Acute renal failure caused by nephrotoxins.
Renal micropuncture studies have greatly changed our views on the pathophysiology of acute renal failure caused by nephrotoxins. Formerly, this type of renal insufficiency was attributed to a direct effect of the nephrotoxins on tubule epithelial permeability. According to that theory, glomerular filtration was not greatly diminished, the filtrate formed being absorbed almost quantitatively and nonselectively across damaged tubule epithelium. Studies in a wide variety of rat models have now shown glomerular filtration to be reduced to a level which will inevitably cause renal failure in and of itself. Passive backflow of filtrate across tubular epithelium is either of minor degree or nonexistent even in models where frank tubular necrosis has occurred. This failure of filtration cannot be attributed to tubular obstruction since proximal tubule pressure is distinctly subnormal in most models studied. Instead, filtration failure appears best attributed to intrarenal hemodynamic alterations. While certain facts tend to incriminate the renin-angiotensin system as the cause of the hemodynamic aberrations, others argue to the contrary. The issue is underactive investigation.
D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000503:physiopathology / Q000517:prevention & control; D000818:Animals; D001834:Body Water / Q000502:physiology; D002712:Chlorides / Q000633:toxicity; D003681:Dehydration; D004285:Dogs; D005919:Glomerular Filtration Rate; D005990:Glycerol / Q000633:toxicity; D007668:Kidney / Q000187:drug effects*; D007684:Kidney Tubules / Q000503:physiopathology; D008628:Mercury / Q000633:toxicity; D009399:Nephrons / Q000503:physiopathology; D011312:Pressure; D011453:Prostaglandins; D011817:Rabbits; D051381:Rats
D002712:Chlorides; D011453:Prostaglandins; D008628:Mercury; D005990:Glycerol