Histopathological Changes in the Kidney following Congestive Heart Failure by Volume Overload in Rats.

Noureddin B Aboryag,Michael Schäfer,Mohammed Shaqura,Lukas Dehe,Shaaban A Mousa,Doaa M Mohamed,Sacha Treskatsch,Mehdi Shakibaei

doi:10.1155/2017/6894040

Abstract

Background This study investigated histopathological changes and apoptotic factors that may be involved in the renal damage caused by congestive heart failure in a rat model of infrarenal aortocaval fistula (ACF). Methods Heart failure was induced using a modified approach of ACF in male Wistar rats. Sham-operated controls and ACF rats were characterized by their morphometric and hemodynamic parameters and investigated for their histopathological, ultrastructural, and apoptotic factor changes in the kidney. Results ACF-induced heart failure is associated with histopathological signs of congestion and glomerular and tubular atrophy, as well as nuclear and cellular degeneration in the kidney. In parallel, overexpression of proapoptotic Bax protein, release of cytochrome C from the outer mitochondrial membrane into cell cytoplasm, and nuclear transfer of activated caspase 3 indicate apoptotic events. This was confirmed by electron microscopic findings of apoptotic signs in the kidney such as swollen mitochondria and degenerated nuclei in renal tubular cells. Conclusions This study provides morphological evidence of renal injury during heart failure which may be due to caspase-mediated apoptosis via overexpression of proapoptotic Bax protein, subsequent mitochondrial cytochrome C release, and final nuclear transfer of activated caspase 3, supporting the notion of a cardiorenal syndrome.

Highlights

Heart failure, a progressive disease marked by repeated hospitalizations for episodes of acute decompensation, is frequently complicated by kidney dysfunction—one of the most important risk factors for poor clinical outcome and death [1]
In vivo hemodynamic measurements of control and aortocaval fistula (ACF) rats showed that central venous (CVP) and left end-diastolic pressure (LVEDP) were significantly increased in ACF rats (p < 0 01) (Table 1)
This study investigated the possible mechanisms that underlie renal damage following heart dysfunction using the rat model of infrarenal aortocaval fistula-induced heart failure

Summary

Introduction

A progressive disease marked by repeated hospitalizations for episodes of acute decompensation, is frequently complicated by kidney dysfunction—one of the most important risk factors for poor clinical outcome and death [1]. Overexpression of proapoptotic Bax protein, release of cytochrome C from the outer mitochondrial membrane into cell cytoplasm, and nuclear transfer of activated caspase 3 indicate apoptotic events. This was confirmed by electron microscopic findings of apoptotic signs in the kidney such as swollen mitochondria and degenerated nuclei in renal tubular cells. This study provides morphological evidence of renal injury during heart failure which may be due to caspase-mediated apoptosis via overexpression of proapoptotic Bax protein, subsequent mitochondrial cytochrome C release, and final nuclear transfer of activated caspase 3, supporting the notion of a cardiorenal syndrome

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Conclusion