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Animal Models to Study Links between Cardiovascular Disease and Renal Failure and Their Relevance to Human Pathology.

Hewitson TD, Holt SG, Smith ER - Front Immunol (2015)

Bottom Line: However, patients with pure or primary renal dysfunction also have metabolic changes (e.g., oxidant stress, inflammation, nitric oxide, or endocrine changes) that affect the cardiovascular system.Whilst we understand several of these links, some of the mechanisms for these connections remain incompletely explained.In this article, we review various experimental models used, and examine critically how representative they are of the human condition.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Royal Melbourne Hospital (RMH) , Melbourne, VIC , Australia ; Department of Medicine - RMH, University of Melbourne , Melbourne, VIC , Australia.

ABSTRACT
The close association between cardiovascular pathology and renal dysfunction is well documented and significant. Patients with conventional risk factors for cardiovascular disease like diabetes and hypertension also suffer renal dysfunction. This is unsurprising if the kidney is simply regarded as a "modified blood vessel" and thus, traditional risk factors will affect both systems. Consistent with this, it is relatively easy to comprehend how patients with either sudden or gradual cardiac and or vascular compromise have changes in both renal hemodynamic and regulatory systems. However, patients with pure or primary renal dysfunction also have metabolic changes (e.g., oxidant stress, inflammation, nitric oxide, or endocrine changes) that affect the cardiovascular system. Thus, cardiovascular and renal systems are intimately, bidirectionally and inextricably linked. Whilst we understand several of these links, some of the mechanisms for these connections remain incompletely explained. Animal models of cardiovascular and renal disease allow us to explore such mechanisms, and more importantly, potential therapeutic strategies. In this article, we review various experimental models used, and examine critically how representative they are of the human condition.

No MeSH data available.


Related in: MedlinePlus

Pathophysiological mediators of cardiorenal syndrome and renocardiac syndrome. MBD, mineral bone disorder; NO, nitric oxide; RAAS, renal–angiotensin–aldosterone system; RBF, renal blood flow; SNS, sympathetic nervous system.
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Figure 1: Pathophysiological mediators of cardiorenal syndrome and renocardiac syndrome. MBD, mineral bone disorder; NO, nitric oxide; RAAS, renal–angiotensin–aldosterone system; RBF, renal blood flow; SNS, sympathetic nervous system.

Mentions: Given its importance, and the wide spectrum of primary disease and clinical presentation, a number of classification systems have been proposed. Ronco et al. have classified CRS on time frame (acute, chronic or secondary) and which organ is involved first (heart or kidney) recognizing five different types of the CRS or renocardiac syndromes (RCS) (7, 8). Other approaches are based on pathophysiological links (9–11) (Figure 1), arguing that effects are bidirectional (11), and that temporal differences in organ involvement are artificial (9).


Animal Models to Study Links between Cardiovascular Disease and Renal Failure and Their Relevance to Human Pathology.

Hewitson TD, Holt SG, Smith ER - Front Immunol (2015)

Pathophysiological mediators of cardiorenal syndrome and renocardiac syndrome. MBD, mineral bone disorder; NO, nitric oxide; RAAS, renal–angiotensin–aldosterone system; RBF, renal blood flow; SNS, sympathetic nervous system.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4585255&req=5

Figure 1: Pathophysiological mediators of cardiorenal syndrome and renocardiac syndrome. MBD, mineral bone disorder; NO, nitric oxide; RAAS, renal–angiotensin–aldosterone system; RBF, renal blood flow; SNS, sympathetic nervous system.
Mentions: Given its importance, and the wide spectrum of primary disease and clinical presentation, a number of classification systems have been proposed. Ronco et al. have classified CRS on time frame (acute, chronic or secondary) and which organ is involved first (heart or kidney) recognizing five different types of the CRS or renocardiac syndromes (RCS) (7, 8). Other approaches are based on pathophysiological links (9–11) (Figure 1), arguing that effects are bidirectional (11), and that temporal differences in organ involvement are artificial (9).

Bottom Line: However, patients with pure or primary renal dysfunction also have metabolic changes (e.g., oxidant stress, inflammation, nitric oxide, or endocrine changes) that affect the cardiovascular system.Whilst we understand several of these links, some of the mechanisms for these connections remain incompletely explained.In this article, we review various experimental models used, and examine critically how representative they are of the human condition.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Royal Melbourne Hospital (RMH) , Melbourne, VIC , Australia ; Department of Medicine - RMH, University of Melbourne , Melbourne, VIC , Australia.

ABSTRACT
The close association between cardiovascular pathology and renal dysfunction is well documented and significant. Patients with conventional risk factors for cardiovascular disease like diabetes and hypertension also suffer renal dysfunction. This is unsurprising if the kidney is simply regarded as a "modified blood vessel" and thus, traditional risk factors will affect both systems. Consistent with this, it is relatively easy to comprehend how patients with either sudden or gradual cardiac and or vascular compromise have changes in both renal hemodynamic and regulatory systems. However, patients with pure or primary renal dysfunction also have metabolic changes (e.g., oxidant stress, inflammation, nitric oxide, or endocrine changes) that affect the cardiovascular system. Thus, cardiovascular and renal systems are intimately, bidirectionally and inextricably linked. Whilst we understand several of these links, some of the mechanisms for these connections remain incompletely explained. Animal models of cardiovascular and renal disease allow us to explore such mechanisms, and more importantly, potential therapeutic strategies. In this article, we review various experimental models used, and examine critically how representative they are of the human condition.

No MeSH data available.


Related in: MedlinePlus