Cardiovascular Calcification in Patients With End‐stage Renal Disease

Pečovnik-Balon, Breda

doi:10.1111/j.1774-9987.2005.00255.x

Cited by 18 publications

(9 citation statements)

References 27 publications

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“…It is produced by the liver and secreted into the bloodstream and plays an anti-inflammatory role by inhibiting lipopolysaccharide-induced tumor necrosis factor-α. Furthermore, recent studies suggested that fetuin-A could act as a protective factor to inhibit ectopic calcification in uremic patients and that the decreased serum fetuin-A concentration was associated with a higher mortality in dialysis patients [18,19,20,21,22]. However, the role of fetuin-A in patients with AKI is not well studied.…”

Section: Discussionmentioning

confidence: 98%

Identification of Nestin as a Urinary Biomarker for Acute Kidney Injury

Zhang

Chen

et al. 2014

Am J Nephrol

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Objectives: Acute kidney injury (AKI) is a common complication in hospitalized patients and the incidence of AKI is rapidly increasing. Despite the advances in treatment of AKI, many patients still progress to end-stage renal disease and depend on dialysis. Therefore, early diagnosis and adequate treatment of AKI could improve prognosis. Methods: We established rat models of AKI induced by cisplatin nephrotoxicity and renal ischemia-reperfusion (I/R). Urine samples were collected, labeled with isobaric tags for relative and absolute quantification agents, and then subjected to nano-LC-MS/MS-based proteomic analysis. Results of the proteomic study were confirmed by Western blot. We also performed RNAi to silence nestin and investigate its role in renal I/R injury. We then validated its clinical application by studying urine nestin levels in AKI patients with cardiovascular surgeries. Results: Our proteomic analysis showed that fetuin-A, nestin, hamartin and T-kininogen were differentially expressed in the urine samples of rats after cisplatin or I/R treatment. Western blot confirmed the differential expression of these proteins in animal models and ELISA confirmed the differential expression of nestin in human urine samples. To explore the expression of nestin in the development of AKI, our results showed that nestin was primarily detected in the glomeruli and barely detected in tubular cells but increased in tubular cells during I/R- and cisplatin-induced AKI. The urine nestin-to-creatinine ratio increased earlier than serum creatinine in AKI patients with postcardiovascular surgeries. The role of nestin in AKI might be related to the p53 signaling pathway. Conclusions: Thus, our results demonstrated that urinary nestin could be a urinary biomarker for patients with AKI and its role in AKI might be related to the p53 signaling pathway.

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Section: Discussionmentioning

confidence: 98%

Identification of Nestin as a Urinary Biomarker for Acute Kidney Injury

Zhang

Chen

et al. 2014

Am J Nephrol

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“…Calcification in atherosclerotic lesions is relatively common and is implicated as a risk factor for increased cardiovascular morbidity and mortality [24, 25]. Vascular calcification is enhanced with advanced age, chronic renal failure, diabetes and inflammation [26]. We have previously demonstrated that carotid atherosclerotic plaque calcification is a structural surrogate marker for carotid plaque stability [18].…”

Section: Discussionmentioning

confidence: 99%

Human Carotid Plaque Calcification and Vulnerability

et al. 2009

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Background: Inflammation is a key mechanism in human atherosclerotic plaque vulnerability and disruption. The objective was to determine the differential gene expression of pro- and anti-inflammatory factors in the fibrous cap and shoulder region of noncalcified and calcified carotid endarterectomy plaques. Methods: Thirty carotid endarterectomy plaques were classified as type Va (noncalcified, n = 15) and type Vb (calcified, n = 15) in accordance with the American Heart Association consensus. Using laser capture microdissection, fibrous cap and shoulder regions were excisedfrom frozen sections. Gene expression of pro- [interleukin 1 (IL-1), IL-8 and monocyte chemoattractant protein 1 (MCP-1)] and anti-inflammatory (IL-10) factors, and bone formation (bone morphogenetic protein 6 and osteocalcin) mediators were quantitated by real-time PCR. Protein levels were determined using Western blotting. Results: Mean percent carotid stenosis and calcification area were 79 and 5% in Va-plaques (40% symptomatic) and 77 and 42% in Vb-plaques (20% symptomatic). Macrophages infiltrating the region of the fibrous cap and the shoulder were more numerous in non-calcified plaques compared with calcified plaques (p < 0.01]. mRNA expression of MCP-1 and IL-8, and protein levels of IL-8 were also greater in Va plaques compared to Vb plaques (p < 0.05). Protein levels and mRNA expression of osteocalcin were greater in Vb compared to Va plaques (p < 0.05). Conclusions: Fibrous cap inflammation is more likely to occur in noncalcified than in calcified plaques. These findings suggest that carotid atherosclerotic plaque calcification is a structural marker of plaque stability.

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“…Hi per tan si yon, dia be tes mel li tus, hi per li pi de mi ve si ga ra içi mi bu tip kal si fi kas yon lar için risk fak tör le ri dir. 6 Me di al kalsi fi kas yon lar ise di a be tik ler de, ile ri yaş lar da ve kronik böb rek yet mez li ği var lı ğın da sık lık la iz le nir. Me di al kal si fi kas yon lu has ta la rın ya şa ma oran la rı -nın in ti mal kal si fi kas yon lu has ta la ra gö re da ha iyi ol du ğu göz len miş tir.…”

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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Cardiovascular Calcification in Patients With End‐stage Renal Disease

Cited by 18 publications

References 27 publications

Identification of Nestin as a Urinary Biomarker for Acute Kidney Injury

Identification of Nestin as a Urinary Biomarker for Acute Kidney Injury

Human Carotid Plaque Calcification and Vulnerability

Vascular Calcification in Chronic Renal Failure and Calcification Inhibitors: Review

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