Ponad 7000 publikacji medycznych!
Statystyki za 2021 rok:
odsłony: 8 805 378
Artykuły w Czytelni Medycznej o SARS-CoV-2/Covid-19

Poniżej zamieściliśmy fragment artykułu. Informacja nt. dostępu do pełnej treści artykułu tutaj
© Borgis - Postępy Nauk Medycznych 9/2016, s. 611-619 | DOI: 10.5604/08606196.1219837
Danuta Fedak1, Marek Kuźniewski2, Paulina Dumnicka3, Maria Kapusta1, Grzegorz Chmiel2, Bogdan Solnica1, *Władysław Sułowicz2
Association between serum fetuin-A concentrations and vascular calcifications among patients on maintenance hemodialysis**
Związek pomiędzy stężeniem fetuiny-A w surowicy i zwapnieniami naczyniowymi u chorych leczonych powtarzanymi hemodializami
1Department of Diagnostics, Chair of Clinical Biochemistry, Jagiellonian University Medical College, Kraków
Head of Department: Professor Bogdan Solnica, MD, PhD
2Chair and Department of Nephrology, Jagiellonian University Medical College, Kraków
Head of Department: Professor Władysław Sułowicz, MD, PhD
3Department of Medical Diagnostics, Jagiellonian University Medical College, Kraków
Head of Department: Associate Professor Ryszard Drożdż, MD, PhD
Streszczenie
Wstęp. Zwapnienia naczyniowe u pacjentów ze schyłkową niewydolnością nerek leczonych powtarzanymi hemodializami są główną przyczyną zdarzeń sercowo-naczyniowych i zgonów. W badaniach epidemiologicznych wykazano, że duże zwapnienia naczyniowe i związane z nimi ryzyko chorobowości i śmiertelności występują szczególnie u chorych z niskimi stężeniami fetuiny-A w surowicy.
Cel pracy. Celem badania była ocena nasilenia zwapnień w układzie sercowo-naczyniowym u chorych leczonych powtarzanymi hemodializami w zależności od stężenia w surowicy fetuiny-A, gęstości mineralnej kości (BMD) i wskaźników zapalenia.
Materiał i metody. Badania przeprowadzono w grupie 71 pacjentów (31 kobiet, 40 mężczyzn) w wieku 60 ± 12 lat leczonych powtarzanymi dializami z powodu schyłkowej niewydolności nerek przez okres 75 ± 57,2 miesiąca. Nasilenie zwapnień w naczyniach oceniano w oparciu o wskaźnik uwapnienia naczyń wieńcowych (CaSc) i grubość kompleksu błony wewnętrznej i środkowej tętnicy szyjnej wspólnej (CCA-IMT). Gęstość mineralną kości mierzono przy użyciu aparatu Lunar DPX. Stężenie w surowicy rutynowo badanych wskaźników oceniano w aparacie Modular P analyzer (Roche Diagnostics), iPTH w oparciu o metodę Nicholsa, hsCRP i IL-6 przy użyciu techniki nefelometrycznej, podczas gdy fetuinę-A oznaczano w oparciu o zestawy ELISA.
Wyniki. W badaniu densytometrycznym wykazano obniżoną gęstość w zakresie kości udowej (Tscore = -2,0 ± 1,00) i odcinka lędźwiowego kręgosłupa (Tscore = -1,03 ± 1,51). Wskaźnik uwapnienia wskazywał na nasilone zwapnienia; CaSc – 511 (158-2394) jednostek Agatstona, a CCA-IMT – 0,90 ± 0,42. Stężenia fetuiny-A były istotnie ujemnie związane z wiekiem pacjentów (r = -0,26; p = 0,04), log (iPTH) (r = -0,31; p = 0,02), log (CRP) (r= -0.31, p = 0.02), log (IL-6) (r = -0.41, p = 0.001), log (CaSc) (r = -0,29; p = 0,03) i log (CCA-IMT) (r = -0,28; p = 0,04). Stężenia fetuiny-A dodatnio korelowały z albuminą (r = 0,37; p = 0,003) i BMD w okolicy szyjki kości udowej (r = 0,26; p = 0,04).
Wnioski. Pacjenci leczeni powtarzanymi hemodializami mają zaawansowane zwapnienia w układzie naczyniowym. Niskie stężenia fetuiny-A w surowicy są ujemnie związane ze wskaźnikami uwapnienia, zapaleniem i nadczynnością przytarczyc.
Summary
Introduction. Vascular calcifications in patients with end stage renal disease on maintenance hemodialysis is the leading cause of cardiovascular events and death. Epidemiological studies have shown that severe vascular calcifications and associated increased risk of morbidity and mortality occur particularly in patients with reduced serum fetuin-A levels.
Aim. The aim of the study was to assess the severity of calcifications in the cardiovascular system of patients treated with repeated hemodialysis depending on the concentrations of serum fetuin-A, bone mineral density (BMD) and markers of inflammation.
