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PubMed1998

Changes in pericardial calcification due to antiplatelet agents: in vitro studies.

To develop tissue valves for prolonged use in the cardiovascular system, the complicated process of surface induced calcification must be better understood. Calcification was examined for 60 days on glutaraldehyde treated bovine pericardium (GABP) and enzyme extracted tissues fixed in glutaraldehyde (GATBP) incubated in metastable solutions of calcium phosphate, and the roles of aspirin and persantine in conjunction with vitamins C, B, or E, gentamycin (antibiotic), or pentothal sodium (anesthetic) in the medium were examined. Further, the diffusion of calcium across the GATBP was evaluated using a diffusion cell with 2 compartments. Pericardial calcification was also observed using scanning electron microscopy (SEM) techniques. It seems that the examined antiplatelet agents can modify the pericardial surfaces and subsequently their mineralization processes (GATBP, 31.7 micrograms/mg tissue; in the presence of 5 mg% vitamin C, 13.1 micrograms/mg tissue; in 1.5 mg% aspirin, 17.2 micrograms/mg tissue; and 1 mg% gentamycin, 14.8 micrograms/mg tissue) on exposure with the metastable calcium phosphate solution for 60 days. In addition, these agents may modify calcium transport and interfere with the adsorption at the surface, hence reducing calcium nodulation on GATBP. Scanning electron micrographs also revealed a reduction in calcium deposition on the pericardium due to these antiplatelet agents. It may be hypothesized that the influx of calcium on GATBP may be due to the cellular components or the involvement of plasma proteins like the fibrinogen molecule. The exact mechanism of these changes in the calcification of the pericardium are still unknown. From these in vitro findings, it appears that a combined vitamin therapy with low doses of aspirin may be beneficial for platelet suppression and thereby for prevention of thrombosis and calcification. However, more in vivo studies are needed to develop applications.

Anesthetics, Intravenous↗
PubMed2003

Vascular calcification in dialysis patients: pathogenesis and consequences.

BACKGROUND: Vascular calcification is believed to have a crucial role in the excess cardiovascular mortality and morbidity in patients with end-stage renal disease (ESRD). METHODS AND RESULTS: Recent evidence suggests that uremic vascular calcification is an active cell-mediated process resembling osteogenesis in bone, rather than passive precipitation of calcium and phosphorus in the setting of deranged mineral metabolism. To date, several bone-associated proteins (osteopontin, bone sialoprotein, alkaline phosphatase, and type I collagen) have been shown in histological sections of vessels obtained from patients with ESRD or calcific uremic arteriolopathy. In in vitro experiments, the addition of uremic serum upregulates osteopontin expression by cultured vascular smooth muscle cells (VSMCs). CONCLUSION: We are only beginning to understand the process by which VSMCs transform into osteoblast-like cells, although phosphorus may have a key role. Additional factors mediating or modulating the development of vascular calcification in patients with ESRD remain to be identified. Further understanding of the pathophysiological state of uremic vascular calcification is needed to design effective therapeutic strategies to intervene with this devastating condition in the ESRD population.

Calcinosis↗
PubMed2004

Vascular calcification in chronic kidney disease.

Dialysis patients have increased cardiovascular morbidity, mortality, and vascular calcification, and the latter appears to impact the former. Recent evidence indicates that vascular calcification is an active, cell-mediated process. Osteoblast differentiation factor Cbfa1 and several bone-associated proteins (osteopontin, bone sialoprotein, alkaline phosphatase, type I collagen) are present in histologic sections of arteries obtained from patients with end-stage renal disease (chronic kidney disease stage V [CKD-V]). This supports the theory that vascular smooth muscle cells can dedifferentiate or transform to osteoblast-like cells, possibly by up-regulation of Cbfa1. In in vitro experiments, addition of pooled serum from dialysis patients (versus normal healthy controls) accelerated mineralization and increased expression of Cbfa1, osteopontin, and alkaline phosphatase in cultured vascular smooth muscle cells. Clinically, the pathogenesis of vascular calcification is not completely understood, although increased levels of phosphorus and/or other potential uremic toxins may play an important role by transforming vascular smooth muscle cells into osteoblast-like cells. Presumably, once this process begins, increased serum calcium X phosphorus product, or calcium load from binders, accelerates this process. In addition, it is likely that circulating inhibitors of calcification are also important. Further understanding of the pathophysiology of vascular calcification is needed to intervene appropriately.

