David Jayne

University of Cambridge, Cambridge, England, United Kingdom

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Publications (266)1815.76 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Patients with anti-glomerular basement membrane (GBM) disease are at increased risk of morbidity and mortality from renal failure, pulmonary haemorrhage or complications of treatment. One-third also have circulating anti-neutrophil cytoplasmic antibodies (ANCA). The aim of this study was to determine the clinicopathologic predictors of patient and renal outcomes in anti-GBM disease with or without ANCA. Retrospective review of 43 patients diagnosed with anti-GBM disease over 20 years in two centres, including nine with dual anti-GBM and ANCA positivity. Renal biopsies from 27 patients were scored for the presence of active and chronic lesions. Dual-positive patients were almost 20 years older than those with anti-GBM positivity alone (P = 0.003). The overall 1-year patient and renal survivals were 88 and 16%, respectively. Oligoanuria at diagnosis was the strongest predictor of mortality; none of the 16 patients without oligoanuria died. In a Cox regression model excluding oligoanuria, age was the only other independent predictor of survival. Pulmonary haemorrhage and dialysis dependence did not influence mortality. Thirty-five of the forty-three (81%) patients required dialysis at presentation, including all nine dual-positive patients. Of them, only two (5.7%) regained renal function at 1 year. By logistic regression, oligoanuria at diagnosis and percentage of crescents were independent predictors of dialysis independence at 3 months. However, in biopsied patients, the presence of crescents (>75%) added little to the presence of oligoanuria in predicting dialysis independence. Histological activity and chronicity indices did not predict renal outcome. Two of the nine (22%) dual-positive patients relapsed compared with none of the anti-GBM alone patients. Seven patients received kidney transplants without disease recurrence. Oligoanuria is the strongest predictor of patient and renal survival while percentage of glomerular crescents is the only pathologic parameter associated with poor renal outcome in anti-GBM disease. Kidney biopsy may not be necessary in oligoanuric patients without pulmonary haemorrhage. © The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
    01/2015;
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    ABSTRACT: Takayasu arteritis (TAK) and giant cell arteritis (GCA) are 2 major variants of large vessel vasculitis (LVV). The frequent involvement of large vessels in GCA has raised the possibility that TAK and GCA should be regarded as 1 disease. By detailed phenotyping of a single-center cohort, we aimed to define the differences between TAK and GCA.
    The Journal of Rheumatology 11/2014; · 3.17 Impact Factor
  • David Jayne
    New England Journal of Medicine 11/2014; 371(19):1839-40. · 54.42 Impact Factor
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    ABSTRACT: Airway stenosis occurs in patients with granulomatosis with polyangiitis (GPA or Wegener granulomatosis). It produces significant morbidity and contributes to mortality.
    JAMA otolaryngology-- head & neck surgery. 10/2014;
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    ABSTRACT: The monoclonal anti-CD20 antibody rituximab depletes B cells in the treatment of lymphoma and autoimmune disease, and contributes to alloantibody reduction in transplantation across immunological barriers. The effects of rituximab on T cells are less well described. T follicular helper cells (Tfh) provide growth and differentiation signals to germinal center (GC) B cells to support antibody production, and suppressive T follicular regulatory cells (Tfr) regulate this response. In mice, both Tfh and Tfr are absolutely dependent on B cells for their formation and on the GC for their maintenance. Here, we demonstrate that rituximab treatment results in a lack of GC B cells in human lymph nodes without affecting the Tfh or Tfr cell populations. These data demonstrate that human Tfh and Tfr do not require an on-going GC response for their maintenance. The persistence of Tfh and Tfr following rituximab treatment may permit rapid reconstitution of the pathological GC response once the B cell pool begins to recover. Strategies for maintaining remission after rituximab therapy will need to take this persistence of Tfh into account.
    Blood 09/2014; 124(17). · 9.78 Impact Factor
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    ABSTRACT: Granulomatosis with polyangiitis and microscopic polyangiitis are ANCA-associated vasculitides (AAVs). The Vasculitis Damage Index (VDI) quantifies damage. This study aims to determine the factors associated with long-term damage in the AAVs.