Material and methods. The study was performed in 71 patients (31 women, 40 men) aged 60 ± 12 years on chronic dialysis because of end-stage renal failure for a period of approximately 75 ± 57.2 months. The level of vascular calcifications was examined based on coronary artery calcification score (CaSc) and common carotid artery intima-media thickness (CCA-IMT). Bone mineral density was measured using Lunar DPX. The serum concentrations of routine laboratory test were performed based on Modular P analyzer (Roche Diagnostics), iPTH using Nichols method, hsCRP and IL-6 using nephelometric techniques while fetuin A, was measured using commercially available ELISA kits.
Results. Densitometry showed a decrease in bone mineral density both within the ranks of the femur (Tscore = -2.10 ± 1.00) and lumbar spine (Tscore = -1.03 ± 1.51). Calcium scoring performed in patients showed severe calcification; CaSc – 511 (158-2394) Agatston units and the CCA-IMT was 0.90 ± 0.42. Fetuin-A concentrations were significantly negatively associated with patients age (r = -0.26, p = 0.04), log (iPTH) (r = -0.31, p = 0.02), log (CRP) (r= -0.31, p = 0.02), log (IL-6) (r = -0.41, p = 0.001), log (CaSc) (r = -0.29, p = 0.03) and log (CCA-IMT) (r = -0.28, p = 0.04). Concentrations of fetuin-A were positively correlated with albumin (r = 0.37, p = 0.003) and BMD in the region of femoral neck (r = 0.26, p = 0.04).
Conclusions. Patients on maintenance hemodialysis suffer from severe calcifications of vascular system. Low serum fetuin-A levels are negatively associated with calcification parameters, inflammation and hyperparathyroidism.
Introduction
Cardiovascular diseases are the leading cause of death in the population of patients with end stage renal disease on maintenance hemodialysis. The increased cardiovascular mortality in dialysis patients may be influenced by many factors, such as advanced age, atherosclerosis, chronic inflammation, malnutrition, hypertension, anemia, diabetes, left ventricular hypertrophy (LVH) and vascular calcification in the course of secondary hyperparathyroidism (1-3). Vascular calcifications may be observed even in the early decades of life in patients with end-stage renal disease (ESRD) and severity of calcification increases with the progression of renal failure (2-6).
Epidemiological studies have shown that severe vascular calcifications and associated increased risk of mortality occur particularly in patients with reduced serum fetuin-A levels (7-9). The fetuin-A acts as an inhibitor of extraosseous calcification (10-14), it inhibits the de novo formation of hydroxyapatite crystals, at least in part, causing the sequestration of calcium and phosphate, and preventing their precipitation in serum containing these minerals (12, 15). The fetuin-A accumulates in the vascular calcification (16) and its serum levels reduction in patients with ESRD is inversely correlated with the occurrence of calcification of the coronary arteries (17-20).
It was also found that in patients with ESRD calcified plaques were higher in those with low bone density (21). It was also demonstrated that reduced bone mineralization in patients with chronic kidney disease (CKD), or in post-menopausal women are accompanied with increased calcifications of tissues, especially vascular system (22-24).
Aim
The aim of the study was to assess the severity of calcifications in the cardiovascular system in patients treated with repeated hemodialysis depending on the concentrations of serum fetuin-A, bone mineral density and markers of inflammation.
Material and methods
The study included 71 patients (31 women, 40 men) aged 60 ± 12 years on chronic dialysis because of end-stage renal failure for a period of approximately 75 ± 57.2 months. The cause of ESRD was chronic glomerulonephritis – 16 patients, chronic pyelonephritis – 16, kidney cirrhosis – 18, polycystic kidney disease – 10, diabetic nephropathy – 3 and not known cause of ESRD – 8. From the study group 55 patients had been treated for hypertension, and 8 had diabetes mellitus type 2. None of the patients had an active infections at the time of the study.
In 35 patients ischemic heart disease was diagnosed.