Calcinosis↗
PubMedDate not supplied

[Sclerochoroidal calcification--a rare disease pattern--report on two patients, differential diagnosis and review of the literature].

BACKGROUND: Idiopathic sclerochoroidal calcification is a benign calcification at the level of the choroid and the sclera. Due to the location of the lesions mainly between the superior temporal vascular arcade and the equator, there is no visual disturbance. Diagnosis of idiopathic sclerochoroidal calcification is made by the typical fundus appearance in combination with ultrasonic findings. PATIENTS: 1. A 55-year old male patient showed multifocal slightly prominent lesions in the superiotemporal fundus of the left eye. 2. In a 60-year old male patient found multifocal slight prominent whitish lesions were found in the superior fundus from temporal to nasal of both eyes. Visual acuity was unaffected by the lesions. The borderlines of visual field were normal. RESULTS: Echography revealed a highly reflective lesion with orbital shadowing. Fluorescein angiography showed a normal pattern besides the lesions with a late hyperfluorescence staining of the lesion itself. Calcium and phosphorus levels were normal with no signs of abnormal calcium metabolism. CONCLUSIONS: Idiopathic sclerochoroidal calcification is a benign disorder which is diagnosed by the typical ophthalmoscopic picture in combination with standardised echography. Computed tomography can confirm the diagnosis. The most important differential diagnosis is choroidal osteoma, others are choroidal metastasis, choroidal amelanotic naevus and choroiditis. The early diagnosis of a sclerochoroidal calcification is important to avoid all the implications for the patient to which a misdiagnosis can lead.

Calcinosis↗
PubMed1981

Early stenosis and calcification of glutaraldehyde-preserved porcine xenografts in children.

Thirty-four glutaraldehyde-preserved porcine aortic valves have been implanted in children at the Center of Thoracic and Cardiovascular Surgery in Göttingen since 1972. Severe stenosis of the right ventricular outflow tract (RVOT) due to massive calcification of the bioprosthetic valve was detected 15 to 76 months after surgery in 2 of 3 children with hospital-made, and in one of 25 children with commercially available valved conduits. The results with Hancock xenograft valves in mitral position were even more alarming. Five out of 6 children, aged 5 to 15 years (mean 9 years) presented similar massive calcification patterns of the bioprosthesis, necessitating reoperation from 23 to 63 months (mean 38.8 months) after implantation. Focal calcium deposits were found mostly in the central layers of the cusps; severe stenosis and regurgitation were due to immobilization of the leaf-lets which were fixed in a semi-open position. The causes for early valve dysfunction and calcification of glutaraldehyde-fixed porcine aortic bioprostheses in children remain to be further investigated. Degenerative changes have been shown to commence early after implantation, resulting in collagen disruption as early as 2 years later (3, 7, 19). There is evidence that these lesions could be predisposing factors for calcification, leading to accelerated calcification rats in children and patients with a high-calcium-turnover. The use of bioprostheses in children and adolescents must therefore be questioned since they appear to carry a high prospect to early valve deterioration.

Adolescent↗
PubMed1990

[Intracranial calcification--how much more information can be obtained by MR than CT?].

Thirty-four patients known to have intracerebral calcification that had been demonstrated by CT, were also examined by MR to determine which modality would provide more information concerning the underlying pathology. There were seven patients with intra- or extracerebral intracranial calcification without any known cause, seven cavernous haemangiomas, six meningiomas, five oligodendrogliomas, one astrocytoma, one optic nerve glioma, one plexus papilloma, one pinealoma, one histologically unclassified tumour, one healed tuberculous meningitis, one old haematoma, one tuberous sclerosis and one case of basal ganglia calcification due to hypoxia. In 16 cases the two methods were of equal value, in four cases CT was more valuable than MR, but in 14 cases MR provided more information than CT. In cases of tumour calcification, MR was frequently more valuable than CT in demonstrating the tumour and its extent. It was also better in diagnosing vascular malformations and old bleedings. MR provided more information in tuberous sclerosis, but less in inflammatory lesions. MR was better than CT in excluding pathology in cases of isolated calcification.

Astrocytoma↗
PubMed1984

Abdominal calcifications in infants and children.