    Rheumatology (Oxford, England) 09/2014; · 4.44 Impact Factor
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    ABSTRACT: Granulomatosis with polyangiitis and microscopic polyangiitis are anti-neutrophil cytoplasmic antibody-associated vasculitides (AAVs) that are prone to cycles of remission and relapse. The introduction of cytotoxic therapy has changed the prognosis for these diseases from typically fatal to manageable chronic illnesses with a relapsing course. Despite improvements in outcomes, recurrence of disease and drug-related toxicity continue to produce significant morbidity and mortality. Better understanding of the pathogenesis of AAV and the mechanism of action of cyclophosphamide has led to investigation of therapies that target B cells. Two randomized controlled trials have shown that rituximab is not inferior to cyclophosphamide for induction of remission in severe AAV, with no significant difference in the incidence of overall adverse events in rituximab- versus cyclophosphamide-treated patients. Data from ongoing clinical trials will determine the role of rituximab in the maintenance of remission.
    Journal of nephrology 09/2014; 28(1). · 2.00 Impact Factor
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    ABSTRACT: Treatment with azathioprine within 3 months of remission induction with cyclophosphamide is a common treatment strategy for patients with ANCA-associated vasculitis. This study comprised patients undergoing long-term follow-up who were randomly allocated to azathioprine after 3-6 months or after 12 months of cyclophosphamide treatment.DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Patients from 39 European centers between 1995 and 1997 with a new diagnosis of ANCA-associated vasculitis that involved the kidneys or another vital organ were eligible. At the time of diagnosis, participants were randomly allocated to convert to azathioprine after 3-6 months (the azathioprine group) or after 12 months of cyclophosphamide (the cyclophosphamide group). Patients who did not achieve a remission within 6 months were excluded. This study assessed relapses, ESRD, and death during long-term follow-up.RESULTS: Patients were allocated to the azathioprine group (n=71) and the cyclophosphamide group (n=73). Of these patients, 63 (43.8%) developed a relapse, 35 (24.3%) developed a renal relapse, 13 (9.0%) developed ESRD, and 21 (14.6%) died. Although there were worse outcomes in the azathioprine group, none were statistically significant. The subdistribution hazard ratio [sHR] for relapse was 1.63 (95% confidence interval [95% CI], 0.99 to 2.71), the composite of relapse or death hazard ratio [HR] was 1.59 (95% CI, 1.00 to 2.54), the ESRD sHR was 1.71 (95% CI, 0.56 to 5.19), and the death HR was 0.75 (95% CI, 0.32 to 1.79).CONCLUSIONS: It remains uncertain whether converting to azathioprine after 3-6 months of induction cyclophosphamide therapy is as effective as converting after 12 months. Outcomes are still poor for this group of patients and further research is required to determine the optimal timing of maintenance therapy.
    Clinical Journal of the American Society of Nephrology 06/2014; · 5.25 Impact Factor
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    ABSTRACT: Rituximab is a B cell depleting anti-CD20 monoclonal antibody. CD20 is not expressed on mature plasma cells and accordingly rituximab does not have immediate effects on immunoglobulin levels. However, after rituximab some patients develop hypogammaglobulinaemia.
    BMC Musculoskeletal Disorders 05/2014; 15(1):178. · 1.90 Impact Factor
    This article is viewable in ResearchGate's enriched format
  • David Jayne
    Rheumatology (Oxford, England) 05/2014; 53(suppl 2):i12. · 4.44 Impact Factor
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    ABSTRACT: The phenotype of renal involvement in anti-neutrophil cytoplasmic antibodies (ANCA) vasculitis has a major influence on survival, and histological subgrouping of diagnostic renal biopsies has been proposed to aid in the prediction of renal outcome. We aimed to validate this histological subgrouping and to investigate the additional value of ANCA serotype in the prediction of renal outcome. Data were retrospectively collected from the time of diagnosis by systematic review of medical records from 136 patients with renal biopsies recruited to cohorts from the UK and Spain, over 15 years. The end point, renal survival, was the composite of end-stage renal disease (ESRD) or death from any cause. The occurrence of ESRD, Stage 4 Kidney Disease Outcomes Quality Initiative-Chronic Kidney Disease, was assessed separately, in order to establish a severity index risk of chronic kidney disease. Renal survival at 5 years was 96% in the focal, 86% in the crescentic, 81% in the mixed and 61% in the sclerotic subgroups (P = 0.03). Myeloperoxidase (MPO)-ANCA was associated with more severe disease when compared with PR3-ANCA, as demonstrated by a lower frequency of focal and higher frequency of sclerotic subgroups, by more advanced interstitial fibrotic change and by lower glomerular filtration rate at diagnosis and worse renal function at 1 and 2 years. We have confirmed the predictive value for renal survival of the ANCA vasculitis histology classification in a multi-centre study. We found a worse renal outcome in patients with tubulointerstitial fibrosis and atrophy. MPO-ANCA positive patients had a worse renal prognosis due to more severe glomerular injury. These results contribute to patient stratification in renal vasculitis for therapeutic, epidemiological and basic research.
