Key result
The nephrectomy 5/6 animal model of chronic kidney disease demonstrated increased Troponin I, TNF-α, and angiotensin expression, alongside left ventricular hypertrophy and fibrosis over 8 weeks.
Why the study?
Does the nephrectomy 5/6 animal model of CKD induce changes in cardiac biomarkers and histology indicative of cardio-renal syndrome subtype 4?
Does the nephrectomy 5/6 animal model of CKD induce changes in cardiac biomarkers and histology indicative of cardio-renal syndrome subtype 4?
In a CKD animal model, cardiac injury (elevated TnI), inflammation (TNF-α), and fibrosis develop over 8 weeks, supporting the role of the renin-angiotensin axis in cardio-renal syndrome subtype 4.
Answers are grounded in this paper and cite their sources.
May inform experimental models of cardio-renal syndrome type 4; leaves open human translation and clinical relevance.
INTRODUCTION: Cardio-renal syndrome subtype 4 (CRS4) is a condition of primary chronic kidney disease that leads to reduction of cardiac function, ventricular hypertrophy, and risk of cardiovascular events. Objective: Our aim was to understand the mechanisms involved on the onset of CRS4. METHODS: We used the nephrectomy 5/6 (CKD) animal model and compared to control (SHAM). Serum biomarkers were analyzed at baseline, 4, and 8 weeks. After euthanasia, histology and immunohistochemistry were performed in the myocardium. RESULTS: Troponin I (TnI) was increased at 4 weeks (W) and 8W, but nt-proBNP showed no difference. The greater diameter of cardiomyocytes indicated left ventricular hypertrophy and the highest levels of TNF-α were found at 4W declining in 8W while fibrosis was more intense in 8W. Angiotensin expression showed an increase at 8W. CONCLUSIONS: TnI seems to reflect cardiac injury as a consequence of the CKD however nt-proBNP did not change because it reflects stretching. TNF-α characterized an inflammatory peak and fibrosis increased over time in a process connecting heart and kidneys. The angiotensin showed increased activity of the renin-angiotensin axis and corroborates the hypothesis that the inflammatory process and its involvement with CRS4. Therefore, this animal study reinforces the need for renin-angiotensin blockade strategies and the control of CKD to avoid the development of CRS4.
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Dionísio et al. (2018) studied Cardio-renal syndrome subtype 4 (CRS4). Nephrectomy 5/6 (CKD) vs. SHAM control was evaluated on Serum biomarkers (TnI, nt-proBNP), histology, and immunohistochemistry. The nephrectomy 5/6 animal model of chronic kidney disease demonstrated increased Troponin I, TNF-α, and angiotensin expression, alongside left ventricular hypertrophy and fibrosis over 8 weeks.
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