Aortic calcification in haemodialysis patients with diabetes mellitus

Taniwaki, Hiromichi; Ishimura, Eiji; Tabata, Tsutomu; Tsujimoto, Yoshihiro; Shioi, Atushi; Shoji, Tetsuo; Inaba, Masaaki; Inoue, Takashi; Nishizawà, Yoshiki

doi:10.1093/ndt/gfi039

Cited by 94 publications

(79 citation statements)

References 22 publications

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“…105 In concert with signals arising from the macrophage, tumor necrosis factor-␣ has emerged as a key stimulus for osteogenic differentiation in vascular cells. 62 As further evidence of biological heterogeneity in medial calcification, patients with diabetes exhibit more severe vascular calcification at every stage of declining renal function, 107 and the association with hyperphosphatemia is not significant in diabetic patients, 108 suggesting the presence of nonredundant mechanisms. Altogether, it appears that different but overlapping mechanisms guide medial calcification in vitamin D toxicity, chronic kidney disease, and diabetes.…”

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confidence: 99%

Vascular Calcification

2008

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M ost individuals aged Ͼ60 years have progressively enlarging deposits of calcium mineral in their major arteries. 1 This vascular calcification reduces aortic and arterial elastance, which impairs cardiovascular hemodynamics, resulting in substantial morbidity and mortality [2][3][4] in the form of hypertension, aortic stenosis, cardiac hypertrophy, myocardial and lower-limb ischemia, congestive heart failure, and compromised structural integrity. [5][6][7] The severity and extent of mineralization reflect atherosclerotic plaque burden 8 and strongly and independently predict cardiovascular morbidity and mortality. 9 Previously considered passive and degenerative, vascular calcification is now recognized as a pathobiological process sharing many features with embryonic bone formation. As evidence of this change in paradigm, research on vascular calcification has accelerated dramatically in the past decade. A search of PubMed (www.ncbi.nlm.nih.gov; US National Library of Medicine) under the key words vascular calcification returned Ϸ16 articles in 1982, 100 in 1994, and 250 in 2004. This year, 400 new publications are expected, for a total Ͼ3500.A breakthrough in this field was the recognition of its similarity to bone development and metabolism, in which endothelial, mesenchymal, and hematopoietic cells interact and respond to mechanical, inflammatory, metabolic, and morphogenetic signals governing skeletal mineralization; their counterparts in the artery wall govern arterial mineralization. With increasing age and dysmetabolic conditions in our population, the clinical burden of vascular calcification will continue to increase. Clinical Impact of Arterial CalcificationAortic calcification promotes congestive heart failure by eroding compliance and elastance. The hemodynamic demands of the cardiovascular system require that the aorta store energy in its elastance during systole and release it during diastole, which minimizes cardiac work and is the basis for balloon counterpulsation. This function, known as Windkessel physiology, is reflected in the high density of elastin in the arch, where mechanical energy is highest. Its loss is detectable as increased arterial pulse wave velocity in calcified arteries, resulting in thoracic summation of reflected and orthograde pressure waves, thereby increasing systolic and pulse pressures. It also increases cardiac work, promoting heart failure, left ventricular hypertrophy, and diastolic dysfunction, independently of atherosclerosis, aging, or diabetes. The link between aortic rigidity and heart failure is most evident in the hypertensive cardiomyopathy observed in patients with idiopathic infantile arterial calcification and in animal models with aortic banding.In the aortic valve, calcification produces life-threatening aortic stenosis. Although previously considered a passive, degenerative, untreatable disorder of "wear and tear" unrelated to atherosclerosis, recent findings now show that valvular calcification is regulated in a manner similar to that of atheroscler...

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Vascular Calcification

2008

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“…[6,7] Several reports have discussed methods for estimating vascular calcification in hemodialysis patients, including the allocation of a coronary artery calcification score using electron beam CT or spiral CT, measurement of areas of abdominal aortic calcification using abdominal CT, and creating an aortic calcification score using a cross-section of the abdominal aorta that has been divided into 12 sections on the abdominal CT image. [6][7][8][9][10][11][12][13][14][15][16][17] All of these procedures are difficult to do routinely.…”

Section: Discussionmentioning

confidence: 99%

“…was evaluated using the method previously reported by Taniwaki et al [13] The area of aortic arch calcification on chest x-ray films and the ACI were measured separately by two operators who were blinded to the patients' information.…”

