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- W1983129220 abstract "Impaired renal function with loss of nephron number in chronic renal disease is associated with increased cardiovascular mortality and morbidity. However, the structural and functional cardiac response to a mild reduction in renal mass is not fully characterized. We hypothesized that early experimental chronic kidney disease produced by uninephrectomy (UNX) would activate myocardial apoptotic genes and lead to early myocardial fibrosis. Cardiorenal function and structure were assessed in rodents at 4 weeks following UNX or sham operation (Sham); (n=10 per group). At 4 weeks UNX resulted in LV myocardial fibrosis compared to Sham (S:2.4±0.1, UNX:4.2±0.4%, p<0.001). Importantly, changes in the apoptotic pathway were observed in the LV. 47 genes were altered after UNX when compared to sham control. These changes were associated a lower early diastolic strain rate (Csr-E) in the UNX group and decreased Csr-E/A ratio indicating myocardial diastolic dysfunction but with preserved LVEF (S:6.4±0.5, UNX:5.2±0.8 and S:1.8±0.5, UNX:1.2±0.4;p<0.05). Blood pressure (BP), aldosterone, glomerular filtration rate (GFR), proteinuria, and plasma B-type natriuretic peptide (BNP) were not significantly altered by UNX. These studies demonstrate that mild renal insufficiency in the rodent results in activation in the apoptosis pathway in the LV 4 weeks after UNX. This is associated with early cardiac fibrosis and impaired diastolic function." @default.
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- W1983129220 date "2011-08-01" @default.
- W1983129220 modified "2023-09-23" @default.
- W1983129220 title "Early Experimental Chronic Kidney Disease Activates Myocardial Apoptotic Genes and Leads to Early Myocardial Fibrosis" @default.
- W1983129220 doi "https://doi.org/10.1016/j.cardfail.2011.06.044" @default.
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