Investigation of the renal injury caused by liver ischemia-reperfusion in rats

Abstract

To explain the mechanism of renal injury caused by liver ischemia-reperfusion, we investigated biochemical and morphological changes in the liver and kidney in rats. After reperfusion following 60 min of liver ischemia, numerous changes were found. The level of serum transaminases and lipid peroxide formation in the liver tissue increased significantly. Electron microscopic studies revealed that most of the hepatocytes had swollen mitochondria and clumping of the nuclear chromatin. The sinusoidal endothelium was disrupted and the sinusoidal lumen was filled with numerous erythrocytes. Blood endotoxin concentration, plasma lipid peroxide levels, and serum beta-glucuronidase activities were significantly higher than in the control group. Biochemical and morphological renal injury was also observed. Tissue lipid peroxide levels increased in both the kidney and the liver. Microscopic examination revealed damage to the renal tubules, including interstitial edema, dilatation of the lumen, and granular casts derived from necrotic cells in the proximal convoluted tubule. The levels of urinary N-acetyl-beta-D-glucosaminidase (NAG) in the liver ischemia-reperfusion group were also higher than in the control group. These results suggest that the renal injury was caused by an increase in endotoxin, lipid peroxide, and lysosomal enzymes in the blood following the liver injury induced by the ischemia-reperfusion.

Acute kidney injury after hepatic ischemia and reperfusion injury in mice

“…Correspondingly, the kidneys from rats subjected to liver IR showed little morphological damage and they failed to see increases in apoptosis (caspase-3) and neutrophil infiltration (myeloperoxidase activity). Their study confirms previous observations in rats that renal dysfunction was mild with little or no histological changes after liver IR (9,41). Polat et al .…”

Renoprotective effect of vildagliptin following hepatic ischemia/reperfusion injury

“…Morphological alterations in the liver and kidneys following liver I/R injury were also reported including degeneration in hepatocytes, congestion, and necrosis in the liver and degeneration in the renal tubular epithelium, tubular dilatation with loss of brush border, congestion, leukocyte infiltration, hyaline cast in the kidney. Similar findings were observed in previous studies [5,11,[14][15][16][17] suggesting that hepatic I/R injury damages both the morphology and the function of the kidney [16,18,19]. Moreover, several studies reported pathological alterations in kidneys according to the period of reperfusion ranging from 1 to 24 h. After 1-h kidney showed moderate hemorrhage and congestion [20], eosinophilic appearance and perinuclear vacuolic formation in tubular cells [17] after 8 h showing loss of brush border and tubular epithelium with hyaline casts and congestion [21], while other researches showed tubular dilatation and necrosis, cellular swelling, and granular casts after 24-h reperfusion [5,14,22].…”

Alteration of renal functional, oxidative stress and inflammatory indices following hepatic ischemia-reperfusion

“…A B C of Polat et al (2006) on rats showed no or little morphological damage of the kidney subjected to 45 min total hepatic ischemia followed by 1 hour of reperfusion. On the other hand, Lee et al (2009) showed that mice subjected to 60 min partial liver ischemia develop severe AKI in less than 24 h. During reperfusion following 60 min of liver ischemia, numerous changes were found including biochemical and renal morphological injury as well as increase in endotoxin, lipid peroxide, and lysosomal enzymes in the blood (Kudo et al 1993). Remote organ injuries are largely consequences of the endogenously produced mediators rather than the exogenous factors and toxins (Weinbroum et al 1999).…”