BACKGROUND/AIMS: Apoptosis, a form of cell death characterized by DNA fragmentation and minimal inflammation, is induced by intrarenal hypoxia in rats. The objective of this study was to test whether apoptosis participates in human acute renal injury. METHODS: We examined kidneys obtained from autopsies of 40 patients following hemodynamic compromise and from 9 controls following sudden death. Nuclear DNA fragmentation was assayed by in situ 3' end labeling (TUNEL stain) and compared to histological findings. RESULTS: DNA fragmentation along renal tubular cells was observed in 23 (57%) of the study patients but in none of the controls (p < 0.005). Acute tubular necrosis was seen by formal histology in 27% of the patients and correlated with clinical acute renal dysfunction, while DNA fragmentation did not. CONCLUSION: DNA fragmentation often occurs after renal hypoperfusion and does not imply renal failure. Apoptosis may participate in the adaptive response of the kidney to hypoxia.
BACKGROUND/AIMS: Apoptosis, a form of cell death characterized by DNA fragmentation and minimal inflammation, is induced by intrarenal hypoxia in rats. The objective of this study was to test whether apoptosis participates in humanacute renal injury. METHODS: We examined kidneys obtained from autopsies of 40 patients following hemodynamic compromise and from 9 controls following sudden death. Nuclear DNA fragmentation was assayed by in situ 3' end labeling (TUNEL stain) and compared to histological findings. RESULTS: DNA fragmentation along renal tubular cells was observed in 23 (57%) of the study patients but in none of the controls (p < 0.005). Acute tubular necrosis was seen by formal histology in 27% of the patients and correlated with clinical acute renal dysfunction, while DNA fragmentation did not. CONCLUSION: DNA fragmentation often occurs after renal hypoperfusion and does not imply renal failure. Apoptosis may participate in the adaptive response of the kidney to hypoxia.