[Effect of inhibition of angiotensin converting enzyme on XXXX following kidney transplantation].

@entity1 @entity8 @entity101 @entity1372 @entity2791 @entity3371 @entity1504 @entity1011 @entity916
The activation of the @entity916 angiotensin system is thought to be an important factor contributing to @entity101 following kidney transplantation (TX). We studied 21 @entity101 renal transplant recipients, without evidence of acute graft rejection or transplant @entity2791 , 6 to 60 months post-TX. The acute responses of mean arterial pressure (MAP) and renal hemodynamics (ERPF: effective renal plasma flow, 131I-Hippuran clearance) and function (GFR: glomerular filtration rate, @entity1011 clearance; UNaV: urinary @entity1372 excretion rate) to converting enzyme inhibition (CEI) by @entity3371 were assessed. CEI induced a decrease in MAP (118 +/- 2 to 110 +/- 2 mmHg), renal resistance (RR: 0.27 +/- 0.02 to 0.21 +/- 0.01) and filtration fraction (FF: 0.31 +/- 0.02 to 0.23 +/- 0.01). ERPF (307 +/- 24 to 333 +/- 18 ml/min/1.73 m2) and GFR (88 +/- 5 to 78 +/- 5 ml/min/1.73 m2) were not significantly changed. UNaV increased by 53 +/- 24 mumol/min. Changes in MAP (r = -0.66), ERPF (r = 0.74) and FF (r = -0.88) were significantly correlated with the log of control plasma @entity916 activity (PRA). In 10 @entity1 with an increase of ERPF (range: + 30 to + 70%) and no change in GFR, the activated @entity916 system could originate from the recipient's own kidneys. In the remaining 11 @entity1 , CEI was associated with no increase in ERPF (change: + 2 to - 27%) and a fall in GFR, a response suggesting a possible @entity1504 . These results indicate that RAS participates in the regulation of systemic and @entity8 , with a possible predominant effect on efferent glomerular arteriole.
