Comparison of renal impairment post-myocardial infarction with reduced and preserved left ventricular function in rats with normal renal function

Abstract

This study aimed to compare the renal impairments in post-myocardial infarction (MI) rats with normal renal biochemical parameters at baseline with versus without cardiac dysfunction and explore the potential mechanisms involved in these differences. Sprague-Dawley rats with permanent ligation of coronary artery were used as MI models. Renal function, histological and molecular changes were compared between the reduced ejection fraction (EF) (EF < 40%) group and the preserved EF (EF ! 40%) group 3 or 9 weeks post-MI. The results revealed that blood cystatin C increased significantly at 9 but not 3 weeks, but it was not associated with cardiac dysfunction. Renal fibrosis and inflammatory cell infiltrations increased significantly in the reduced EF group than in the preserved EF group at 3 and 9 weeks. Glomerular podocyte injury, identified by increased immunostaining for desmin and decreased immunostaining for Wilms' tumor-1, was more significant in the reduced EF group than in the preserved EF group at 9, but not 3 weeks. The number of p16 ink4a-positive and 8-hydroxy-2 0-deoxyguanosine-positive podocytes was greater in the reduced EF group than in the preserved EF group at both time points. These changes were associated with increased expression of angiotensin II type 1/2 receptors at both time points. In conclusion, our study demonstrated that cardiac dysfunction accounted for substantially severity in renal parenchymal impairment in a partially time-dependent manner, and local activation of angiotensin II receptors, increased cell senescence and oxidative stress, and enhanced inflammatory reaction may be potential modulators participated in the deterioration of renal parenchymal injury.

Any heart failure treatments associated with worsening renal function in patients admitted due to acute heart failure?

“…Previous studies have examined the risk factors for WRF in acute heart failure [ 5 ], which include baseline serum creatinine (odds ratio 3.02), atrial fibrillation (odds ratio 0.35), age over 80 years (odds ratio 2.72), and high systolic blood pressure (odds ratio 1.61) [ 6 , 7 ]. An animal study also showed that renal fibrosis and renal dysfunction may be occurred in ischemic heart disease [ 8 ]. Even though there are several heart failure treatment, there are limited data available regarding the effects of heart failure treatment on the risk of WRF.…”

Modulatory effect of Ovothiol‐A on myocardial infarction induced by epinephrine in rats

“…MI induced renal injury in the current study, which was observed by a significant increase in creatinine, urea, and uric acid and histopathological investigation. Cardiac dysfunction resulted in local angiotensin II receptor activation, cell senescence, and oxidative stress, all of which contributed to the severity of renal parenchymal damage (Wen et al, 2020).…”

Association between physical activity and changes in renal function in patients after acute myocardial infarction: A dual-center prospective study

“…Although this observational study did not elucidate the mechanism for the effect of higher physical activity on renal function in AMI patients, some potential mechanisms are suggested. The onset of AMI induces the renin-angiotensin system (RAS) activity in the kidney, increases oxidative stress, and enhances inflammatory response, causing damage to the renal parenchyma [37] . Increased physical activity has been shown to improve vascular endothelial function and have multifaceted and beneficial effects on the body, such as increased nitric oxide, suppression of RAS activity, and antioxidant and anti-inflammatory effects [ 38 , 39 ].…”