Pathophysiology of ischaemic acute renal failure.
This chapter summarizes the pathophysiology of ischaemic acute renal failure from both the experimental and clinical points of view. Traditionally, the abrupt fall in glomerular filtration rate (GFR) is thought to be due to an interplay of haemodynamic and tubular abnormalities. The intrarenal haemodynamic alterations include renal vasoconstriction, leukocyte-endothelium interactions and loss of blood flow and GFR autoregulation. During recent years it has become evident that pronounced outer medulary ischaemia makes an important contribution. In severe and prolonged ischaemia, the tubular epithelial cells can undergo either sublethal or lethal cell damage. Cell death occurs by necrosis and apoptosis. The different mechanisms of post-ischaemic cell damage are discussed. The post-ischaemic kidney also shows a dramatic capacity for recovery. During this recovery phase some of the damaged cells undergo de-differentiation--which is an important step in regeneration of the tubular epithelium. Recent evidence points to the possibility that infiltration of the kidney with bone-marrow-derived stem cells contributes to the repair process. The molecular mechanisms and the effect of growth factors are summarized.
Lameire
Norbert H
NH
Renal Division, Department of Medicine, University Hospital, De Pintelaan, 185, 9000 Ghent, Belgium. norbert.lameire@rug.ac.be
Vanholder
Raymond
R
D058186:Acute Kidney Injury / Q000473:pathology / Q000503:physiopathology*; D006133:Growth Substances / Q000502:physiology; D006801:Humans; D007511:Ischemia / Q000473:pathology / Q000503:physiopathology*; D007683:Kidney Tubular Necrosis, Acute / Q000473:pathology / Q000503:physiopathology; D007684:Kidney Tubules / Q000473:pathology / Q000503:physiopathology; D012079:Renal Circulation / Q000502:physiology*
D006133:Growth Substances