Screening of vascular calcifications in patients with end-stage renal diseases

Abstract. Vascular calcifications (VC) are a major contributor to the massively increased mortality in hemodialysis (HD) patients. The present study aimed to detect arterial media and intima calcifications in HD patients and to evaluate potential risk factors. 214 patients aged 59.0 ± 11.0 years on HD for 6.39 ± 4.59 years were studied. VC were scored based on to plain radiographs. Potential risk factors were assessed. Out of the 214 patients studied, only 14% did not display any detectable VC. Using plain radiographs calcifications could be detected in 136 (63.6%) patients. Calcified plaques on carotid arteries were detected in 168 (78.4%) patients. There was the highest frequency of patients with the most pronounced calcifications. Calcifications of heart valves were detected in 89 (44.1%) patients. Univariante analysis indicate that risk to develop VC is present in older patients, patients with longer dialysis vintage, thicker intima media, higher lumen diameter and mitral valve calcifications. Multivariate multinomial logistic regression analysis revealed these factors as independent predictors of VC in dialysis patients. Our data confirm a high prevalence of VC in HD patients, their association with older ages, longer dialysis vintage, and presence of valvular calcifications and early markers of atherosclerosis

Renoprotective effect of calcium channel blockers

The advancing chronic renal failure is at most the consequence of secondary haemodynamic and metabolic factors as intraglomerular hypertension and glomerular hypertrophy. Although tight blood pressure control is the major preventive mechanism for progressive renal failure, ACE inhibitors and angiotensin receptor blockers have some other renoprotective mechanisms beyond the blood pressure control. That is why these two groups of antihypertensive drugs traditionally have advantages in treating renal patients especially those with proteinuria over 400-1000 mg/day. Even if earlier experimental studies have shown renoprotective effect of calcium channel blockers, later clinical studies did not prove that calcium channel blockers have any advantages in renal protection over ACE inhibitors given as monotherapy or in combination with ACE inhibitors. It was explained by action of calcium channel blockers on afferent but not on efferent glomerular arterioles; a well known mechanism that leads to intraglomerular hypertension. New generations of dihydropiridine calcium channel blockers can dilate even efferent arterioles not causing unfavorable haemodynamic disturbances. This finding was confirmed in clinical studies which showed that renoprotection established by calcium channel blockers was not inferior to that of ACE inhibitors and that calcium channel blockers and ACE inhibitors have additive effect on renoprotection. Newer generation of dihydropiridine calcium channel blockers seem to offer more therapeutic possibilities in renoprotection by their dual action on afferent and efferent glomerular arterioles and, possibly by other effects beyond the blood pressure control

Vascular access calcification predicts mortality in hemodialysis patients

Vascular calcification is a recognized risk factor for cardiovascular mortality in patients with end-stage renal disease. The aim of this study was to identify risk factors for vascular access calcification and to determine if patients with this disorder are at increased risk of death. Vascular access calcification was found in 49 of 212 hemodialysis patients as measured by plain X-ray (arteriovenous fistula or synthetic graft) in two dimensions. Male gender, diabetes mellitus, and length of time on dialysis were independent predictors for access calcification determined by logistic regression multivariate analysis. Serum parameters were not independently related to access calcification. Kaplan–Meier analysis showed an increased mortality risk, and Cox regression analysis confirmed that vascular access calcification was an independent mortality predictor. Our study suggests that detection of vascular access calcification is a cost-effective method to identify patients at increased mortality risk