Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/12121
Title: Glomerular haemodynamics, the renal sympathetic nervous system and sepsis-induced acute kidney injury.
Authors: Calzavacca, Paolo;May, Clive N;Bellomo, Rinaldo
Affiliation: Department of Anaesthesia and Intensive Care, Uboldo Hospital, Milan, Italy.
Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, VIC, Australia.
Australian and New Zealand Intensive Care Research Centre, Monash University School of Epidemiology and Public Health, Melbourne, Australia Department of Intensive Care, Austin Health, Heidelberg, VIC, Australia.
Issue Date: 11-Mar-2014
Citation: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association 2014; 29(12): 2178-84
Abstract: To describe recent insights into glomerular haemodynamics in septic acute kidney injury (AKI).We reviewed the literature with particular emphasis on recent findings in animal experiments and human studies in relation to renal macro- and micro-renal haemodynamics during septic AKI.The dominant paradigm is that septic AKI is due to decreased renal perfusion with ischaemic loss of glomerular filtration rate (GFR), ischaemic tubular cell injury and acute tubular necrosis (ATN). However, recent experimental and human studies challenge this view of the pathogenesis of septic AKI. In addition, rapid post-mortem and experimental histological studies do not support ATN as the histological substrate of septic AKI. Finally, more recent experimental evidence suggests that changes in the glomerular and peri-glomerular haemodynamics provide a more likely explanation for the loss of GFR seen in the early phases of septic AKI.Despite a long-standing paradigm that septic AKI is due to renal hypo-perfusion and associated ATN, experimental and human studies increasingly suggest that changes in the state of the glomerular and peri-glomerular micro-vasculature are a more likely additional explanation for this condition.
Internal ID Number: 24619060
URI: http://ahro.austin.org.au/austinjspui/handle/1/12121
DOI: 10.1093/ndt/gfu052
URL: http://www.ncbi.nlm.nih.gov/pubmed/24619060
Type: Journal Article
Subjects: acute kidney injury
afferent arteriole
efferent arteriole
renal blood flow
sepsis
Animals
Glomerular Filtration Rate
Humans
Kidney Glomerulus.innervation.physiopathology
Kidney Tubular Necrosis, Acute.etiology.physiopathology
Sepsis.complications
Sympathetic Nervous System.pathology
Appears in Collections:Journal articles

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