Mediators of ischemic renal injury.
Acute renal failure is a serious consequence of renal ischemia. The diagnosis carries an associated high mortality rate. When blood flow to the kidneys is inadequate to supply metabolic demands, a number of pathophysiological changes occur that ultimately result in cell death and tissue dysfunction, characterized by a marked reduction in glomerular filtration rate and associated accumulation of systemic toxins and disorders of fluid and electrolyte metabolism. In this chapter we review the factors that have been implicated as mediators of the renal tissue damage associated with ischemia and reperfusion.
Bonventre
J V
JV
Medical Services, Massachusetts General Hospital, Boston.
D000138:Acidosis / Q000378:metabolism; D058186:Acute Kidney Injury / Q000209:etiology; D000255:Adenosine Triphosphate / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D005919:Glomerular Filtration Rate; D006801:Humans; D007511:Ischemia; D007668:Kidney / Q000098:blood supply* / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D010740:Phospholipases / Q000378:metabolism; D012079:Renal Circulation
D000255:Adenosine Triphosphate; D010740:Phospholipases; D010100:Oxygen; D002118:Calcium