    Nephrology Dialysis Transplantation 04/2014; · 3.37 Impact Factor
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    ABSTRACT: The principle of treating-to-target has been successfully applied to many diseases outside rheumatology and more recently to rheumatoid arthritis. Identifying appropriate therapeutic targets and pursuing these systematically has led to improved care for patients with these diseases and useful guidance for healthcare providers and administrators. Thus, an initiative to evaluate possible therapeutic targets and develop treat-to-target guidance was believed to be highly appropriate in the management of systemic lupus erythematosus (SLE) patients as well. Specialists in rheumatology, nephrology, dermatology, internal medicine and clinical immunology, and a patient representative, contributed to this initiative. The majority convened on three occasions in 2012-2013. Twelve topics of critical importance were identified and a systematic literature review was performed. The results were condensed and reformulated as recommendations, discussed, modified and voted upon. The finalised bullet points were analysed for degree of agreement among the task force. The Oxford Centre level of evidence (LoE, corresponding to the research questions) and grade of recommendation (GoR) were determined for each recommendation. The 12 systematic literature searches and their summaries led to 11 recommendations. Prominent features of these recommendations are targeting remission, preventing damage and improving quality of life. LoE and GoR of the recommendations were variable but agreement was >0.9 in each case. An extensive research agenda was identified, and four overarching principles were also agreed upon. Treat-to-target-in-SLE (T2T/SLE) recommendations were developed by a large task force of multispecialty experts and a patient representative. It is anticipated that 'treating-to-target' can and will be applicable to the care of patients with SLE.
    Annals of the rheumatic diseases 04/2014; · 9.27 Impact Factor
  • Miklos Perenyei, David R W Jayne, Oliver Floßmann
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    ABSTRACT: Gusperimus is an immunosuppressive drug with a unique mode of action. We review its effects on different arms of the immune system and the current evidence for clinical applications, particularly in the treatment of transplant rejection and ANCA-associated vasculitis.
    Rheumatology (Oxford, England) 02/2014; · 4.44 Impact Factor
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    ABSTRACT: Background The clinical course of autoimmune and infectious disease varies greatly even between individuals with the same condition. An understanding of the molecular basis for this heterogeneity could lead to substantial improvements in both monitoring and treatment. Since persistent antigen is targeted in both autoimmunity and chronic infection, similar pathways could dictate the success of that response. However, whereas a successful response to pathogen results in clearance and recovery from disease, a robust response to self-antigen might drive relapsing autoimmunity. During chronic viral infection, CD8 T cells develop progressive loss of function in a process termed exhaustion, characterised by high expression of inhibitory receptors (such as programmed cell death 1 [PD1]) and low expression of memory markers (such as interleukin-7 receptor). These can serve both as biomarkers of viral progression and as targets for therapy. We sought to determine whether an analogous exhausted state exists during autoimmune responses targeting persistent self-antigen. Methods To identify gene expression signatures associated with clinical outcome, we used weighted gene coexpression network analysis of concurrently sampled CD4 and CD8 T-cell transcriptomes from patients with four distinct autoimmune diseases (23 with systemic lupus erythematosus [SLE], 44 with anti-neutrophil cytoplasmic antibody-associated vasculitis [AAV], and 56 with Crohn's disease or ulcerative colitis) and with chronic viral infection (42 with HIV infection). Association with clinical outcome was independently validated in 1145 samples from 504 individuals with infectious disease (HIV, hepatitis C virus, dengue), during vaccination (malaria, yellow fever, influenza), and autoimmunity (type 1 diabetes, SLE, AAV, Crohn's disease and ulcerative colitis, and idiopathic pulmonary fibrosis). We used an artificial antigen presenting cell to modify provision of co-stimulatory and inhibitory signals (as suggested by the network analysis) to primary human T cells during in-vitro differentiation. In this way we tested whether expression signatures associated with clinical outcome might be modified by manipulating co-stimulatory signals and whether they reflected changes in T-cell function. Findings Network analysis of CD8 T-cell transcriptomes identified a common signature of T-cell exhaustion during responses to chronic viral and self-antigen. However, whereas exhausted responses were associated with poor viral clearance, they predicted a less severe course in multiple