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Periton Diyaliz Hastalarında Fetuin-A Düzeyi ile Kardiyovasküler Risk Faktörleri Arasındaki İlişki

Relationship Between Fetuin-A Level and Cardiovascular Risk Factors in Peritoneal Dialysis Patients

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DOI: 
DOI 10.5262/tndt.2013.1001.11
Abstract (2. Language): 
OBJECTIVE: Vascular calcifications and chronic inflammation are the main reasons of the decreased life span and prevalent morbidity for patients on renal replacement therapy due to chronic renal failure. Scoring systems used to determine the chance of cardiovascular (CV) risk and traditional CV risk factors frequently fail to identify the risk in these patients. New markers to predict the risk of CV disease continues to be investigated. One of the most studied marker in recent years is a serum glycoprotein fetuin-A, which is major calcification inhibitor. We aimed to study the relation between fetuin-A subclinical inflammation and cardiovascular risk factors in Peritoneal Dialysis (PD) patients and healthy volunteers. MA TERIAL and M ETHODS: Forty-eight PD patients and 27 healthy volunteers were included in the study. Fetuin-A levels, body weight, body mass index, blood pressure, markers of inflammation (sedimentation, C-reactive protein, ferritin) and lipid profile tests were performed. The relationship between these parameters was compared with fetuin-A. Res ults : CRP and sedimentation levels were significantly higher in the group of PD patients. Fetuin-A levels were significantly lower in PD patients than the control group. There was a negative correlation between serum fetuin-A levels, average arterial blood pressure and CRP. ConclusIo n: Fetuin-A can be used to predict subclinic inflammation, and cardiovascular mortality risk in PD patients.
Abstract (Original Language): 
AMA Ç: Böbrek yerine koyma tedavisi gören, kronik renal yetmezlikli hastalarda subklinik inflamasyon ve vasküler kalsifikasyon, artmış kardiyovasküler ölüm riskinin başlıca sorumlularıdır. Kardiyovasküler riski belirlemek amacıyla kullanılan risk skorlamaları ve geleneksel risk faktörleri, bu hasta grubunda gerçek riski belirlemede yetersiz kalmaktadır. Bu nedenle yeni belirteçler üzerinde çalışılmaktadır. Son yıllarda çalışmaların üzerine yoğunlaştığı fetuin-A, serumda major kalsifikasyon inhibitörü olarak görev yapan bir glikoproteindir. Bu çalışmamızda periton diyaliz (PD) hastaları ve sağlıklı kontrol grubunda serum fetuin-A düzeyi ile subklinik inflamasyon ve kardiyovasküler risk parametreleri arasındaki ilişkiyi inceledik. GEREÇ ve YÖN TEML ER: Çalışmaya 48 PD hastası ve sağlıklı gönüllülerden 27 erişkin kontrol grubu olarak alındı. Hastalar ve kontrol grubunun kilo, boy, beden kitle indeksleri, kan basınçları ölçüldü. İnflamasyon belirteçleri (ferritin, C-reaktif protein (CRP), sedimantasyon, fibrinojen, albumin), lipid profilleri ve fetuin-A düzeyleri çalışıldı. Çalışılan parametreler ile fetuin-A arasındaki ilişki değerlendirildi. Bulgular: CRP düzeyi PD grubunda, kontrol grubuna göre yüksek, fetuin-A düzeyi ise anlamlı düzeyde düşük saptandı. PD grubunda serum fetuin-A düzeyi ile CRP düzeyi ve ortalama arteryel kan basıncı arasında negatif korelasyon olduğu gösterildi. Sonuç: Serum fetuin-A düzeyi, periton diyaliz hastalarında subklinik inflamasyonu, ve kardiyovasküler riski ön görmek amacıyla kullanılabilecek risk faktörlerindendir.
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REFERENCES

References: 

