Key result
Genetic deficiency of eNOS significantly reduced the 8-week survival rate to 23.3% compared to 69% in wild-type mice following 5/6 nephrectomy, and exacerbated renal dysfunction.
Why the study?
Does eNOS deficiency exacerbate renal injury and mortality in a mouse model of chronic renal failure?
Does eNOS deficiency exacerbate renal injury and mortality in a mouse model of chronic renal failure?
Absolute Event Rate: 23.3% vs 69%
p-value: p=<0.01
eNOS-derived nitric oxide plays a protective role against renal injury and mortality in a murine model of chronic renal failure.
We investigated the role of endothelial nitric oxide synthase (eNOS) in the remnant kidney model of chronic renal failure, by using eNOS-deficient (eNOS-/-) and wild-type mice. There were significant increments of blood urea nitrogen level, plasma creatinine concentration and proteinuria in both wild-type and eNOS-/- mice at 8 weeks after 5/6 nephrectomy, but observed changes were more prominent in eNOS-/- mice. Only 7 out of 30 eNOS-/- mice were alive during 8-week experimental period, whereas survival rate in the wild-type mice was 69%. The glomerular size distribution indicated that the glomeruli of 5/6 nephrectomized eNOS-/- mice tended to be larger compared with cases of wild-type mice. It seems likely that eNOS-derived NO is protective against renal injuries in this disease model.
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Yamashita et al. (2008) studied Chronic renal failure (n=56). Genetic deficiency of endothelial nitric oxide synthase (eNOS) vs. Wild-type was evaluated on Survival rate at 8 weeks (p=<0.01). Genetic deficiency of eNOS significantly reduced the 8-week survival rate to 23.3% compared to 69% in wild-type mice following 5/6 nephrectomy, and exacerbated renal dysfunction.
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