The basic demographic data and the results obtained are shown in table 1. Blood samples for routine laboratory tests were taken before hemodialysis start in the middle of the week sessions. The basic biochemical studies have been performed on the analyzer Modular P (Roche Diagnostic), C-reactive protein and IL-6 using immunonephelometric techniques Behring Nephelometer II, Dade Behring, Marburg, Germany while iPTH based on chemiluminescence Nichols method. The serum concentration of fetuin-A were measured using commercially available ELISA kits. Blood samples were centrifuged and the resulting serum/plasma aliquoted and stored at -70°C until immunoassays measurement. Routine laboratory tests were performed in the Diagnostic Laboratory at the University Hospital in Kraków, and immunochemical tests in Diagnostics Department, Jagiellonian University Medical College in Kraków.
Tab. 1. Demographic and clinical data of hemodialysis patients
Studied parametersWhole group (N = 71)Women (N = 31)Men (N = 40)p-value
Age (years)60 ± 1261 ± 1459 ± 120.5
Dialysis vintage (months)60 (36-100)52 (30-108)60 (45-97)0.8
BMI (kg/m2)23.6 (21.0-26.7)22.0 (20.0-25.5)24.8 (22.6-28.0)0.01*
Hypertension 55 (77%)23 (74%)32 (80%)0.6
Diabetes mellitus type 28 (11%)2 (6%)6 (15%)0.5
Ischemic heart disease35 (49%)19 (61%)16 (40%)0.08
Smoking15 (21%)5 (16%)10 (25%)0.4
BMD femoral neck (g/cm2)0.77 ± 0.170.73 ± 0.160.81 ± 0.170.07
BMD lumbar spine (g/cm2)1.08 ± 0.240.96 ± 0.201.17 ± 0.230.0004*
CaSc (Agatstone units)488 (109-1853)462 (41-1428)511 (158-2394)0.5
CCA-IMT (mm)0.90 (0.80-1.05)0.90 (0.75-1.00)0.90 (0.80-1.05)0.3
Values that were normally distributed, expressed as mean ± SD, data that were not normally distributed, expressed as median and (minimum-maximum), categorical variables are presented as %. *Significant associations
BM – body mass index; BMD – bone mineral density; CaSc – calcium scoring; CCA-IMT – common carotid artery intima-media thickness
The study was approved by the Jagiellonian University Bioethics Committee and all the patients gave written informed consent for participation.
Imaging techniques
The calcification score was measured by 64-slice spiral computer tomography scans, MSCT (Siemens Medical Solutions Inc., Germany) using the standard calcium scoring protocol. To quantify the calcification of the coronary arteries indicator of coronary artery calcification was used, expressed in units of numerical values forming the sum of the Agatston score for final calcification of the coronary arteries (CaSc). Common carotid artery intima-media thickness (CCA-IMT) measurements were performed using a ALOKA 5500 SV equipped with a head for vascular studies. The CCA-IMT of the medial trunk-internal carotid artery was measured at three locations: at the height of half the length of the common carotid artery; at a distance of 1 cm from the bifurcation of the common carotid artery and at the height of the pad common carotid artery. In each of the three points a 2-3 medial thickness measurements during the diastolic phase of the cardiac cycle were performed, and the final results were calculated as an average arithmetic values at a point of measurement. Both, CaSc and CCA-IMT were performed at the Center for Diagnosis and Rehabilitation of Heart and Lung Diseases Specialist Pope John Paul II Hospital in Kraków. Bone mineral density (BMD) was performed in the Metabolic Diseases Clinic of the University Hospital in Kraków using Dual Energy X-ray Absorptiometry, Lunar DPX (Lunar, USA). BMD was measured in the lumbar spine (L1-L4) and femoral region (Ward’s triangle).
Statistical analysis
The obtained data were reported as number (percent) and analyzed with Chi-squared test. Mean ± standard deviation (SD) or median (Lower-upper quartile) according distribution were given. Simple and multiple regression models were computed after log10-transformation of right-skewed variables.
The results were considered significant at p ≤ 0.05.
Results
The results of routine laboratory parameters, concentration of fetuin-A and imaging studies in the analyzed group of patients are summarized in table 1. Densitometry showed a decrease in bone mineral density both within the ranks of the femur (Tscore = -2.10 ± 1.00) and lumbar spine (Tscore = -1.03 ± 1.51). Calcium scoring performed in patients showed severe calcification of the vascular system, CaSc – 511 (158-2394) Agatston units and the CCA-IMT was 0.90 ± 0.42.