Section: Methodsmentioning

confidence: 99%

“…It has been reported that vascular calcification increases cardiovascular events and mortality. [1][2][3][4][5] Several reports have discussed the use of different imaging modalities for assessing vascular calcification, including assessment of coronary artery calcification using electron beam computed tomography (CT) or spiral CT and assessment of the calcification index of the abdominal aorta using plain abdominal CT. [6][7][8][9][10][11][12][13][14][15][16][17] However, these modalities are of limited use because of their high cost, and their use as screening tools is restricted. Simple posterior-anterior chest x-rays are carried out regularly in many hemodialysis clinics to adjust patients' post-dialysis dry weights.…”

Section: Introductionmentioning

confidence: 99%

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Switching from Calcium Carbonate to Sevelamer Hydrochloride Has Suppressive Effects on the Progression of Aortic Calcificationin Hemodialysis Patients: Assessment Using Plain Chest X-Ray Films

Izumi¹,

Morita²,

Nishian³

et al. 2008

Renal Failure

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Sevelamer hydrochloride, a non-aluminum-and non-calciumcontaining hydrogel, is an effective phosphate binder in dialysis patients. The suppressive effect of the switching from calcium carbonate to sevelamer hydrochloride on the progression of vascular calcification was examined by measuring areas of calcification on routine chest X-rays using image-analyzing software. The data of 69 maintenance hemodialysis patients were analyzed retrospectively. Over a period of 18 months, 19 patients took only sevelamer hydrochloride as a phosphate binder, while the other 50 patients took only calcium carbonate. The area of calcification increased in the calcium carbonate group, but did not change significantly in the sevelamer group. While the usefulness of computed tomography in detecting vascular calcification in hemodialysis patients has been reported previously, the suppressive effects of switching from calcium carbonate to sevelamer hydrochloride on the progression of aortic calcification can be observed without computed tomography by using the plain chest X-ray films that are routinely performed in hemodialysis clinics.

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“…19 Aortic calcification can be quantitatively measured by abdominal computed tomography (CT) on the aortic calcification index (ACI). ACI is widely used [20][21][22][23] and defines 12 levels of calcification as a percentage. We previously reported the clinical significance of ACI among hemodialysis patients and renal transplant recipients.…”

Section: Introductionmentioning

confidence: 99%

486 The implication of aortic calcification on persistent hypertension after laparoscopic adrenalectomy in patients with primary aldosteronism

Fujita¹,

Yamamoto²,

Imai³

et al. 2016

European Urology Supplements

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Abstract:Objectives: To identify risk factors, including aortic calcification, for persistent hypertension in primary aldosteronism (PA) patients who underwent laparoscopic adrenalectomies. Methods:Between October 2000 and October 2015, we performed consecutive 101 laparoscopic adrenalectomies for unilateral PA patients. Of those, 95 patients who had at least one year follow-up periods were included. The patients were divided into two groups based on whether they had normal blood pressure without antihypertensive medications (resolved group) or still required medications (unresolved group) at one year after surgery.Variables included age, gender, body mass index, history of hypertension, dosage of antihypertensive medication score, presence of type 2 diabetes, subclinical Cushing syndrome, preoperative renal function, aldosteronoma resolution score (ARS), and abdominal calcification index (ACI). Univariate and multivariate logistic regression analyses were used to assess independent risk factors for persistent hypertension one year after surgery. Results:The complete resolution of hypertension without antihypertensive medication one year after adrenalectomy was 36/95 (38%). Preoperative antihypertensive medication score, systolic blood pressure, ACI were significantly higher, and ARS were significantly lower in the unresolved group than in the resolved group. Using multivariate logistic regression analysis, independent risk factors significantly correlating with persistent hypertension one year after surgery were ARS and ACI. Conclusions:Adrenalectomy improved blood pressure and the need for antihypertensive medications, whereas ARS and ACI were potential independent risk factors for persistent hypertension one year after adrenalectomy.

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Aortic calcification in haemodialysis patients with diabetes mellitus

Cited by 94 publications

References 22 publications

Vascular Calcification

Vascular Calcification

Switching from Calcium Carbonate to Sevelamer Hydrochloride Has Suppressive Effects on the Progression of Aortic Calcificationin Hemodialysis Patients: Assessment Using Plain Chest X-Ray Films

486 The implication of aortic calcification on persistent hypertension after laparoscopic adrenalectomy in patients with primary aldosteronism

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