Abdominal and pelvic calcifications are usually incidental findings and require further measures to determine their origin. Most laboratory investigations are of little help. Plain anteroposterior and lateral x-rays are essential. The time of appearance and localisation of a calcification is of diagnostic importance. Amorphous, granular and irregular calcification can be an early sign of malignancy. Mobility of a calcification also helps to clarify its origin. Over the past 15 years abdominal and pelvic calcifications, excluding urological radiodensities, have been found in 63 patients up to fourteen years of age at our institute. A migrating deposit in the omentum, a spontaneously amputated calcified ovary mimicking a vesical calculus and a congenital retroperitoneal xanthofibroma caused the greatest difficulty in establishing a preoperative diagnosis.

Abdomen↗
PubMed1983

[Are foreign body calcifications late reactions following augmentation mammaplasty?].

We describe 47 patients aged 20 to 63 years in whom a mammaplasty had been performed (43 by an injection method, four by surgery). Calcification round the foreign body occurred in 71.5% of the paraffin group (ten out of 14 cases) and in 17% of the silicone group (eight out of 33 cases). The interval between implantation and calcification is fairly constant in the paraffin group; of 11 patients whose implant was older than 15 years, ten showed calcification. In the silicone group, only one out of ten cases showed calcification. In the silicone group, the material itself is thought to be responsible since (with the exception of one case done in 1956) all cases treated between 1966 and 1971 showed calcification irrespective of the interval.

Adult↗
PubMed1989

Encephalopathy with calcifications of the basal ganglia in children. A reappraisal of Fahr's syndrome with respect to 14 new cases.

Calcifications of the basal ganglia are described under the heading of "Fahr's syndrome". The clinical pattern is variable and the syndrome may be sporadic or familial. This study describes a personal series of 14 cases of encephalopathy with calcification of the basal ganglia and reviews the literature cases. A four-group classification is proposed. The first group includes encephalopathy, microcephaly, dwarfism, retinal degeneration or optic atrophy, symmetrical patchy demyelination with calcifications and probable autosomal recessive inheritance. Some cases have an early onset, a rapid evolution. Others have a later onset, longer course and retinal degeneration. In the second group, the children suffer from a congenital encephalopathy or a cerebral palsy without clear deterioration, without short stature, ocular impairment or persistent CSF abnormalities. This group has not been reported in the literature. The cases do not seem to be genetic. The precise cause in unknown but a sporadic non progressive anoxo-ischemic, or viral prenatal disease is suggested. In the third group, the association of encephalopathy, microcephaly, and persistent CSF lymphocytosis, has a high recurrence rate. The pathogenesis is still a matter of dispute. The fourth group is characterized by autosomal dominant calcifications of the basal ganglia with or without neurological abnormalities. Finally calcium metabolism disorders and mitochondrial encephalomyopathy may be associated with calcifications of the basal ganglia.

Basal Ganglia Diseases↗
PubMed1999

Ultrasound therapy for calcific tendinitis of the shoulder.

BACKGROUND AND METHODS: Although ultrasound therapy is used to treat calcific tendinitis of the shoulder, its efficacy has not been rigorously evaluated. We conducted a randomized, double-blind comparison of ultrasonography and sham insonation in patients with symptomatic calcific tendinitis verified by radiography. Patients were assigned to receive 24 15-minute sessions of either pulsed ultrasound (frequency, 0.89 MHz; intensity, 2.5 W per square centimeter; pulsed mode, 1:4) or an indistinguishable sham treatment to the area over the calcification. The first 15 treatments were given daily (five times per week), and the remainder were given three times a week for three weeks. Randomization was conducted according to shoulders rather than patients, so a patient with bilateral tendinitis might receive either or both therapies. RESULTS: We enrolled 63 consecutive patients (70 shoulders). Fifty-four patients (61 shoulders) completed the study. There were 32 shoulders in the ultrasound-treatment group and 29 in the sham-treatment group. After six weeks of treatment, calcium deposits had resolved in six shoulders (19 percent) in the ultrasound-treatment group and decreased by at least 50 percent in nine shoulders (28 percent), as compared with respective values of zero and three (10 percent) in the sham-treatment group (P=0.003). At the nine-month follow-up visit, calcium deposits had resolved in 13 shoulders (42 percent) in the ultrasound-treatment group and improved in 7 shoulders (23 percent), as compared with respective values of 2 (8 percent) and 3 (12 percent) in the sham-treatment group (P=0.002). At the end of treatment, patients who had received ultrasound treatment had greater decreases in pain and greater improvements in the quality of life than those who had received sham treatment; at nine months, the differences between the groups were no longer significant. CONCLUSIONS: In patients with symptomatic calcific tendinitis of the shoulder, ultrasound treatment helps resolve calcifications and is associated with short-term clinical improvement.

