http://cjasn.asnjournals.org Clinical Journal of the American Society of Nephrology RSS feed -- recent Controversies in Nephrology articles 1555-905X Clinical Journal of the American Society of Nephrology 1555-9041 http://cjasn.asnjournals.org/icons/banner/title.gif http://cjasn.asnjournals.org http://cjasn.asnjournals.org/cgi/content/short/3/6/1583?rss=1 2008-11-06 info:doi/10.2215/CJN.03250708 American Society of Nephrology 6 3 1584 2008-11-01 1583 Controversies in Nephrology http://cjasn.asnjournals.org/cgi/content/short/3/6/1585?rss=1 Autopsy studies have demonstrated the near universal presence of fatty streaks and fibroatheromas in the general population from which patients with chronic kidney disease (CKD) arise. The vast majority of patients with CKD have multiple conventional cardiovascular risk factors. Vascular atherosclerotic calcification develops in most patients as they transition from the general population to significant CKD as part of cholesterol crystallization within atherosclerotic lesions. Once present, however, atherosclerotic medial calcification can become prominent and has been previously identified as Mönckeberg's sclerosis. A unifying concept supported by the preponderance of pathologic evidence contends that Mönckeberg's sclerosis is a manifestation of accelerated atherosclerosis in patients with CKD. The term has also been used in rare cases to describe vascular calcinosis not related to CKD. This clarification is critical to advance the field in terms of pathologic diagnosis and treatment of CKD bone and mineral disorder. Factors that seem to promote the osteoblastic transformation of vascular smooth muscle cells and enhance deposition of calcium hydroxyapatite crystals include phosphorus activation of the Pit-1 receptor, bone morphogenic proteins 2 and 4, leptin, endogenous 1,25 dihydroxyvitamin D, vascular calcification activating factor, and measures of oxidative stress. These entities work to accelerate the atherosclerotic process in patients with CKD and may be future targets for diagnosis and treatment because randomized trials with hydroxymethylglutaryl-CoA reductase inhibitors have failed to attenuate the rate of progressive vascular calcification.

]]> 2008-11-06 info:doi/10.2215/CJN.01930408 American Society of Nephrology 6 3 1598 2008-11-01 1585 Controversies in Nephrology http://cjasn.asnjournals.org/cgi/content/short/3/6/1599?rss=1 Calcification of the vascular tree is common in physiologic and pathologic conditions, i.e., aging, diabetes, dyslipidemia, genetic diseases, and diseases with disturbances of calcium metabolism. In chronic kidney disease, vascular calcification is even more common, develops early, and contributes to the markedly increased cardiovascular risk in this particular population. Pathomorphologically, atherosclerosis (i.e., plaque-forming degenerative changes of the aorta and of large elastic arteries) and arteriosclerosis (i.e., concentric media thickening of muscular arteries) can be distinguished. Increasing knowledge about calcification together with improved imaging techniques provided evidence that also vascular calcification has to be divided into two distinct entities according to the specific sites of calcification within the vascular wall: Patchy calcification of the intima in the vicinity of lipid or cholesterol deposits as present in plaque calcification and calcification of the media in the absence of such lipid or cholesterol deposits, known as Mönckeberg-type atherosclerosis. The two types of calcification may vary according to the type of vessel (large elastic versus smaller muscular type artery) and proximal versus distal sites of the arterial tree. Furthermore, clinical studies showed that it is not purely academic to distinguish between intimal and medial calcification but rather relevant for the clinical presentation, treatment, and prognosis because each type leads to different clinical consequences. In vivo studies in animal models provided evidence in favor of common pathomechanisms between vascular calcification and atherosclerosis; however, there is other, strong experimental and clinical evidence that pleads for the continued distinction between intimal and medial calcification.

]]> 2008-11-06 info:doi/10.2215/CJN.02120508 American Society of Nephrology 6 3 1605 2008-11-01 1599 Controversies in Nephrology