Abstract
ABSTRACTIntroduction: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.
Highlights
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
The focus of this study was cardio-renal syndrome (CRS) subtype 4 (CRS4), which is characterized by a condition of primary chronic kidney disease (CKD), which leads to reduction of the cardiac function, ventricular hypertrophy, diastolic dysfunction, and increased risk of adverse cardiovascular events
The comparisons of Troponin I (TnI) levels showed a significant difference between the 4 weeks (4W) and 8W (p < 0.05) when CKD was compared to SHAM (Figure 1)
Summary
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. To cover the vast array of interrelated derangements and stress the bidirectional nature of heart-kidney interactions, Ronco et al presented a classification of the CRS with 5 subtypes based on pathophysiology, the time-frame, and the nature of concomitant cardiac and renal dysfunction providing a more concise and logical approach.[2] The focus of this study was CRS subtype 4 (CRS4), which is characterized by a condition of primary chronic kidney disease (CKD), which leads to reduction of the cardiac function, ventricular hypertrophy, diastolic dysfunction, and increased risk of adverse cardiovascular events. More than 50% of deaths in stage 5 cohorts are attributed to cardiovascular disease,[1] but the mechanisms underlying the CRS within of the context of CKD are not well understood
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