Calcinosis↗
PubMed2003

Coronary artery calcification in black women and white women.

BACKGROUND: Coronary calcification is a potent independent predictor of coronary risk. Sex-specific risk categories based on calcium scores have been established, but ethnic differences in coronary calcification have been little studied. This prospective cohort study compares coronary calcification, assessed by computed tomography, in postmenopausal black women and white women. METHODS AND RESULTS: Computed tomographic scans were performed on 128 black women and 733 white women without known coronary artery disease (mean age 63 +/- 8 years). Although coronary risk factors were more prevalent among black women (P <.0001), total calcium scores were similar to those in white women. By use of the Framingham algorithm, higher calcium scores were associated with higher 10-year risk of myocardial infarction or coronary death. In multiple regression analysis, age was independently associated with higher calcium scores in both ethnic groups (P =.002 for black women, P <.0001 for white women). Diabetes mellitus and not exercising at least 3 times per week were independently associated with higher calcium scores in white women but not black women. Educational level, body mass index, current hormone replacement therapy, hysterectomy, dietary fat consumption, family history of premature coronary disease, hypertension, self-reported high cholesterol, and current smoking were not independently associated with coronary calcium score in black women, white women, or the combined cohort; neither was ethnicity an independent predictor of coronary calcification. CONCLUSIONS: Despite higher dietary fat consumption, higher body mass index, and greater prevalence of hypertension, diabetes, and smoking, black women had coronary calcium scores similar to those of white women. Ethnicity was not an independent predictor of coronary calcification.

Black or African American↗
PubMed2003

Sonographic features of hepatic artery calcification in chronic renal failure.

PURPOSE: Little is known about radiological aspects of hepatic artery calcification. For this reason, the sonographic features of calcified hepatic arteries were studied in patients with chronic renal failure who frequently develop tissue calcification due to hyperparathyroidism. MATERIAL AND METHODS: Ultrasound was performed in 314 patients on dialysis who underwent examination of the liver, spleen and kidney twice in the past 4 years and were reevaluated with particular attention to acoustic shadowing. Abdominal CT was carried out in 219 of these 314 patients, and ultrasound findings were reevaluated with reference to CT findings. RESULTS: A large acoustic shadow was seen in the hilum that corresponded to the calcified hepatic artery on CT in 8 patients, and in another 9, a similar large shadow was seen in the hilum without CT confirmation. Acoustic shadows of various sizes were definitely or most likely due to arterial calcification within the liver in 36 patients. The strength of shadow depended on the angle at which the ultrasound beam hit the artery. Probable calcification of small arteries accompanying portal veins was seen in 70 patients. These changes are different from those due to pneumobilia and biliary tract diseases. CONCLUSION: Calcification of the hepatic artery can be identified by its acoustic shadow.

Aged↗
PubMed2004

Improved image contrast of calcifications in breast tissue specimens using diffraction enhanced imaging.

The contrast of calcifications in images of breast tissue specimens using a synchrotron-based diffraction enhanced imaging (DEI) apparatus has been measured and is compared to the contrast in images acquired using a conventional synchrotron-based radiographic imaging modality. DEI is an imaging modality which derives image contrast from x-ray absorption, refraction and small-angle scatter-rejection (extinction), unlike conventional radiographic techniques, which can only derive contrast from absorption. DEI is accomplished by inserting an analyser crystal in the beam path between the sample and the detector. Two of the three breast tissue specimens contained calcifications associated with cancer, while a third contained benign calcifications. Results of the image analysis indicate that the DEI contrast of images taken with the analyser crystal tuned to the peak of its rocking curve, was as much as 19 times that of the conventional radiograph, with an average of 5.5 for all calcifications. This improved image contrast for even near-pixel-size calcifications suggests potential utility for DEI in breast imaging.

Breast Diseases↗
PubMed2004

Breast vascular calcification and risk of coronary heart disease, stroke, and heart failure.

