Special characteristics of @entity731 in XXXX .

@entity1 @entity32 @entity8 @entity583 @entity6 @entity301 @entity1133 @entity2232 @entity740 @entity177 @entity3151 @entity453 @entity460 @entity729 @entity731 @entity204 @entity65
@entity65 are a major clinical problem in @entity1 with @entity740 and end @entity177 . @entity204 from cardiac causes accounts for 40%-50% of all @entity204 in these @entity1 and is thus up to 20 times more common in uremic @entity1 than in the general population. @entity65 in @entity1 with @entity177 is complex, but accelerated @entity731 has repeatedly been discussed as one major cause. The prevalence of @entity301 in uremic @entity1 is approximately 30% by autopsy and coronary angiography studies. Not only is the prevalence of @entity731 very high, but also the case fatality rate of @entity583 . Recently, excess mortality in uremic @entity1 having had a @entity583 was noted; the one year mortality was 55.4% and 62.3% in uremic @entity1 with and without @entity6 , respectively, compared to about 10-15% in non-uremic @entity1 . This study goes beyond the well-known notion that @entity1133 is associated with more severe @entity731 and shows that, in addition, the adaptation to coronary perfusion deficits is inappropriate. Recent clinical and autoptical studies in pre-dialysis and dialysis cohorts have documented increased intima and media thickness which appear early in the course of @entity8 ; Vascular wall thickening in @entity177 seems to be modified at least in part by parathyroidhormone (PTH) and @entity2232 (ET-1) which are both elevated in @entity1 with @entity177 . In experimental @entity177 a direct effect of high @entity3151 diet in arterial wall thickening was also documented. In addition to thickening of the vascular wall marked structural alterations were noted in @entity177 i.e. a decrease in elastic fibre content and an increase in extracellular matrix. Furthermore, increased calcification of @entity453 and of the media of the aorta and some peripheral arteries has been documented in @entity1 with @entity177 . Factors contributing to this increased calcification process may be deposition of abundant circulating @entity460 , microinflammation, oxidative stress, de novo expression of bone morphogenous proteins and lack of inhibitors of calcifcation. These changes in vascular wall composition may alter vessel elasticity and thus contribute to impaired vessel function in @entity177 . It is obvious from the above mentioned facts that @entity65 in the renal @entity1 is certainly multifaetorial in origin. There are, however, important issues to adress in the future, like (I) the characterization of vascular morphology in the different vascular beds, (II) the pathomechanisms of @entity729 as well as the potential beneficial effect of rigorous control of non-classical risk factors (i.e. high P or Ca x P, @entity32 , oxidative stress, etc.), (III) an additive or supraadditive effect of various classical and non-classical risk factors and (IV) the role of @entity6 in modifying these vascular alterations.