Powyżej zamieściliśmy fragment artykułu, do którego możesz uzyskać pełny dostęp.
Mam kod dostępu
  • Aby uzyskać płatny dostęp do pełnej treści powyższego artykułu albo wszystkich artykułów (w zależności od wybranej opcji), należy wprowadzić kod.
  • Wprowadzając kod, akceptują Państwo treść Regulaminu oraz potwierdzają zapoznanie się z nim.
  • Aby kupić kod proszę skorzystać z jednej z poniższych opcji.

Opcja #1

19

Wybieram
  • dostęp do tego artykułu
  • dostęp na 7 dni

uzyskany kod musi być wprowadzony na stronie artykułu, do którego został wykupiony

Opcja #2

49

Wybieram
  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 30 dni
  • najpopularniejsza opcja

Opcja #3

119

Wybieram
  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 90 dni
  • oszczędzasz 28 zł
Piśmiennictwo
London GM, Guèrin AP, Marchais SJ et al.: Arterial medial calcification in end-stage renal disease: Impact on all-cause and cardiovascular mortality. Nephrol Dial Transplant 2003; 18: 1731-1740.
Haydar AA, Hujairi NM, Covic AA et al.: Coronary artery calcification is related to coronary atherosclerosis in chronic renal disease patients: A study comparing EBCT-generated coronary artery calcium scores and coronary angiography. Nephrol Dial Transplant 2004; 19: 2307-2312.
Agatston AS, Janowitz WR, Hildner FJ et al.: Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol 1990; 15: 827-832.
Alexopoulos N, Raggi P: Calcification in atherosclerosis. Nat Rev Cardiol 2009; 6: 681-688.
Johnson RC, Leopold JA, Loscalzo J: Vascular calcification: pathobiological mechanisms and clinical implications. Circ Res 2006; 99: 1044-1059.
McCullough PA, Agrawal V, Danielewicz E, Abela GS: Accelerated atherosclerotic calcification and Monckeberg’s sclerosis: a continuum of advanced vascular pathology in chronic kidney disease. Clin J Am Soc Nephrol 2008; 3: 1585-1598.
Cozzolino M, Galassi A, Biondi ML et al.: Serum fetuin-A levels link inflammation and cardiovascular calcification in hemodialysis patients. Am J Nephrol 2006; 26: 423-429.
Ketteler M, Bongartz P, Westenfeld R et al.: 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.
Hermans MMH, Brandenburg V, Ketteler M et al.: Association of serum fetuin-A levels with mortality in dialysis patients. Kidney Int 2007; 72: 202-207.
Roos M, Lutz J, Salmhofer H et al.: Relation between plasma fibroblast growth factor-23, serum fetuin-A levels and coronary artery calcification evaluated by multislice computed tomography in patients with normal kidney function. Clin Endocrinol 2008; 68: 660-665.
Ix JH, Chertow GM, Shlipak MG et al.: Fetuin-A and kidney function in persons with coronary artery disease: data from the Heart and Soul Study. Nephrol Dial Transplant 2006; 21: 2144-2151.
Schafer C, Heiss A, Schwarz A et al.: The serum protein alpha 2-Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification. J Clin Invest 2003; 112: 357-366.
Dellegrottaglie S, Sanz J, Rajagopalan S: Molecular determinants of vascular calcification: A bench to bedside view. Curr Mol Med 2006; 6: 515-524.
Suliman ME, García-López E, Anderstam B et al.: Vascular calcification inhibitors in relation to cardiovascular disease with special emphasis on fetuin-A in chronic kidney disease. Adv Clin Chem 2008; 46: 217-262.