OBJECTIVE: Vascular calcification holds promise as a useful cardiovascular risk maker. Our objective was to examine the association between breast vascular calcification and risk of cardiovascular disease (CVD) outcomes. METHODS: A cohort study was performed among 12,761 women, 40-79 years of age at baseline (1968-1973), who attended multiphasic health checkups that included mammography. The outcome measures included coronary heart disease (CHD), ischemic stroke, transient ischemic attack (TIA), hemorrhagic stroke, and heart failure, ascertained using discharge diagnosis codes and death records through December 31, 2000 (median follow-up, 24.8 years). RESULTS: Breast vascular calcification was present in 424 (3%) women. It was independently and positively associated with age, high parity, and diabetes and inversely associated with education level and current cigarette smoking. After adjustment for age, education level, race, cigarette smoking, alcohol use, body mass index (BMI), serum total cholesterol, hypertension, diabetes, parental history of myocardial infarction (MI), parity, and hormone replacement therapy (HRT), breast vascular calcification was associated with a 1.32-fold increased risk of CHD (95% confidence interval [CI] 1.08-1.60), a 1.41-fold increased risk of ischemic stroke (95% CI 1.11-1.78), and a 1.52-fold increased risk of heart failure (95% CI 1.18-1.98). CONCLUSIONS: Breast vascular calcification detected as part of a screening mammogram was an independent risk factor for multiple cardiovascular outcomes among women. The value of mammography in cardiovascular risk stratification deserves further investigation.

Adult↗
PubMed2001

The amino bisphosphonate ibandronate prevents vitamin D toxicity and inhibits vitamin D-induced calcification of arteries, cartilage, lungs and kidneys in rats.

Experiments were carried out to determine whether the doses of the amino bisphosphonate ibandronate that inhibit bone resorption inhibit soft tissue calcification and death in rats treated with a toxic dose of vitamin D. These studies were prompted by the recent discovery that ibandronate doses that inhibit bone resorption potently inhibit artery calcification induced by treatment with the vitamin K antagonist warfarin. All 16 rats treated with the toxic dose of vitamin D (12.5 mg cholecalciferol x kg(-1)) died by d 6 after the first vitamin D injection (median survival: 4.5 d), whereas the 12 rats treated with vitamin D plus ibandronate (0.25 mg x kg(-1) x d(-1)) were alive and in good health at d 10. Rats treated with vitamin D alone and examined at d 4 had extensive Alizarin red staining for calcification in the aorta, the carotid, hepatic, mesenteric, renal and femoral arteries, kidneys and lungs, whereas rats treated with vitamin D plus ibandronate had no evidence for calcification at any of these tissues when examined at d 7 and 10. Ibandronate treatment also inhibited the dramatic increase in the levels of calcium and phosphate seen in the abdominal aorta, kidneys, lungs and trachea of the vitamin D-treated rats (P < 0.001). Serum calcium levels were, however, not different in rats treated with vitamin D alone (3.4 +/- 0.2 mmol x L(-1)) and in rats treated with vitamin D plus ibandronate (3.5 +/- 0.2 mmol x L(-1)). Treatment with vitamin D alone increased levels of matrix Gla protein, an inhibitor of soft tissue calcification, in the arteries, kidneys, lungs and trachea by 10- to 100-fold, and ibandronate treatment prevented this increase. The importance of these studies in the rat model is that they identify a class of drugs in current clinical use that can be used to treat patients with vitamin D toxicity and that they identify the dose of the drug that is predicted to be effective, namely the dose that inhibits bone resorption. Because there is no other known treatment for vitamin D toxicity, there would seem to be good reason to try bisphosphonates such as ibandronate in future studies aimed at treating patients who have been exposed to toxic levels of vitamin D.

Animals↗
PubMed2004

Natural history of vascular calcification in dialysis and transplant patients.

BACKGROUND: The purpose of the present study was to determine the natural history of coronary artery and aorta calcification by spiral computed tomography (CT) in patients who undergo a renal transplant and patients on haemodialysis. METHODS: Two cohorts were evaluated for the natural history of vascular calcification: (i) 23 patients who underwent a baseline CT scan at the time of renal transplant and a repeat evaluation 15-20 months later; and (ii) 33 chronic kidney disease, stage 5 haemodialysis subjects who underwent a baseline CT scan, all followed for a minimum of 15 months, and 17 of whom underwent a second CT scan. RESULTS: In the patients undergoing a renal transplant, there was no net change in CAC with time, suggesting stabilization of calcification. In the haemodialysis patients, the median CAC increased by 1.27+/-1.88 score/days, P = 0.013. There was a trend towards increasing AoC score in both groups. All patients without calcification at baseline remained calcification free at follow-up. In the 15 months following baseline, the six dialysis patients who died had a significantly greater CAC score at baseline compared with the 24 patients who remained alive. Similarly, those patients who were hospitalized had a greater baseline CAC than patients who were not hospitalized. CONCLUSION: In this preliminary study, renal transplantation appears to slow down or arrest CAC, whereas CAC progresses in haemodialysis patients. In haemodialysis patients, CAC was greater in patients who died or were hospitalized compared with those who remained alive or were not hospitalized.

