Original ArticlesRegulation of renal tubular cell apoptosis and proliferation after ischemic injury to a solitary kidney☆,☆☆
Section snippets
Rats
Male Sprague-Dawley rats weighing 263 to 328 g were anesthetized with Inactin, 100 mg/g body wt intraperitoneally. The rats were placed on a temperature-regulated table, received a rectal thermo probe, and were kept at 36.5°C during right nephrectomy and 30 minutes of cross-clamping of the left renal artery. A 200-μL sample of tail vein blood was drawn in all animals, at all time points indicated until the animals were killed, for the measurement of serum creatinine with the standardized
Histomorphology and kidney function
Kidney function data and body weight over time are shown in Table I. h, Hours; d, days; wEmpty Cell Time 0 1h 1d 3d 7d 5w 20w Body ARF 298 ± 17 301 ± 11 279 ± 15 264 ± 13* 268 ± 22* 389 ± 13* 461 ± 15* weight (g) Control 286 ± 14 285 ± 13 277 ± 2 286 ± 8 305 ± 10 432 ± 5 501 ± 24 Serum ARF 0.5 ± 0.1 0.8 ± 0 4.0 ± 0.1* 3.2 ± 0.8* 0.9 ± 0.4 0.5 ± 0.2 0.8 ± 0.1* creatinine (mg/dL) Control 0.4 ± 0 0.5 ± 0.1 0.4 ± 0 0.5 ± 0.1 0.5 ± 0.1 0.5 ± 0.1 0.4 ± 0
Discussion
The present study investigated the time course and molecular regulation of apoptotic cell death and cellular proliferation after ischemic injury to a solitary kidney. This model was chosen because it resembles the clinical setting of kidney transplantation and allows the discrimination between ischemia and alloimmune-mediated injury. Recently three articles were published about apoptosis and apoptosis regulation in rodent kidneys subjected to bilateral clamping of the renal arteries. Basile et
Acknowledgements
We thank Miaofen Chou for technical assistance.
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Supported by the Josef Skoda Funds, the Else Kröner Fresenius Funds, FWF P-12037MED, and NIH-RO1 DK52841.
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Reprint requests: Rainer Oberbauer, MD, Klinik für Innere Medizin III, Abteilung für Nephrologie und Dialyse, Währinger Gürtel 18-20, A-1090 Vienna, Austria.