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Lui Forni


Honorary Professor
BSc, PHD, MB.BS, MRCPI, AFICM

Biography

Professor Lui Forni originally trained in basic science with a subsequent PhD in fast reaction physical chemistry, which was then followed by medical training at St George's Hospital Medical School. After house jobs, he undertook specialist training on the London Postgraduate Medical Schools Rotation.  Registrar Training in renal medicine and intensive care medicine was at St Thomas' hospital followed by ICU and Nephrology training at St Thomas' and St George's.  He was a consultant Intensivist/Nephrologist at the Western Sussex Hospitals Trust and Honorary Senior Lecturer at University of Sussex for over 10 years before moving to his current post at the Royal Surrey County Hospital NHS Foundation Trust in intensive care medicine.  

Research Interests

His research interests include pre-operative assessment of high-risk surgical candidates, all aspects of renal replacement therapy, diagnosis, pathophysiology and treatment of acute kidney injury and predictive modeling in acute medical admissions.  He has published over 100 papers including several book chapters as well as being a co-editor on one book.  He is a referee for over 20 journals and is on the editorial board of several.  He has been the UK Principal investigator for several international studies as well as currently being the lead investigator for a UK based study.  

Research Collaborations

Professor Forni has been an advisor for NCEPOD and was a founder member of the ESICM AKI group being elected chair of the section in 2013 and now has been elected chair of the research committee for the European Society of intensive care medicine. He has been a faculty member for numerous international conferences including the ESICM, SRLF, SMART and GREAT meetings as well as the ICS.  He is invited to lecture nationally and internationally.

My publications

Publications

Hodgson LE, Dimitrov BD, Roderick PJ, Venn R, Forni L (2017) Predicting AKI in emergency admissions: an external validation study of the acute kidney injury prediction score (APS), BMJ Open 7 (3) pp. e013511-e013511
Objectives Hospital-acquired acute kidney injury (HA-AKI) is associated with a high risk of mortality. Prediction models or rules may identify those most at risk of HA-AKI. This study externally validated one of the few clinical prediction rules (CPRs) derived in a general medicine cohort using clinical information and data from an acute hospitals electronic system on admission: the acute kidney injury prediction score (APS).

Design, setting and participants External validation in a single UK non-specialist acute hospital (2013?2015, 12?554 episodes); four cohorts: adult medical and general surgical populations, with and without a known preadmission baseline serum creatinine (SCr).

Methods Performance assessed by discrimination using area under the receiver operating characteristic curves (AUCROC) and calibration.

Results HA-AKI incidence within 7?days (kidney disease: improving global outcomes (KDIGO) change in SCr) was 8.1% (n=409) of medical patients with known baseline SCr, 6.6% (n=141) in those without a baseline, 4.9% (n=204) in surgical patients with baseline and 4% (n=49) in those without. Across the four cohorts AUCROC were: medical with known baseline 0.65 (95% CIs 0.62 to 0.67) and no baseline 0.71 (0.67 to 0.75), surgical with baseline 0.66 (0.62 to 0.70) and no baseline 0.68 (0.58 to 0.75). For calibration, in medicine and surgical cohorts with baseline SCr, Hosmer-Lemeshow p values were non-significant, suggesting acceptable calibration. In the medical cohort, at a cut-off of five points on the APS to predict HA-AKI, positive predictive value was 16% (13?18%) and negative predictive value 94% (93?94%). Of medical patients with HA-AKI, those with an APS e5 had a significantly increased risk of death (28% vs 18%, OR 1.8 (95% CI 1.1 to 2.9), p=0.015).

Conclusions On external validation the APS on admission shows moderate discrimination and acceptable calibration to predict HA-AKI and may be useful as a severity marker when HA-AKI occurs. Harnessing linked data from primary care may be one way to achieve more accurate risk prediction.

Hoste EAJ, Bagshaw SM, Bellomo R, Cely CM, Colman R, Cruz DN, Edipidis K, Forni LG, Gomersall CD, Govil D, Honore PM, Joannes-Boyau O, Joannidis M, Korhonen A-M, Lavrentieva A, Mehta RL, Palevsky P, Roessler E, Ronco C, Uchino S, Vazquez JA, Vidal Andrade E, Webb S, Kellum JA (2015) Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study, INTENSIVE CARE MEDICINE 41 (8) pp. 1411-1423 SPRINGER
Lambden Simon, Creagh-Brown Ben C., Hunt Julie, Summers Charlotte, Forni Lui G. (2018) Definitions and pathophysiology of vasoplegic shock, Critical Care 22 (174) pp. 1-8 BioMed Central
Vasoplegia is the syndrome of pathological low systemic vascular resistance, the dominant clinical feature of which
is reduced blood pressure in the presence of a normal or raised cardiac output. The vasoplegic syndrome is
encountered in many clinical scenarios, including septic shock, post-cardiac bypass and after surgery, burns and
trauma, but despite this, uniform clinical definitions are lacking, which renders translational research in this area
challenging. We discuss the role of vasoplegia in these contexts and the criteria that are used to describe it are
discussed. Intrinsic processes which may drive vasoplegia, such as nitric oxide, prostanoids, endothelin-1, hydrogen
sulphide and reactive oxygen species production, are reviewed and potential for therapeutic intervention explored.
Extrinsic drivers, including those mediated by glucocorticoid, catecholamine and vasopressin responsiveness of the
blood vessels, are also discussed. The optimum balance between maintaining adequate systemic vascular resistance
against the potentially deleterious effects of treatment with catecholamines is as yet unclear, but development of
novel vasoactive agents may facilitate greater understanding of the role of the differing pathways in the
development of vasoplegia. In turn, this may provide insights into the best way to care for patients with this
common, multifactorial condition.
Lambden Simon, Creagh-Brown Ben C., Hunt Julie, Summers Charlotte, Forni Lui G. (2018) Definitions and pathophysiology of vasoplegic shock, Critical Care 22 174 pp. 1-8 BioMed Central Ltd.
Vasoplegia is the syndrome of pathological low systemic vascular resistance, the dominant clinical feature of which is reduced blood pressure in the presence of a normal or raised cardiac output. The vasoplegic syndrome is encountered in many clinical scenarios, including septic shock, post-cardiac bypass and after surgery, burns and trauma, but despite this, uniform clinical definitions are lacking, which renders translational research in this area challenging. We discuss the role of vasoplegia in these contexts and the criteria that are used to describe it are discussed. Intrinsic processes which may drive vasoplegia, such as nitric oxide, prostanoids, endothelin-1, hydrogen sulphide and reactive oxygen species production, are reviewed and potential for therapeutic intervention explored. Extrinsic drivers, including those mediated by glucocorticoid, catecholamine and vasopressin responsiveness of the blood vessels, are also discussed. The optimum balance between maintaining adequate systemic vascular resistance against the potentially deleterious effects of treatment with catecholamines is as yet unclear, but development of novel vasoactive agents may facilitate greater understanding of the role of the differing pathways in the development of vasoplegia. In turn, this may provide insights into the best way to care for patients with this common, multifactorial condition. © 2018 The Author(s).