1. U.S. Renal Data System: USRDS 2011 Annual Data Report: Atlas of
Chronic Kidney Disease and End-Stage Renal Disease in the United
States, National Institutes of Health, National Institute of Diabetes
and Digestive and Kidney Diseases, Bethesda, MD, 2011;1:27
2. Nascimento MM, Pecoits-Filho R, Lindholm B, Riella MC,
Stenvinkel P: Inflammation, malnutrition and atherosclerosis in
end-stage renal disease: A global perspective. Blood Purif 2002; 20:
454–458
3. Registry of the Nephrology, Dialysis and Transplantation in Turkey.
Registry 2010; 1: 7
4. Foley RN, Parfrey PS, Sarnac MJ: Clinical epidemiology of
cardiovascular disease in chronic renal disease. Am J Kidney Dis
1998; 32: 112-119
5. Coresh J, Longenecker JC, Miller ER, Young HJ, Klag MJ:
Epidemiology of cardiovascular risk factors in chronic renal
disease. J Am Soc Nephrol 1998; 9: 24–30
6. Levey AS: Controlling the epidemic of cardiovascular disease in
chronic renal disease: Where do we start? Am J Kidney Dis 1998;
32: 5-13
7. Longenecker J Coresh J, Powe N, Levey A, Fink N, Martin A, Klag
M: Traditional cardiovascular disease risk factors in dialysis patients
compared with the general population: The CHOICE Study. J Am
Soc Nephrol 2002; 13: 1918–1927
8. Cheung AK, Sarnak MJ, Yan G, Dwyer JT, Heyka RJ, Rocco MV,
Teehan BP, Levey AS: Atherosclerotic cardiovascular disease risks
in chronic hemodialysis patients. Kidney Int 2000; 58: 353-362
9. Stenvinkel P, Alvestrand P: Inflammation in end-stage renal disease:
Sources, consequences and therapy. Semin Dial 2002; 15: 329-337
10. Himmelfarb J, Stenvinkel P, Ikizler TA, Hakim RM: The elephant
of uremia: Oxidative stress as a unifying concept of cardiovascular
disease in uremia. Kidney Int 2002; 62: 1524-1538
11. London GM, Guerin AP, Marchais SJ, Metivier F, Pannier B, Adda
H: Arterial media calcification in end-stage renal disease: Impact
on all-cause and cardiovascular mortality. Nephrol Dial Transplant
2003; 18: 1731–1740
12. Wang AY, Wang M, Woo J, Lam CW, Li PK, Lui SF, Sanderson JE:
Cardiac valve calcification as an important predictor for all-cause
mortality and cardiovascular mortality in long-term peritoneal
dialysis patients: A prospective study. J Am Soc Nephrol 2003; 14:
159-168
13. Shioi A, Katagi M, Okuno Y, Mori K, Jono S, Koyama H, Nishizawa
Y: Induction of bone-type alkaline phosphatase in human vascular
smooth muscle cells: Roles of tumor necrosis factor-alpha and
oncostatin M derived from macrophages. Circ Res 2002; 91: 9-16
14. Moe SM, Duan D, Doehle BP, O’Neill KD, Chen NX: Uremia
induces the osteoblast differentiation factor cbfa1 in human blood
vessels. Kidney Int 2003; 63: 1003–1011
15. ADHR Consortium: Autosomal dominant hypophosphataemic
rickets is associated with mutations in FGF23. Nature Genetics
2000; 26 (3): 345–348
16. Imanishi Y, Inaba M, Nakatsuka K, Nagasue K, Okuno S, Yoshihara
A, Miura M, Miyauchi A, Kobayashi K, Miki T, Shoji T, Ishimura
E, Nishizawa Y: FGF-23 in patients with end-stage renal disease on
hemodialysis. Kidney Int 2004; 65: 1943–1946
17. Ketteler M, Bongartz P, Westenfeld R, Wildberger JE, Mahnken
AH, Böhm R, Metzger T, Wanner C, Jahnen-Dechent W, Floege J:
Association of low fetuin-A (AHSG) concentrations in serum with
cardiovascular mortality in patients on dialysis: A cross-sectional
study. Lancet 2003; 361: 827–833
