Arterial Calcifications in Severe Chronic Renal Disease and their Relationship to Dialysis Treatment, Renal Transplant, and Parathyroidectomy

He, Meema; Dg, Oreopoulos; Ga, Deveber

doi:10.1148/121.2.315

Cited by 90 publications

(43 citation statements)

References 13 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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“…Aortic calcification occurs in very high incidence in patients with chronic renal failure, especially in hemodialysis patients [18, 19]. High serum phosphate, unchanged serum calcium and high Ca × P products in the control group may have caused metastatic calcification, especially aortic calcification.…”

Section: Discussionmentioning

confidence: 99%

Effect of Oral Adsorbent (AST-120) on Renal Function, Acquired Renal Cysts and Aortic Calcification in Rats with Adriamycin Nephropathy

Ishikawa

Araya²,

Hayama³

et al. 2002

Nephron

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Aims: The effect of oral adsorbent, AST-120, on the experimental renal disease induced by adriamycin, uninephrectomy and high protein diet proposed as a model of acquired cystic disease of the kidney was investigated. Methods: 3 mg of adriamycin was injected into the tail vein of rats and 4 weeks later right-side nephrectomy was performed, 2 weeks thereafter 26 rats with urinary protein excretion between 100 and 358 mg/day were selected from 60 rats. Two groups, 13 rats in each group, namely the AST-120-treated group and control group, both of which had equal renal damage before the administration of AST-120 or placebo. AST-120 (0.4 g/100 g BW/day) was administered for 19 weeks. Results: Serum creatinine and BUN in the AST-120-treated group were significantly lower (serum creatinine: 3.3 ± 2.1 vs. 7.1 ± 2.7 mg/dl, p < 0.003) and creatinine clearance was higher (0.62 ± 0.49 vs. 0.29 ± 0.30 ml/min, p < 0.05) at the final examination than in the control group. Survival rate which was examined using another set of 9 rats was higher in AST-120-treated rats than in AST-120-untreated rats. Serum indoxyl sulfate was significantly lower at all times after using AST-120 in the AST-120-treated group than in contrast to the control group. Histological examination revealed less severe interstitial and cystic changes in the AST-120-treated group. This suggests that AST-120 can prevent or retard the development of acquired renal cystic disease in this model. Aortic calcification tended to be less severe in the AST-120-treated group because of less serum Ca × P products. Conclusion: The AST-120-treated group significantly decreased serum creatinine and increased creatinine clearance with less severe renal cystic changes in this model during the later weeks of administration of AST-120 or at death, accompanied with the tendency of less severe aortic calcification.

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“…1,2 Kro nik böb rek yet mez lik li has ta lar da vas kü ler kal si fi kasyon di rekt gra fi ler de ilk ola rak 1976 yı lın da ta nım -lan mış tır. 3 1969-1977 yıl la rı ara sın da ölen he mo di ya liz has ta la rı nın otop si le ri in ce len di ğin de vas kü ler kal si fi kas yon sık lı ğı nın %50-80 gi bi dikka te de ğer bir şekil de yük sek oran lar da ol du ğu tespit edil miş tir. 4,5 Kal si fi kas yon ge nel lik le bü yük ve kü çük ar terler de, myo kar di um ve kalp ka pak la rın da iz le nen bir du rum ol mak la bir lik te tüm yu mu şak do ku larda da kal si fi kas yon ge li şe bi lir.…”

Section: Kro Ni̇k Böb Rek Yet Mez Li̇ ğİ Ve Vas Kü Ler Kal Si̇ Fi̇ Kas Yonunclassified

Vascular Calcification in Chronic Renal Failure and Calcification Inhibitors: Review