autoimmune diseases. In autoimmunity, we found that where CD8 T-cell exhaustion was high a concurrent signature of CD4 T-cell co-stimulation was low. We used this signature to identify CD2 as a co-stimulatory signal preventing the development of T-cell exhaustion during controlled in-vitro assays, recreating expression patterns seen in patients with severe autoimmunity and leading to enhanced T-cell survival during primary and repeated stimulation. Finally, exogenous signals through the inhibitory receptor PD1 restricted development of this robust population. Interpretation Here we show that the process of CD8 T-cell exhaustion is important not only in facilitating viral persistence during chronic infection, but also in shaping the immune response to persistent self-antigen during autoimmunity. The observed correlation between T-cell exhaustion, co-stimulation, and subsequent prognosis increases our understanding of the pathogenesis of severe autoimmune disease and might help stratify patients for personalised therapy. Furthermore, our data suggest that future modulation of T-cell exhaustion may lead to new therapeutic opportunities in autoimmunity. Funding Wellcome Trust, Biomedical Research Centre, National Institute for Health Research.
    The Lancet 02/2014; 383:S12. · 39.21 Impact Factor
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    ABSTRACT: Objectives. ANCA-associated vasculitis (AAV) commonly affects those of working age. Since survival rates have been transformed by immunotherapeutics, the measurement of other outcomes has become increasingly relevant. Work disability is an important outcome for both patient and society that has yet to be fully evaluated in AAV. We aimed to assess employment status in AAV patients and identify putative predictors of their work disability.Methods. A cross-sectional study was undertaken. AAV cases were recruited according to consecutive clinic attendance. Subjects completed a questionnaire that determined employment status and other psychosocial measures. Clinical factors were concurrently recorded by the attending physician. From the data of those subjects of working age, a multivariable model was developed using forward stepwise logistic regression to identify the independent associations of work disability, defined by those subjects reporting unemployment secondary to ill-health. Results are expressed as odds ratios (ORs) and 95% CIs.Results. Of the 410 participants (84.4% response rate), 149 (36.7%) were employed, 197 (48.6%) retired and 54 (13.3%) unemployed secondary to ill health. Of those of working age, 26.0% were considered work disabled. Fatigue (OR 7.1, 95% CI 1.5, 33.1), depression (OR 4.4, 95% CI 1.8, 10.8), severe disease damage [Vasculitis Damage Index (VDI) > 4 (OR 3.9, 95% CI 1.01, 14.7)] and being overweight (OR 3.4, 95% CI 1.3, 8.9) were independently associated with their unemployment.Conclusion. A quarter of working-age AAV subjects reported unemployment as a result of ill health and are characterized by high levels of fatigue, depression, disease damage and being overweight. These potentially modifiable factors may inform future multidisciplinary interventions aimed at alleviating work disability.
    Rheumatology (Oxford, England) 01/2014; · 4.44 Impact Factor
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    ABSTRACT: There are differences between Europe and Japan in the incidence and antineutrophil cytoplasmic antibody (ANCA) serotype of patients with microscopic polyangiitis (MPA). However, differences in phenotype or outcome have not been explored. We aimed to identify differences in phenotype and outcome of MPA between Europe and Japan. Sequential cohorts of patients with MPA and renal limited vasculitis were collected from European and Japanese centers (n = 147 and n = 312, respectively). Trial databases from the European Vasculitis Society and the Japanese patients with Myeloperoxidase (MPO)-ANCA-Associated Vasculitis (JMAAV) trial were studied (n = 254 and n = 48, respectively). We evaluated baseline characteristics including ANCA status and organ involvement, treatment, survival, and renal survival. Differences in survival and renal survival were studied using multivariate analysis. The non-trial cohorts showed patients with MPA in Japan had a higher age at onset, more frequent MPO-ANCA positivity, lower serum creatinine, and more frequent interstitial pneumonitis than those in Europe (all p < 0.01). Comparisons between the trial databases demonstrated similar results. Cumulative patient survival and renal survival rates were not different between Europe and Japan (p = 0.71 and p = 0.38, respectively). Multivariate analysis identified age at onset, serum creatinine, gastrointestinal, and respiratory involvement as factors with higher risk of death. For endstage renal failure, serum creatinine and use of plasma exchange were identified as factors with higher risk, and immunosuppressant use as lower risk factors. Phenotypes in patients with MPA were different between Europe and Japan. However, the outcomes of patient survival and renal survival were similar.
