title: PAH extraction and estimation of plasma flow in human postischemic acute renal failure.
abstract: We determined the effect of postischemic injury to the human renal allograft on p-aminohippurate (PAH) extraction (E(PAH)) and renal blood flow. We evaluated renal function in 44 allograft recipients on two occasions: 1-3 h after reperfusion (day 0) and again on postoperative day 7. On day 0 subsets underwent intraoperative determination of renal blood flow (n = 35) by Doppler flow meter and E(PAH) (n = 25) by renal venous assay. Blood flow was also determined in another subset of 16 recipients on postoperative day 7 by phase contrast-cine-magnetic resonance imaging, and E(PAH) was computed from the simultaneous PAH clearance. Glomerular filtration rate (GFR) on day 7 was used to divide subjects into recovering (n = 23) and sustained (n = 21) acute renal failure (ARF) groups, respectively. Despite profound depression of GFR in the sustained ARF group, renal plasma flow was only slightly depressed, averaging 296 +/- 162 ml. min(-1). 1.73 m(-2) on day 0 and 202 +/- 72 ml. min(-1). 1.73 m(-2) on day 7, respectively. These values did not differ from corresponding values in the recovering ARF group: 252 +/- 133 and 280 +/- 109 ml. min(-1). 1.73 m(-2), respectively. E(PAH) was profoundly depressed on day 0, averaging 18 +/- 14 and 10 +/- 7% in recovering and sustained ARF groups, respectively, vs. 86 +/- 6% in normal controls (P < 0.001). Corresponding values on day 7 remained significantly depressed at 65 +/- 20 and 11 +/- 22%, respectively. We conclude that postischemic injury to the renal allograft results in profound impairment of E(PAH) that persists for at least 7 days, even after the onset of recovery. An ensuing reduction in urinary PAH clearance results in a gross underestimate of renal plasma flow, which is close to the normal range in the initiation, maintenance, and recovery stages of this injury.
authors.affiliation: Department of Medicine, Division of Nephrology, Department of Health Research and Policy, Stanford University School of Medicine, Stanford, California 94305, USA.
authors.forename: G
authors.initials: G
authors.lastname: Corrigan
authors.forename: D
authors.initials: D
authors.lastname: Ramaswamy
authors.forename: O
authors.initials: O
authors.lastname: Kwon
authors.forename: F G
authors.initials: FG
authors.lastname: Sommer
authors.forename: E J
authors.initials: EJ
authors.lastname: Alfrey
authors.forename: D C
authors.initials: DC
authors.lastname: Dafoe
authors.forename: R A
authors.initials: RA
authors.lastname: Olshen
authors.forename: J D
authors.initials: JD
authors.lastname: Scandling
authors.forename: B D
authors.initials: BD
authors.lastname: Myers
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology*; D000328:Adult; D000368:Aged; D005260:Female; D006801:Humans; D007511:Ischemia / Q000150:complications*; D007668:Kidney / Q000503:physiopathology; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D011183:Postoperative Complications; D012079:Renal Circulation; D015424:Reperfusion; D013997:Time Factors; D010130:p-Aminohippuric Acid / Q000097:blood / Q000378:metabolism*
chemical_list: D010130:p-Aminohippuric Acid