Advances in pathogenesis and current therapeutic strategies for cardiorenal syndrome
Mina Rizk Aziz Rizk;
Abstract
The heart and the kidneys share responsibility for maintaining hemodynamic stability and end-organ perfusion through a tight-knit relationship that controls cardiac output, volume status, and vascular tone. Communication between the heart and kidneys occurs through a variety of pathways. These include perfusion pressure, filling pressure, and neurohormonal activity.
The cardiorenal syndrome (CRS) is a condition characterized by the initiation and/or progression of renal insufficiency secondary to heart failure, the term CRS should also be used to describe conditions of renal dysfunction leading to heart dysfunction (renocardiac syndrome)
It is classified into five subtypes based on the primary organ dysfunction, whether heart (“cardiorenal” syndromes) or kidney (“renocardiac” syndromes) and on whether the organ dysfunction is acute or chronic
Several mechanisms have been implicated in the pathogenesis of renal dysfunction and worsening renal function in heart failure patients. The hemodynamic consequences of reduced cardiac output (CO) with low renal perfusion and activation of the sympathetic and renin-angiotensin-aldosterone system (RAAS) probably play the most prominent role in initiating renal dysfunction, .Salt and water retention, and venous congestion. can in turn, further worsen renal function through several mechanisms
Anemia, a common comorbidity in HF, can also worsen renal function. Drugs, such as blockers of RAAS used for the treatment of HF or nonsteroidal anti-inflammatory drugs and cyclosporine, may contribute to worsening renal function
Several factors have also been reported to independently predict the development of worsening renal function (type 1 CRS) during the treatment of ADHF. These factors include history of coronary artery disease, hypertension, diabetes mellitus, and history of prior HF. In addition, the presence of systolic hypertension, tachycardia, pulmonary edema, and use of high doses of diuretics .
One of the cornerstones of CRS therapy is the early identification of worsening kidney function. This can be accomplished with the use of biomarkers that become detectable before the traditional tests for kidney function, including glomerular filtration rate or serum creatinine
The management of these acute CRS subtypes is challenging because of the multitude and complexity of pathophysiological interactions between heart and kidney.
Preventive strategies in general for all patients with CKD and cardiac diseases and especially those in high-risk patients, will help decrease the incidence of acute deterioration of organ function Importantly, early recognition of heart failure decompensation, via application of novel methods of detection of pulmonary venous congestion and remote monitoring of volume status, would lead to use of diuretics or other decongestive regimen to prevent florid venous congestion and abort worsening of renal function.
The cardiorenal syndrome (CRS) is a condition characterized by the initiation and/or progression of renal insufficiency secondary to heart failure, the term CRS should also be used to describe conditions of renal dysfunction leading to heart dysfunction (renocardiac syndrome)
It is classified into five subtypes based on the primary organ dysfunction, whether heart (“cardiorenal” syndromes) or kidney (“renocardiac” syndromes) and on whether the organ dysfunction is acute or chronic
Several mechanisms have been implicated in the pathogenesis of renal dysfunction and worsening renal function in heart failure patients. The hemodynamic consequences of reduced cardiac output (CO) with low renal perfusion and activation of the sympathetic and renin-angiotensin-aldosterone system (RAAS) probably play the most prominent role in initiating renal dysfunction, .Salt and water retention, and venous congestion. can in turn, further worsen renal function through several mechanisms
Anemia, a common comorbidity in HF, can also worsen renal function. Drugs, such as blockers of RAAS used for the treatment of HF or nonsteroidal anti-inflammatory drugs and cyclosporine, may contribute to worsening renal function
Several factors have also been reported to independently predict the development of worsening renal function (type 1 CRS) during the treatment of ADHF. These factors include history of coronary artery disease, hypertension, diabetes mellitus, and history of prior HF. In addition, the presence of systolic hypertension, tachycardia, pulmonary edema, and use of high doses of diuretics .
One of the cornerstones of CRS therapy is the early identification of worsening kidney function. This can be accomplished with the use of biomarkers that become detectable before the traditional tests for kidney function, including glomerular filtration rate or serum creatinine
The management of these acute CRS subtypes is challenging because of the multitude and complexity of pathophysiological interactions between heart and kidney.
Preventive strategies in general for all patients with CKD and cardiac diseases and especially those in high-risk patients, will help decrease the incidence of acute deterioration of organ function Importantly, early recognition of heart failure decompensation, via application of novel methods of detection of pulmonary venous congestion and remote monitoring of volume status, would lead to use of diuretics or other decongestive regimen to prevent florid venous congestion and abort worsening of renal function.
Other data
| Title | Advances in pathogenesis and current therapeutic strategies for cardiorenal syndrome | Other Titles | التقدم فى المرضية والأستراتيجيات العلاجية الحالية فى متلازمة قلبى كلوى | Authors | Mina Rizk Aziz Rizk | Issue Date | 2014 |
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