Sr. Vercauteren et al., Chronic reduction in renal mass in the rat attenuates ischemia/reperfusioninjury and does not impair tubular regeneration, J AM S NEPH, 10(12), 1999, pp. 2551-2561
It is not known whether a kidney with chronic structural and functional cha
nges is more vulnerable to an acute renal insult, and whether its regenerat
ion capacity after injury is altered. To study this question, Lewis rats we
re submitted 10 wk after 5/6 nephrectomy to an ischemic insult of 60 min (r
emnant kidney [RK] group). Functional and morphologic data of the RK group
were compared with data obtained in IO-wk uninephrectomized (1K) and normal
(2K) Lewis rats with unilateral and bilateral renal ischemia, respectively
. The acute postischemic decrease in creatinine clearance was smallest in t
he RK group, followed by the 2K and 1K groups, respectively. At days 1 and
3, fewer proximal tubules in the outer stripe of the outer medulla of the R
K and 2K groups had undergone acute tubular necrosis compared with the 1K g
roup. The mean percentage of tubules with signs of regeneration was maximal
at day 3 in the three experimental groups. At day 10, regeneration was alm
ost complete in the three groups. The number of leukocytes (OX1(+) cells) p
resent in the RK before ischemia did not increase after ischemia/reperfusio
n injury (377 +/- 146 cells/mm(2) at day 0) in contrast to the 1K and 2K gr
oups. In the latter groups, the number of leukocytes had increased graduall
y, reaching a maximum at day 15 (1K: 960 +/- 308 cells/mm(2)) and day 10 (2
K: 668 +/- 164 cells/mm(2)), respectively. In conclusion, this study has sh
own that an RK exhibiting chronic morphologic changes of interstitial fibro
sis and tubular atrophy is protected against ischemia/reperfusion injury, a
nd that its regeneration capacity is preserved. The reperfusion injury is n
ot followed by further accumulation of leukocytes, which were already prese
nt in the RK before ischemia.