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Review
. 2004 Aug;90(8):961-6.
doi: 10.1136/hrt.2003.015503.

Renal dysfunction and acceleration of coronary disease

M W Yerkey  1 , S J Kernis, B A Franklin, K R Sandberg, P A McCullough
Affiliations
Review

Renal dysfunction and acceleration of coronary disease

M W Yerkey et al. Heart. 2004 Aug.
No abstract available

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Figures

Figure 1
Figure 1
Risk of coronary heart disease death by gradations of chronic kidney disease (CRD) and diabetes (DM). Adapted from Levin A, Steven L, McCullough PA. Cardiovascular disease and the kidney. Tracking a killer in chronic kidney disease. Postgrad Med 2002;111:53–60.
Figure 2
Figure 2
Angiotensinogen is secreted by the liver and is cleaved by renin, which is secreted into the lumen of renal afferent arterioles by juxtaglomerular cells. Angiotensin I is then converted to angiotensin II by angiotensin converting enzyme, primarily in endothelial cells. In the zona glomerulosa of the adrenal cortex, angiotensin II stimulates the production of aldosterone. Aldosterone production is also stimulated by potassium, corticotropin, catecholamines (for example, noradrenaline (norepinephrine)), and endothelins. Points of therapeutic impact are shown as ACE (angiotensin converting enzyme inhibition), ARB (angiotensin II receptor blockade), and AldB (aldosterone receptor blockade). Adapted from Weber KT. Aldosterone in congestive heart failure. N Engl J Med 2001;345:1689–97.
Figure 3
Figure 3
The renin–angiotensin system, creating the formation of angiotensin II, directly upregulates oxidised low density lipoprotein receptors on the endothelium and accelerates the progression of coronary atherosclerosis. EC, endothelial cell; LDL-C, low density lipoprotein cholesterol; LOX-1, oxidised low density lipoprotein receptor; NADH, nicotinamide adenine dinucleotide; NO nitric oxide.
Figure 4
Figure 4
Processes related to the acceleration of coronary disease and plaque rupture in patients with renal disease. AGE, advanced glycation end products; LDL-C, low density lipoprotein cholesterol; NO, nitric oxide.
Figure 5
Figure 5
The disproportionately increased rates of coronary artery disease are caused in part by an excess burden of novel cardiovascular risk factors. CAD, coronary artery disease.
See this image and copyright information in PMC

References

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