Vascular Calcifications

Abstract

The predisposition to vascular calcifications in patients with chronic kidney disease (CKD) has gained great interest in recent years as many studies have described its likely impact on morbidity and mortality. The mechanism by which the process of vascular calcification is produced is complex, and it does not consist in a simple precipitation of calcium and phosphate but is instead an active and modifiable process. Several "modifiable and nonmodifiable" factors that are able to promote vascular calcification are extremely frequent in patients with CKD. Most of the present strategies to decrease vascular calcifications are based in the control of the more prevalent modifiable risk factors. Unfortunately, the extremely important nonmodifiable risk factors, which are highly prevalent, such as older age, time on dialysis, and diabetes, are not under one's control. Recent studies also have shown that vascular calcifications in some localizations were associated with increased osteoporotic fractures not only in dialysis patients but also in the general population, and interestingly, mortality also was associated significantly and positively with vascular calcifications and nontraumatic bone fractures. Despite that new strategies may improve the management of vascular diseases and specifically have a positive impact on the high prevalence of vascular calcifications, still the best possible control of the bone metabolic and inflammatory parameters are in the primary line. The horizon of the coming decade looks promising, but solid clinical and epidemiologic data are needed to manage better the bone- and cardiovascular-related disorders in patients with CKD.

Niacin Lowers Serum Phosphate and Increases HDL Cholesterol in Dialysis Patients

“…Calcium's role in the progression of cardiovascular disease is gaining more and more attention as a result of better understanding of mechanisms that control calcification processes (11,12). Although effective and well tolerated, feeding calcium salts may promote coronary artery and aortic valve calcification (13,14); therefore, hyperphosphatemia treatment protocols must carefully balance potential benefits and adverse effects.…”

New approaches to assessing cardiovascular risk

“…19 This is secondary to disorders of mineral metabolism and results in increasing arterial stiffness (aggravating hypertension and its end-organ effects). 20 The balance between FGF-23 and the membrane-bound protein Klotho becomes disturbed well before even a fall in GFR 21 and recent evidence suggests this may contribute directly to endothelial dysfunction, left ventricular hypertrophy and CV risk. 22 Paradoxically, treatments for renal failure, such as dialysis, may greatly exacerbate these calcium-phosphate-related mechanisms for arterial disease and modified strategies for renal replacement therapies may reduce progression of arterial damage.…”

Stężenia parathormonu w surowicy oznaczane metodą chemiluminescencji i elektrochemiluminescencji — czy wyniki są porównywalne u hemodializowanych chorych na przewlekłą chorobę nerek?

“…Clinical symptoms accompanying the impaired calcium-phosphorus balance, such as abnormalities in imaging tests and renal osteodystrophy, are known as chronic kidney disease -mineral and bone disorders (CKD-MBD) [5]. The clinical importance of developing CKD-MBD is increased cardiovascular and overall mortality caused mainly by vascular calcification [6].…”