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Cardiovascular–renal disorders
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Cardiovascular–renal disorders
- Authors: Shelly L. Vaden, Clarke Atkins and Mark A. Oyama
- From: BSAVA Manual of Canine and Feline Nephrology and Urology
- Item: Chapter 16, pp 196 - 204
- DOI: 10.22233/9781910443354.16
- Copyright: © 2017 British Small Animal Veterinary Association
- Publication Date: January 2017
Abstract
There is a complex interaction between the renal and cardiovascular systems, both in health and in disease states. In disease states, this complex interaction can present both diagnostic and therapeutic challenges. This chapter discusses definitions, classification, epidemiology and pathophysiology; clinical staging and evaluation; biomarkers, imaging and blood pressure measurement; and management of CvRD.
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16.2
The complexities of the cardiorenal axis as it relates to cardiovascular–renal disorders (CvRD). The diseased heart (CHF, congestive heart failure) and kidney (CKD, chronic kidney disease) are depicted, as are the renin–angiotensin–aldosterone and sympathetic nervous systems (RAAS and SNS, respectively) and the normal heart and kidney. The failing heart activates the SNS and RAAS via a fall in CO (cardiac output) and blood pressure, while the diseased kidney activates the RAAS via renin release associated with a fall in glomerular filtration rate. The RAAS causes vasoconstriction (with increased afterload), potassium wasting (with resultant cardiac arrhythmias, renal damage and muscular weakness), myocardial and renal remodelling with fibrosis (via angiotensin II [Ang II] and aldosterone [Aldo]). The SNS increases heart rate, contributes to cardiac remodelling and arrhythmias, and causes vasoconstriction, all deleterious to cardiac function. The fall in CO and possibly congestion of the kidney result in azotaemia and reduced drug and hormone clearance via renal excretion. CKD and acute kidney injury both activate the RAAS, damaging the heart, vessels and the kidney itself. If left-sided heart failure and pulmonary oedema exist, tissue oxygenation falls and this is compounded by diminished oxygen-carrying capacity of the blood, which is rendered anaemic in CKD (via reduction in erythropoietin production). In glomerular disease, proteinuria can result in hypoalbuminaemia and reduced plasma oncotic pressure, which contribute to signs of congestion (pulmonary oedema, ascites). RAAS activation by cardiac, vascular (high blood pressure, HBP) or kidney disease and by anaemia increases the presence of reactive oxygen species (ROS) which are generally toxic to living tissues, including the heart, vessels and kidney. HBP, a cardiovascular disease, can be produced by chronic kidney disease, by other (endocrine) disease, or be idiopathic. Therefore HBP is an important lynchpin in the concept of CvRD, because it may produce cardiac disease with left ventricular hypertrophy, diastolic dysfunction and heart failure (CvRDK or CvRDO, depending on whether there is renal or idiopathic HBP) and kidney disease with glomerular hypertension, glomerulosclerosis and renal failure (CvRDH or CvRDO, depending on whether the HBP is idiopathic or caused by another disease such as hyperthyroidism). HBP causes vascular hypertrophy and dysfunction, worsening HBP. © 2017 British Small Animal Veterinary Association
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16.2
The complexities of the cardiorenal axis as it relates to cardiovascular–renal disorders (CvRD). The diseased heart (CHF, congestive heart failure) and kidney (CKD, chronic kidney disease) are depicted, as are the renin–angiotensin–aldosterone and sympathetic nervous systems (RAAS and SNS, respectively) and the normal heart and kidney. The failing heart activates the SNS and RAAS via a fall in CO (cardiac output) and blood pressure, while the diseased kidney activates the RAAS via renin release associated with a fall in glomerular filtration rate. The RAAS causes vasoconstriction (with increased afterload), potassium wasting (with resultant cardiac arrhythmias, renal damage and muscular weakness), myocardial and renal remodelling with fibrosis (via angiotensin II [Ang II] and aldosterone [Aldo]). The SNS increases heart rate, contributes to cardiac remodelling and arrhythmias, and causes vasoconstriction, all deleterious to cardiac function. The fall in CO and possibly congestion of the kidney result in azotaemia and reduced drug and hormone clearance via renal excretion. CKD and acute kidney injury both activate the RAAS, damaging the heart, vessels and the kidney itself. If left-sided heart failure and pulmonary oedema exist, tissue oxygenation falls and this is compounded by diminished oxygen-carrying capacity of the blood, which is rendered anaemic in CKD (via reduction in erythropoietin production). In glomerular disease, proteinuria can result in hypoalbuminaemia and reduced plasma oncotic pressure, which contribute to signs of congestion (pulmonary oedema, ascites). RAAS activation by cardiac, vascular (high blood pressure, HBP) or kidney disease and by anaemia increases the presence of reactive oxygen species (ROS) which are generally toxic to living tissues, including the heart, vessels and kidney. HBP, a cardiovascular disease, can be produced by chronic kidney disease, by other (endocrine) disease, or be idiopathic. Therefore HBP is an important lynchpin in the concept of CvRD, because it may produce cardiac disease with left ventricular hypertrophy, diastolic dysfunction and heart failure (CvRDK or CvRDO, depending on whether there is renal or idiopathic HBP) and kidney disease with glomerular hypertension, glomerulosclerosis and renal failure (CvRDH or CvRDO, depending on whether the HBP is idiopathic or caused by another disease such as hyperthyroidism). HBP causes vascular hypertrophy and dysfunction, worsening HBP.