Mönckeberg's medial sclerosis and inorganic phosphate in uremia

Shioi, Atsushi; Taniwaki, Hiromichi; Jono, Shuichi; Okuno, Yasuhisa; Koyama, Hideki; Mori, Katsuhito; Nishizawà, Yoshiki

doi:10.1053/ajkd.2001.27396

Cited by 54 publications

(37 citation statements)

References 17 publications

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“…Vascular calcification (VC), especially in the arterial media, is probably a major contributor to arteriosclerosis in CKD (127)(128)(129)(130). Numerous autopsy and radiologic studies in the past several decades have demonstrated high rates of calcification of peripheral and central arteries (131)(132)(133)(134)(135)(136)(137)(138)(139)(140), and coronary artery calcification is even common and progressive in young adult hemodialysis patients (141). VC is probably primarily due to abnormal mineral metabolism that is seen in renal failure (141)(142)(143)(144)(145), perhaps through a complex process involving osseous metaplasia of the vascular wall components (118,119,146).…”

Section: Pathophysiology Of Cvd In Ckdmentioning

confidence: 99%

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

Nogueira

Weir

2007

Clinical Journal of the American Society of Nephrology

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D uring the past several decades, the advent and refinement of maintenance dialysis and kidney transplantation have essentially eliminated kidney failure per se as a cause of death in developed countries. However, as patients survive many years after the development of renal failure, comorbidities develop, progress, and ultimately cause death in these individuals. Cardiovascular disease (CVD) has ranked prominent among these comorbidities, accounting for nearly half of the deaths (1). All along the continuum of chronic kidney disease (CKD)-from microalbuminuria to ESRD-a higher risk for CVD has been observed (see Epidemiology of CVD in CKD). In fact, individuals with early CKD are more likely to die of CVD than to develop ESRD (2,3). Then, among those who survive to ESRD, the all-cause CVD mortality in patients with ESRD is many-fold higher than in the general population (4). Unfortunately, the reasons for the association of CKD with CVD are not clearly understood, and the role of various clinical interventions in stemming the CVD epidemic are not well defined. Complicating the issue is the potential variation in the pathophysiology and clinical behavior of CVD through the stages of CKD.3-Hydroxyl-3-methylglutaryl CoA reductase inhibitors (statins) and other lipid-lowering drugs (LLD) have been clearly demonstrated to lessen the morbidity and mortality of CVD in the general population; therefore, there is hope that the use of these drugs may likewise help patients with CKD (In addition, it has been theorized that dyslipidemia may contribute to the progression of CKD, such that LLD may prove to slow CKD progression.) Nevertheless, given differences in epidemiology and pathophysiology of CVD in CKD, there are reasons to question whether the cardiovascular benefits of LLD that are observed in the general population will also be realized in the CKD population. It is widely acknowledged that the current medical literature provides insufficient data to guide the use of LLD in the CKD population, in large part because renal insufficiency has been an exclusion criterion for most of the randomized, controlled studies that have addressed this issue. Although consensus-based guidelines on the treatment of dyslipidemias in individuals with CKD and with kidney transplants have been published by the National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI) Work Groups, the nephrology and cardiology communities recognize the urgent need for high-quality clinical studies on this issue, and this has fueled the publication of subgroup analyses of previous large studies in the general population and the launching of large-scale clinical trials in the CKD population, as summarized in Table 1. To provide the reader with a better appreciation of the important issues that are germane to management of dyslipidemia in CKD, this article (1) briefly summarizes the literature on the benefits of LLD in the general population, (2) demonstrates the limited involvement of individuals with CKD in the studies in the ge...

