PAH extraction and estimation of plasma flow in human postischemic acute renal failure
PAH extraction and estimation of plasma flow in human postischemic acute renal failure
复制标题
DOI：
10.1152/ajprenal.1999.277.2.f312
复制
发表时间：
1999-08-01
影响因子：
4.2
通讯作者：
Myers, BD
中科院分区：
文献类型：
--
作者：
Corrigan, G;Ramaswamy, D;Myers, BD
对44例同种异体肾移植受者分别于再灌注后1~3h(第0天)和术后第7天测定肾功能。第0天分别用多普勒血流仪测定35例移植肾血流量(n=35)，用肾静脉血流法测定25例移植肾血流量(n=25)。另一组16名受者在术后第7天通过相位对比-电影-磁共振成像测定血流量，并根据同时的PAH清除量计算EPAH。根据第7天肾小球滤过率(GFR)将受试者分为恢复期(n=23)和持续性(n=21)急性肾功能衰竭(ARF)组。持续性ARF组肾小球滤过率(GFR)显著降低，但肾血流量仅轻度降低，0d平均为296+/-162ml.min(-1)、1.73m(-2)，第7天平均为202+/-72ml.min(-1)、1.73m-2。分别为252+/-133和280+/-109ml.min(-1)，1.73m(-2)，E(PAH)在第0天显著降低，恢复期和持续性组分别为18+/-14和10+/-7%，而正常对照组为86+/-6%(P<；0.001)。粘土7上的相应数值分别保持在65+/-20和11+/-22%。我们的结论是，移植肾的缺血后损伤导致EPAH的严重损害，这种损害至少持续7天，即使在开始恢复之后也是如此。随之而来的尿PAH清除量的减少导致肾血浆流量的严重低估，这接近于这种损伤的起始、维持和恢复阶段的正常范围。
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 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 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 clay 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 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.