Acute renal failure is a complex clinical syndrome characterized by a sudden and significant reduction in kidney function, often caused by either intrinsic kidney damage or external factors. Symptoms typically include oliguria or anuria, elevated blood urea nitrogen (BUN) and creatinine levels, 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 acute IR injury on rat kidneys. Researchers from the Department of Nephrology at Zhongshan Hospital, Fudan University, created an IR model by clamping the bilateral 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 post-operation—and monitored kidney function, histopathology, and survival rates over time.

Using advanced techniques such as transmission electron microscopy, TUNEL assays, Masson staining, and Western blotting, the researchers were able to observe structural changes in the tubular epithelial cells, detect apoptosis, assess the degree of interstitial fibrosis, and measure the expression of α-smooth muscle actin (α-SMA). Immunohistochemistry was also used to evaluate the distribution and expression of α-SMA and TGF-β1 in the kidney tissue.

The findings showed that in the IR group, serum creatinine (Scr) and BUN levels gradually increased after reperfusion, peaking at 48 hours. The mortality rate in the IR group was 32% (8 out of 25), compared to 0% in the sham group. At 48 hours post-reperfusion, the peripheral renal tubular epithelium exhibited widespread necrosis and some apoptosis. By 5 and 10 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, with TGF-β1 levels remaining higher than those in the sham group despite a slight decrease.

In conclusion, severe ischemia-reperfusion injury not only leads to early tubular necrosis, a sharp decline in kidney function, and higher mortality, but also contributes to long-term fibrotic changes that impair renal recovery. The overexpression of TGF-β1 and the accumulation of myofibroblasts appear to be key mediators of these fibrotic processes. Understanding these mechanisms is essential for developing effective therapeutic strategies to prevent or reduce the long-term consequences of acute kidney injury.

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