    The Journal of Rheumatology 01/2014; · 3.17 Impact Factor
  • Shunsuke Furuta, David Jayne
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    ABSTRACT: The current standard therapy for antineutrophil cytoplasm antibody-associated vasculitis (AAV), high-dose glucocorticoid and cyclophosphamide followed by azathioprine, has improved the disease prognosis. However, there are still unmet needs. For example, reducing relapse risk and glucocorticoid toxicity. Newer therapies are needed. Potential newer drugs are emerging following a better understanding of disease mechanisms and the availability of targeted therapies to B cells, T cells, proinflammatory cytokines and complement. Rituximab, an anti-CD20 monoclonal antibody, has proven efficacy in remission induction therapy for AAV, and two trials with rituximab as remission maintenance therapy are ongoing. Clinical trials evaluating mycophenolate mofetil as remission induction therapy, gusperimus, belimumab and complement factor C5a inhibition are also ongoing, and many other potential candidates are being investigated both clinically and experimentally. B-cell therapy is now an established treatment in AAV and several other therapies are under evaluation. However, the unmet need in vasculitis therapy remains large and newer therapies either alone or in combination will need to both improve efficacy and permit reductions in glucocorticoid and immunosuppressive exposure.
    Current opinion in rheumatology 11/2013; · 5.07 Impact Factor
  • Shunsuke Furuta, David Jayne
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    ABSTRACT: The current standard therapy for antineutrophil cytoplasm antibody-associated vasculitis (AAV), high-dose glucocorticoid and cyclophosphamide followed by azathioprine, has improved the disease prognosis. However, there are still unmet needs. For example, reducing relapse risk and glucocorticoid toxicity. Newer therapies are needed. Potential newer drugs are emerging following a better understanding of disease mechanisms and the availability of targeted therapies to B cells, T cells, proinflammatory cytokines and complement. Rituximab, an anti-CD20 monoclonal antibody, has proven efficacy in remission induction therapy for AAV, and two trials with rituximab as remission maintenance therapy are ongoing. Clinical trials evaluating mycophenolate mofetil as remission induction therapy, gusperimus, belimumab and complement factor C5a inhibition are also ongoing, and many other potential candidates are being investigated both clinically and experimentally. B-cell therapy is now an established treatment in AAV and several other therapies are under evaluation. However, the unmet need in vasculitis therapy remains large and newer therapies either alone or in combination will need to both improve efficacy and permit reductions in glucocorticoid and immunosuppressive exposure.
    Current opinion in rheumatology 11/2013; · 5.07 Impact Factor
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    ABSTRACT: To describe short-term (up to 12 months) and long-term (up to 7 years) damage in patients with newly diagnosed antineutrophil-cytoplasm antibody-associated vasculitis (AAV). Data were combined from six European Vasculitis Study group trials (n=735). Long-term follow-up (LTFU) data available for patients from four trials (n=535). Damage accrued was quantified by the Vasculitis Damage Index (VDI). Sixteen damage items were defined a priori as being potentially treatment-related. VDI data were available for 629 of 735 patients (85.6%) at baseline, at which time 217/629 (34.5%) had ≥1 item of damage and 32 (5.1%) ≥5 items, reflecting disease manifestations prior to diagnosis and trial enrolment. LTFU data were available for 467/535 (87.3%) at a mean of 7.3 years postdiagnosis. 302/535 patients (56.4%) had VDI data at LTFU, with 104/302 (34.4%) having ≥5 items and only 24 (7.9%) no items of damage. At 6 months and LTFU, the most frequent items were proteinuria, impaired glomerular filtration rate, hypertension, nasal crusting, hearing loss and peripheral neuropathy. The frequency of damage, including potentially treatment-related damage, rose over time (p<0.01). At LTFU, the most commonly reported items of treatment-related damage were hypertension (41.5%; 95% CI 35.6 to 47.4%), osteoporosis (14.1%; 9.9 to 18.2%), malignancy (12.6%; 8.6 to 16.6%), and diabetes (10.4%; 6.7 to 14.0%). In AAV, renal, otolaryngological and treatment-related (cardiovascular, disease, diabetes, osteoporosis and malignancy) damage increases over time, with around one-third of patients having ≥5 items of damage at a mean of 7 years postdiagnosis.
