PAH extraction and estimation of plasma flow in human postischemic acute renal failure

We determined the effect of postischemic injury to the human renal allograft on p-aminohippurate (PAH) extraction (EPAH) 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 EPAH( 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 EPAH 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. EPAH 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 7remained significantly depressed at 65 ± 20 and 11 ± 22%, respectively. We conclude that postischemic injury to the renal allograft results in profound impairment of EPAH 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.