIVAS trial which found that the addition of plasma exchange to standard therapy does not reduce the risk for all-cause mortality among patients with severe ANCA-associated vasculitis. Moreover, a reduced-dose regimen of glucocorticoids is non-inferior to a standard-dose protocol, while reducing the risk for serious infections.Diffuse alveolar haemorrhage (DAH) is not treatable with arterial embolization or bronchoscopic methods due to the diffuse nature of the bleeding. Extracorporeal membrane oxygenation (ECMO) has been used to support patients with DAH but the use of ECMO is controversial due to the need for anticoagulation.The conference will help me deepen my understanding of epidemic rheumatology which will be useful for my clinical practice going forward, especially if there is a second wave of the COVID-19 pandemic. I am keen to use this event to engage with other clinicians on immunosuppression in the context of infection so that I may confidently manage similarly complex cases in the future.