    Annals of the rheumatic diseases 11/2013; · 9.27 Impact Factor
  • Mikkel Faurschou, David R W Jayne
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    ABSTRACT: Several monoclonal antibodies targeting B cells have been tested as therapeutics for inflammatory rheumatic diseases. We review important observations from randomized clinical trials regarding the efficacy and safety of anti-B cell antibody-based therapies for rheumatoid arthritis, systemic lupus erythematosus, antineutrophil cytoplasmic antibody-associated vasculitis, polymyositis/dermatomyositis, and primary Sjögren's syndrome. For some anti-B cell agents, clinical benefits have been convincingly demonstrated, while other B cell targeted therapies failed to improve outcomes when added to standard-of-care treatment or were associated with increased rates of adverse events. Although the risk-benefit balance seems to be acceptable for currently licensed anti-B cell agents, additional studies are required to fully assess the safety of treatment regimens involving prolonged interference with B cell counts and functions in rheumatic disorders. Future studies should also evaluate how to maintain disease control by means of conventional and/or biologic immunosuppressants after remission-induction with anti-B cell antibodies. Expected final online publication date for the Annual Review of Medicine Volume 65 is January 14, 2014. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.
    Annual review of medicine 10/2013; · 9.94 Impact Factor

Publication Stats

10k Citations
1,815.76 Total Impact Points

Institutions

  • 1990–2015
    • University of Cambridge
      • Department of Medicine
      Cambridge, England, United Kingdom
    • Papworth Hospital NHS Foundation Trust
      Papworth, England, United Kingdom
  • 2012–2014
    • Cambridge Institute for Medical Research
      Cambridge, England, United Kingdom
    • Aarhus University Hospital
      Aarhus, Central Jutland, Denmark
  • 2009–2014
    • Cambridge University Hospitals NHS Foundation Trust
      • Addenbrooke's Hospital
      Cambridge, England, United Kingdom
  • 2012–2013
    • McMaster University
      • Department of Clinical Epidemiology and Biostatistics
      Hamilton, Ontario, Canada
  • 2008–2013
    • University of Oxford
      • Oxford e-Research Centre
      Oxford, England, United Kingdom
  • 2011
    • University of Birmingham
      • School of Immunity and Infection
      Birmingham, ENG, United Kingdom
  • 2006–2011
    • Leiden University Medical Centre
      • Department of Pathology
      Leiden, South Holland, Netherlands
  • 2010
    • National Jewish Health
      Denver, Colorado, United States
    • University of Aberdeen
      Aberdeen, Scotland, United Kingdom
    • The Bracton Centre, Oxleas NHS Trust
      Дартфорде, England, United Kingdom
    • Second University of Naples
      Caserta, Campania, Italy
    • Royal Berkshire NHS Foundation Trust
      Reading, England, United Kingdom
  • 2007
    • The University of Calgary
      • Department of Medicine
      Calgary, Alberta, Canada
    • Vrije Universiteit Brussel
      Bruxelles, Brussels Capital Region, Belgium
  • 1999–2007
    • St. George's School
      • Division of Renal Medicine
      Middletown, Rhode Island, United States
    • St George's, University of London
      Londinium, England, United Kingdom
  • 1999–2002
    • Epsom and St Helier University Hospitals NHS Trust
      Эпсом, England, United Kingdom
  • 2001
    • Queen Elizabeth Hospital Birmingham
      Birmingham, England, United Kingdom
  • 1996
    • University of London
      Londinium, England, United Kingdom