What question did this study set out to answer?

To examine the cardiac and renal structural and functional consequences of inducing myocardial infarction against a backdrop of pre-existing chronic kidney disease.

October 10, 2017Journal of Cellular and Molecular MedicineOpen Access

Chronic kidney disease with comorbid cardiac dysfunction exacerbates cardiac and renal damage

Q: What is the clinical evidence from this study?

Study design: RCT. Population: Cardiorenal syndrome (n=36). Intervention: Myocardial infarction (MI) combined with 5/6 nephrectomy (STNx) vs. Sham+Sham, Sham+MI, and STNx+Sham. Primary outcome: Renal tubulointerstitial fibrosis and kidney injury molecule-1 expression (p=<0.01).

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Key result

In male rats, adding myocardial infarction to 5/6 nephrectomy exacerbated renal tubulointerstitial fibrosis (P<0.01) and cardiac interstitial fibrosis (P<0.01) compared to nephrectomy alone.

Why the study?

Does myocardial infarction exacerbate renal and cardiac damage in a rat model of chronic kidney disease?

Key Points

To examine the cardiac and renal structural and functional consequences of inducing myocardial infarction against a backdrop of pre-existing chronic kidney disease.
Male Sprague-Dawley rats (n = 36) were randomized into four groups: Sham+Sham, Sham+MI, subtotal nephrectomy (STNx)+Sham, and STNx+MI.
STNx or Sham surgery was induced initially, followed by MI or Sham surgery 4 weeks later, with a total follow-up duration of 8 additional weeks.
STNx+MI rats showed significantly increased renal tubulointerstitial fibrosis (P < 0.01) and kidney injury molecule-1 expression (P < 0.01) compared with STNx+Sham, though renal function did not decline further.
Heart weight was increased in STNx+MI compared to STNx+Sham or Sham+MI (P < 0.05), alongside greater cardiomyocyte cross-sectional area and increased cardiac interstitial fibrosis versus STNx+Sham (P < 0.01) or Sham+MI (P < 0.01).
Left ventricular tissue in STNx+MI animals exhibited heightened diastolic dysfunction associated with upregulation of ANP, cTGF, and collagen I mRNA as well as phospho-p38 and phospho-p44/42 MAPK proteins.

Study Design

Type

RCT (n=36)

Randomization

randomized

Structured PICO

Does myocardial infarction exacerbate renal and cardiac damage in a rat model of chronic kidney disease?

Population

36 male Sprague-Dawley rats subjected to 5/6 nephrectomy followed by myocardial infarction 4 weeks later, and maintained for a further 8 weeks.

Intervention

Myocardial infarction (MI) induced 4 weeks after 5/6 nephrectomy (STNx)

Comparator

Sham+Sham, Sham+MI, and STNx+Sham groups

Outcome

Renal and cardiac functional and structural damage (including renal tubulointerstitial fibrosis, kidney injury molecule-1 expression, heart weight, cardiomyocyte cross-sectional area, cardiac interstitial fibrosis, and diastolic dysfunction)surrogate

Main Result

p-value: p=<0.01

The addition of myocardial infarction to chronic kidney disease accelerates structural cardiac and renal damage, providing a useful model for studying cardiorenal syndrome.

Discussion

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Implication

Offers an experimental model of accelerated cardiorenal fibrosis; leaves open translation to human cardiorenal syndrome management.

Cite This Study

Wang et al. (2017) conducted an RCT in Cardiorenal syndrome (n=36). Myocardial infarction (MI) combined with 5/6 nephrectomy (STNx) vs. Sham+Sham, Sham+MI, and STNx+Sham was evaluated on Renal tubulointerstitial fibrosis and kidney injury molecule-1 expression (p=<0.01). In male rats, adding myocardial infarction to 5/6 nephrectomy exacerbated renal tubulointerstitial fibrosis (P<0.01) and cardiac interstitial fibrosis (P<0.01) compared to nephrectomy alone.

synapsesocial.com/papers/6a9df6e72bf3873a96f9a3c5 https://doi.org/10.1111/jcmm.13349

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Chronic kidney disease with comorbid cardiac dysfunction exacerbates cardiac and renal damage

Key Points

Study Design

Structured PICO

Main Result

Discussion

Implication

Cite This Study

Chronic kidney disease with comorbid cardiac dysfunction exacerbates cardiac and renal damage

Key Points

Study Design

Structured PICO

Main Result

Discussion

Implication

Cite This Study

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