Mutluay¹,

Değer²,

Derici³

2010

Turkiye Klinikleri J Med Sci

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Ö ÖZ ZE ET T Sağ lık lı bi rey le re gö re kro nik böb rek yet mez li ği olan has ta lar kar di yo vas kü ler mor bi di te ve mor ta li te açı sın dan yük sek ris ke sa hip tir. Bu has ta lar da söz ko nu su olan hız lan mış ate rosk le roz da vas kü ler kal si fi kas yon önem li rol oy nar ve kro nik böb rek yet mez li ği nin ev re si art tık ça da ha da belir gin ha le ge lir. İnti mal kal si fi kas yon kli nik ola rak ken di ni ate rosk le roz la gös te rir ken; me di al kalsi fi kas yon da ha çok di a be tik ler ve böb rek yet mez lik li bi rey ler de göz le nir. Di ya liz has ta la rın da hem in ti mal hem de me di al kal si fi kas yo nun bir ara da ola bi le ce ği de bi lin mek te dir. Son dö nem böb rek yet mez lik li has ta lar da kalp ka pak kal si fi kas yon in si dan sı nın da sağ lık lı top lu lu ğa oran la art tı ğı ve bu grup has ta lar da ste no zun hız la iler le di ği bi lin mek te dir. Vas kü ler kal si fi kas yon ge li şi min de yaş, si ga ra, di a be tes mel li tus gi bi kla sik risk fak tör le ri nin ya nı sı ra uza mış di ya liz sü re si, hi per kal se mi ve hi per fos fa te mi gi bi üre mi ile iliş ki li risk fak tör le ri hem vas kü ler hem de val vu ler kal si fi kas yo nu art tı rı cı rol oy na mak ta dır. Son yıl lar da önem le ri da ha da iyi an la şıl ma ya baş la nan mat riks Gla prote in, fe tu in-A, os te op ro te ge rin ve os te o pon tin gi bi ba zı pro te in le rin dü zey le ri nin art ma sı ise kal sifi kas yo nu in hi be et mek te dir. Bi li nen kal si fi kas yon in hi bi tör le ri ara sın da en yo ğun araş tır ma ko nu su olan pro te in fe tu in-A' dır ve gü nü mü ze de ğin ya pıl mış olan ça lış ma lar di ya liz has ta la rı için azal mış fe tu in-A kon san tras yo nu nu ge le nek sel ol ma yan risk fak tör le rin den bi ri ha li ne ge tir miş tir. Kro nik böb rek yet mez lik li has ta lar da fe tu in-A ve di ğer vas kü ler kal si fi kas yon in hi bi tör le ri nin kal si fi kasyon sü re cin de ki et kin rol le ri nin tam ola rak an la şı la bil me si ile ge le cek te te da vi de kul la nım la rı söz -ko nu su ola bi le cek tir.A An na ah h t ta ar r K Ke e l li i m me e l le er r: : Kronik böbrek yetmezliği; vasküler kalsifikasyon ilişkili faktör, osteoprotegerin A AB BS S T TR RA AC CT T Pa ti ents with chro nic re nal fa i lu re ha ve hig her car di o vas cu lar mor bi dity and mor tality ra tes com pa red to ge ne ral po pu la ti on. Vas cu lar cal ci fi ca ti on plays an im por tant ro le for ac cele ra ted at he rosc le ro sis of the se pa ti ents and be co mes more evi dent as the sta ge of re nal fa i lu re increases. Alt ho ugh in ti mal cal ci fi ca ti on cli ni cally oc curs with at he rosc le ro sis; me di al cal ci fi ca tion is mo re com monly se en in di a be tics and pa ti ents with re nal fa i lu re. It is al so known that both in ti mal and me di al ca li fi ca ti on can be present in at di aly sis pa ti ents. It is known that the in ci dence of car di ac val ve cal ci fi ca ti on is hig her and val ve ste no sis prog res ses mo re ra pidly in end sta ge re...

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Arterial Calcifications in Severe Chronic Renal Disease and their Relationship to Dialysis Treatment, Renal Transplant, and Parathyroidectomy

Cited by 90 publications

References 13 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

Effect of Oral Adsorbent (AST-120) on Renal Function, Acquired Renal Cysts and Aortic Calcification in Rats with Adriamycin Nephropathy

Vascular Calcification in Chronic Renal Failure and Calcification Inhibitors: Review

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