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Section: Pathophysiology Of Cvd In Ckdmentioning

confidence: 99%

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

Nogueira

Weir

2007

Clinical Journal of the American Society of Nephrology

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“…Such vesicles originate from the cell membrane of cells that have undergone apoptosis, and diffuse into the collagen matrix; they eventually coalesce and form a calcium phosphate plaque. 12,13,22 This process has been demonstrated in atheromatous plaques in CRF patients; there is strong evidence suggesting that hypercalcemia and hyperphosphatemia participate in the origin of these vesicles. 22,27 Matrix vesicles also participate in other types of calcification, including tympanosclerosis.…”

Section: Discussionmentioning

confidence: 96%

“…12,13,22 This process has been demonstrated in atheromatous plaques in CRF patients; there is strong evidence suggesting that hypercalcemia and hyperphosphatemia participate in the origin of these vesicles. 22,27 Matrix vesicles also participate in other types of calcification, including tympanosclerosis. 4 Other cellular and hormonal elements have been found to participate actively in tympanosclerotic calcification and in the calcification of other tissues.…”

Section: Discussionmentioning

confidence: 96%

“…20 Certain authors have questioned the role of elevated serum calcium and phosphorus in the pathophysiology of this type of calcification, 20 although various papers have associated these two conditions. [22][23][24] An altered glomerular filtration rate due to kidney disease leads to phosphate retention in the serum. Excess serum phosphorus tends to bind to free calcium to form precipitates that may originate ectopic calcification.…”

Section: Discussionmentioning

confidence: 99%

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Miringosclerose em pacientes com insuficiência renal crônica: análise comparativa com um grupo controle

Neto¹,

Lessa²,

Alves³

et al. 2008

Rev. Bras. Otorrinolaringol.

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Myri ngosclerosis is a scar of the tympanic membrane lamina propria, resulting from trauma or inflammation, characterized by proliferation of collagen, hyalinization, calcium and phosphate deposits and cartilaginous or osseous metaplasia of the middle ear mucosa, a sequence that is similar to that taking place in other types of pathologic calcification, common in chronic renal failure (CRF). Aim: To verify the influence of chronic renal failure on the prevalence of myringosclerosis. Method: The otoscopic examination was done in 341 chronic renal failure patients and in 356 normal control individuals. The frequency of positive otoscopies was compared between the two groups, based on individual variables and those pertaining to CRF. Results: 11.7% of the patients had a positive otoscopy in the CRF group, compared to 5.1% in the control group. There was no statistical diference in the frequency of myringosclerosis acording to gender, ethnic group, time of dialysis or serum minerals. The groups had a wide age range. Conclusion: Although the findings of this study suggest a higher ocurrence of myringosclerosis in patients with renal disease, they do not provide a basis for stating that there is any relation between renal failure and tympanic alterations.

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“…The clinical significance of vascular calcification has been realized only recently. Arterial medial calcification (Monckeberg's type calcification) is the major type of arteriosclerosis in dialysis patients (6,7). The medial sclerosis progresses in proportion to the period of dialysis without any relation to age since it occurs even in young adults in coronary as well as peripheral arteries (1).…”

Section: Introductionmentioning

confidence: 99%

Effect of Etidronate on Aortic Calcification and Bone Metabolism in Calcitoriol-Treated Rats With Subtotal Nephrectomy

et al. 2005

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Abstract. The present study was undertaken to determine the effects of etidronate (ED) on calcitriol-induced aortic calcification and bone metabolism in rats with renal failure. Severe aortic calcification was induced by treatment with calcitriol for 3 weeks in rats in which 5 / 6 of the kidneys were removed (SNx group). Treatment of ED (10 mg / kg) together with calcitriol after subtotal nephrectomy (SNx) significantly inhibited thoracic and abdominal aortic calcification 3 weeks after the operation; however, ED (2 mg / kg) was ineffective. The serum levels of osteocalcin and pyridinoline decreased in ED (10 mg / kg) treated-renal failure rats compared with SNx rats. Total bone mineral density (BMD) in the SNx group was lower than that in the sham group, in which animals were treated with calcitriol after a sham operation. The total BMD value in the ED (10 mg/ kg)-treated group was similar to that in the SNx group, whereas the levels of cancellous BMD were low in the ED (10 mg / kg)-treated rats. Our data show that ED at a dosage that suppresses bone metabolism markedly inhibits vascular calcification in rats with renal failure.

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Mönckeberg's medial sclerosis and inorganic phosphate in uremia

Cited by 54 publications

References 17 publications

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

Miringosclerose em pacientes com insuficiência renal crônica: análise comparativa com um grupo controle

Effect of Etidronate on Aortic Calcification and Bone Metabolism in Calcitoriol-Treated Rats With Subtotal Nephrectomy

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