Acute renal failure is a complex clinical syndrome caused by either intrinsic kidney damage or extrarenal factors, resulting in a sudden drop in urine output and impaired kidney function. This leads to serious imbalances in the body, including oliguria or anuria, elevated blood urea nitrogen (BUN), hyperkalemia, and metabolic acidosis. A study published in the fourth issue of the Chinese Journal of Nephrology investigated the short- and long-term effects of IR injury on rat kidneys and explored the underlying mechanisms.

The researchers created an IR model in rats by clamping both renal pedicles for 40 minutes. They collected blood samples and kidney tissues at various time points—4 hours, 24 hours, 48 hours, 72 hours, one week, five weeks, and ten weeks after surgery. Throughout the study, they monitored renal pathology, function, and survival. Transmission electron microscopy was used to examine the ultrastructure of tubular epithelial cells, while the TUNEL assay was employed to detect apoptosis. Masson staining was used to assess interstitial fibrosis, and Western blotting was performed to measure α-smooth muscle actin (α-SMA) levels. Immunohistochemistry was also used to evaluate the expression and distribution of α-SMA and TGF-β1 in the kidneys.

The results showed that serum creatinine (Scr) and BUN levels in the IR group gradually increased post-reperfusion, peaking at 48 hours. The mortality rate in the IR group reached 32% (8 out of 25), compared to 0% in the sham group. At 48 hours post-surgery, the IR group exhibited widespread necrosis of peripheral tubular epithelial cells, along with some apoptosis. By five and ten weeks after surgery, mild to moderate tubulointerstitial fibrosis was observed in the IR group. One week after the operation, there was a significant increase in α-SMA and TGF-β1 protein expression, although TGF-β1 levels later decreased slightly, still remaining higher than those in the sham group.

In conclusion, severe ischemia-reperfusion injury not only causes acute tubular necrosis, a sharp decline in kidney function, and increased mortality but also contributes to long-term fibrotic changes that negatively affect kidney outcomes. The findings suggest that overexpression of TGF-β1 and the proliferation of myofibroblasts may be key mediators of the fibrotic process. These insights could help guide future research and therapeutic strategies aimed at preventing or reducing kidney damage following IR injury.

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