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Updated: Jul 5, 2026
A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
Published on: November 7, 2017
Exaggerated renal pathology of partial ablation-induced chronic renal failure in eNOS deficient mice
Chika Yamashita1, Naoko Tazawa, Mamoru Ohkita
1Laboratory of Pathological and Molecular Pharmacology, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan.
Abstract:
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.
Insights
Endothelial nitric oxide synthase (eNOS) deficiency worsens chronic renal failure in mice, increasing mortality and kidney damage. eNOS-derived nitric oxide (NO) appears protective against kidney injury in this model.
Area of Science:
- Nephrology
- Cardiovascular Research
- Molecular Biology
Background:
- Chronic renal failure (CRF) is a significant health concern.
- Endothelial nitric oxide synthase (eNOS) plays a crucial role in vascular health.
- The specific role of eNOS in CRF progression is not fully understood.
Purpose of the Study:
- To investigate the role of eNOS in a 5/6 nephrectomy remnant kidney model of CRF.
- To compare renal injury and survival rates between eNOS-deficient and wild-type mice.
Main Methods:
- Utilized eNOS-deficient (eNOS-/-) and wild-type mice.
- Induced chronic renal failure using a 5/6 nephrectomy surgical model.
- Monitored blood urea nitrogen, plasma creatinine, proteinuria, survival rates, and glomerular size over 8 weeks.
Main Results:
- Both wild-type and eNOS-/- mice showed increased blood urea nitrogen, creatinine, and proteinuria post-nephrectomy.
- These changes were significantly more pronounced in eNOS-/- mice.
- Survival rate was drastically lower in eNOS-/- mice (23%) compared to wild-type mice (69%).
- Glomeruli in nephrectomized eNOS-/- mice tended to be larger than in wild-type counterparts.
Conclusions:
- eNOS-derived nitric oxide (NO) appears to have a protective effect against renal injury in the remnant kidney model.
- eNOS deficiency exacerbates the progression of chronic renal failure and reduces survival.