Adult↗
PubMed2005

Atherosclerosis and vascular calcification are independent predictors of left ventricular hypertrophy in chronic haemodialysis patients.

BACKGROUND: Accelerated atherosclerosis and vascular calcification are common in chronic haemodialysis (HD) patients. In this study, we aimed to investigate the relationship between left ventricular hypertrophy (LVH) in HD patients and atherosclerosis and vascular calcification measured by electron beam computed tomography (EBCT). METHODS: In a cohort of 118 HD patients (52 male, 66 female, mean age: 46+/-13 years), we measured biochemical parameters, including BUN, creatinine, albumin, haemoglobin, C-reactive protein and fibrinogen levels, and performed echocardiography, high-resolution B-mode carotid ultrasonography and EBCT in 85 of them. The degree of stenosis was measured at four different sites (communis, bulbus, interna and externa) in both carotid arteries. Carotid plaque scores were calculated by summing the degrees of stenosis measured at all locations. RESULTS: LVH was detected in 89 of the patients (75%). Plaque-positive patients had higher left ventricular mass index (LVMI) than plaque-negative patients (175+/-59 vs 143+/-46 g/m2, P = 0.003). LVMI was correlated with systolic blood pressure (r = 0.62, P<0.001), pulse pressure (r = 0.58, P<0.001), haemoglobin levels (r = - 0.25, P = 0.008), carotid plaque score (r = 0.32, P = 0.001) and coronary (CACS) and aortic wall calcification score (AWCS) (r = 0.34, P = 0.002 and r = 0.43, P<0.001, respectively). Multiple linear regression analysis (model r = 0.76) showed the independent factors related to LVMI to be systolic blood pressure, pulse pressure, CACS and presence of carotid plaques. CONCLUSION: Extra-coronary atherosclerosis and vascular calcification are associated with LVH in HD patients. Whether the treatment of atherosclerosis or vascular calcification may cause regression of or even prevent LVH in HD patients remains to be seen.

Adolescent↗
PubMed2005

Reduced baroreflex sensitivity is associated with increased vascular calcification and arterial stiffness.

INTRODUCTION: Vascular calcification is a critical determinant of cardiovascular morbidity and mortality in chronic haemodialysis (HD) patients. The pathophysiology underlying this observation remains obscure. Baroreceptor sensitivity (BRS) is important in the maintenance of an appropriate cardiovascular status both at rest and under the physiological stress of HD. BRS is determined by both the mechanical properties of the vascular wall, mediating the transfer of transmural pressure, and afferent and efferent autonomic function. We aimed to study the association between arterial structure, function and BRS in chronic HD patients. METHODS: We studied 40 chronic HD patients mean age 62+/-2 (26-86) years who had received HD for a mean 40+/-4 (9-101) months. Spontaneous BRS was assessed using software studying the relationship between inter-beat variability and beat to beat changes in systolic blood pressure. Functional characteristics of conduit arteries (pulse wave analysis) were studied with applanation tonometry at the radial artery. Arterial calcification was assessed in lower limbs using reconstructed multi-slice computed tomography and quantified with volume-corrected calcification scores within the superficial femoral artery. RESULTS: Mean BRS was 4.43+/-0.44 ms/mmHg, with a wide range from 1.0 to 11.5 ms/mmHg. This correlated with arterial stiffness as measured by time to shoulder calculated from the central pulse wave analysis (r = 0.4, P = 0.01). BRS was also associated with vascular calcification (P = 0.01) but not by other factors such as dialysis vintage, age or pre-dialysis systolic/diastolic blood pressure. CONCLUSION: The reduction in BRS and the resulting aberrant blood pressure response to the physiological stress and volume changes of HD may be important in the further understanding of the pathophysiology of the increased mortality in HD patients with vascular calcification.

Adult↗