The role of tubular necrosis in the pathophysiology of acute renal failure.
Renal tubular function was evaluated in vitro by kidney slice uptakes of p-aminohippurate (PAH) and tetraethylammonium (TEA) at 24 and 48 h in water-drinking rats and at 24 h in chronic saline-loaded rats after induction of acute tubular necrosis (ATN) by HgCl2 and glycerol injection. Significant correlations between decrease tubular uptake of PAH and TEA and elevated serum creatinine levels were noted in both models of ATN in water- and saline-drinking rats. However, with the same degree of impairment of PAH and TEA uptakes the creatinine was significantly lower in saline-loaded rats than in water-drinking rats in both forms of ATN. The correlation between impaired tubular function and elevated creatinine suggests that tubular damage and glomerular filtration reduction might be pathophysiologically related in ATN.
D058186:Acute Kidney Injury / Q000503:physiopathology*; D000618:Aminohippuric Acids / Q000378:metabolism; D000818:Animals; D003404:Creatinine / Q000097:blood; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000503:physiopathology; D007683:Kidney Tubular Necrosis, Acute / Q000503:physiopathology*; D007684:Kidney Tubules / Q000503:physiopathology*; D007688:Kidneys, Artificial; D009336:Necrosis; D051381:Rats; D012996:Solutions; D013757:Tetraethylammonium Compounds / Q000378:metabolism
D000618:Aminohippuric Acids; D012996:Solutions; D013757:Tetraethylammonium Compounds; D003404:Creatinine