18. Wang AY, Woo J, Lam CW, Wang M, Chan IH, Gao P, Lui SF, Li PK,
Sanderson JE: Associations of serum fetuin-A with malnutrition,
inflammation, atherosclerosis and valvular calcification syndrome
and outcome in peritoneal dialysis patients. Nephrol Dial Transplant
2005; 20: 1676–1685
19. Moe SM, Reslerova M, Ketteler M, O’neill K, Duan D, Koczman J,
Westenfeld R, Jahnen-Dechent W, Chen NX: Role of calcification
inhibitors in the pathogenesis of vascular calcification in chronic
kidney disease (CKD). Kidney Int 2005; 67: 2295–2304
20. Bergström j, Heimburger O, Lindholm B, Qershi AR: Elevated
serum C-reactive protein is a strong predictor of increased mortality
and low serum albumin in hemodialysis patients. J Am Soc Nephrol
1995; 6: 573 (Abstract)
21. Stenvinkel P, Wang K, Qureshi AR, Axelsson J, Pecoits-Filho R,
Gao P, Barany P, Lindholm B, Jogestrand T, Heimbürger O, Holmes
C, Schalling M, Nordfors L: Low fetuin-A levels are associated
with cardiovascular death impact of variations in the gene encoding
fetuin. Kidney Int 2005; 67: 2383-2392
22. Ketteler M, Bongartz P, Westenfeld R, Wildberger JE, Mahnken
AH, Böhm R, Metzger T, Wanner C, Jahnen-Dechent W, Floege J:
Association of low fetuin-A (AHSG) concentrations in serum with
cardiovascular mortality in patients on dialysis: A cross- sectional
study. Lancet 2003; 361: 827-833
23. Lebreton JP, Joisel F, Raoult JP, Lannuzel B, Rogez JP, Humbert
G: Serum concentration of human alfa-2 HS glycoprotein during
inflammatory process. Evidence that alfa2HS glycoprotein is a
negative acute phase reactant. J Clinic İnvest 1979; 64: 1118-1129
24. Wang H, Zhang M, Soda K, Sama A, Tracey KJ: Fetuin protects the
fetus from TNF. Lancet 1997; 350: 861-862
25. Jersmann HP, Dransfield I, Hart SP: Fetuin/alpha2-HS glycoprotein
enhances phagocytosis of apoptotic cells and macropinocytosis by
human macrophages. Clin Sci (Lond) 2003; 105 (3): 273-278
26. Block GA: Prevalence and clinical consequences of elevated CaxP
product in hemodialysis patients. Clin Nephrol 2000; 54: 318-324
27. Hermans MM, Brandenburg V, Ketteler M, Kooman JP, van der
Sande FM, Gladziwa U, Rensma PL, Bartelet K, Konings CJ, Hoeks
AP, Floege J, Leunissen KM: Study on the relationship of serum
fetuin-A concentration with aortic stiffness in patients on dialysis.
Nephrol Dial Transplant 2006; 21: 1293–1299
28. Jung JY, Hwang YH, Lee SW, Lee H, Kim DK, Kim S, Oh YG, Yang
J, Joo KW, Ahn C, Oh KH: Factors associated with aortic stiffness
and its change over time inperitoneal dialysis patients. Nephrol Dial
Transplant 2010; 25 (12): 4041-4048
29. Savage T, Clarke AL, Giles M, Tomson CR, Raine AE: Calcified
plaque is common in the carotid and femoral arteries of dialysis
patients without clinical vascular disease. Nephrol Dial Transplant
1998; 13: 2004–2012
30. London GM: Alterations of arterial function in end-stage renal
disease. Nephron 2000; 84: 111–118
31. Blacher J, Safar ME, Guerin AP, Pannier B, Marchais SJ, London
GM: Aortic pulse wave velocity index and mortality in end-stage
renal disease. Kidney Int 2003; 63: 1852–1860
32. London GM, Blacher J, Pannier B, Guerin AP, Marchais SJ, Safar
ME: Arterial wave reflections and survival in end-stage renal failure.
Hypertension 2001; 38: 434–438

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