Schinke T, Amendt C, Trindl A et al.: The serum protein alpha2-HS glycoprotein/fetuin inhibits apatite formation in vitro and in mineralizing calvaria cells. A possible role in mineralization and calcium homeostasis. J Biol Chem 1996; 271: 20789-20796.
Reynolds JL, Skepper JN, McNair R et al.: Multifunctional roles for serum protein fetuin-A in inhibition of human vascular smooth muscle cell calcification. J Am Soc Nephrol 2005; 16: 2920-2930.
Oberg BP, McMenamin E, Lucas FL et al.: Increased prevalence of oxidant stress and inflammation in patients with moderate to severe chronic kidney disease. Kidney Int 2004; 65: 1009-1016.
Zheng S, de Las Fuentes L, Bierhals A et al.: Relation of serum fetuin-A levels to coronary artery calcium in African-American patients on chronic hemodialysis. Am J Cardiol 2009; 103: 46-49.
Mori K, Emoto M, Araki T et al.: Association of serum fetuin-A with carotid arterial stiffness. Clin Endocrinol (Oxf) 2007; 66: 246-250.
Turkmen K, Gorgulu N, Uysal M et al.: Fetuin-A, inflammation, and coronary artery calcification in hemodialysis patients. Indian J Nephrol 2011; 21: 90-94.
Kirkpantur A, Altun B, Hazirolan T et al.: Association among serum fetuin-A level, coronary artery calcification, and bone mineral densitometry in maintenance hemodialysis patients. Artif Org 2009; 33: 844-854.
Banks LM, Lees B, MacSweeney JE et al.: Effect of degenerative spinal and aortic calcification on bone density measurements in post-menopausal women: links between osteoporosis and cardiovascular disease? Eur J Clin Invest 1994; 24: 813-817.
London GM, Marty C, Marchais SJ et al.: Arterial calcifications and bone histomorphometry in end-stage renal disease. J Am Soc Nephrol 2004; 15: 1943-1951.
Sari A, Uslu T: The relationship between fetuin-A and bone mineral density in postmenopausal osteoporosis. Turk J Rheumatol 2013; 28: 195-201.
Collins AJ: Cardiovascular mortality in end-stage renal disease. Am J Med Sci 2003; 325: 163-167.
Moe SM, Chen NX: Mechanisms of vascular calcification in chronic kidney disease. J Am Soc Nephrol 2008; 19: 213-216.
Liabeuf S, Okazami H, Desjardins L et al.: Vascular calcification on chronic kidney disease: are biomarkers useful for probing the pathobiology and the health risks of this process in the clinical scenario? Nephrol Dial Transplant 2014; 29: 1275-1284.
Moe SM, Reslerova M, Ketteler M et al.: Role of calcification inhibitors in the pathogenesis of vascular calcification in chronic kidney disease (CKD). Kidney Int 2005; 67: 2295-2304.
Stenvinkel P, Wang K, Qureshi AR et al.: Low fetuin-A levels are associated with cardiovascular death: Impact of variations in the gene encoding fetuin. Kidney Int 2005; 67: 2383-2392.
Wang AY, Woo J, Lam CW et al.: 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.
Mehrotra R, Westenfeld R, Christenson P et al.: Serum fetuin-A in nondialyzed patients with diabetic nephropathy: relationship with coronary artery calcification. Kidney Int 2005; 67: 1070-1077.
Hermans MM, Brandenburg V, Ketteler M et al.: Study on the relationship of serum fetuin-A concentration with aortic stiffness in patients on dialysis. Nephrol Dial Transplant 2006; 21: 293-299.
Mikami S, Hamano T, Fujii N et al.: Serum osteoprotegerin as a screening tool for coronary artery calcification score in diabetic pre-dialysis patients. Hypertens Res 2008; 31: 1163-1170.
Ford ML, Tomlinson LA, Smith ER et al.: Fetuin-A is an independent determinant of change of aortic stiffness over 1 year in non-diabetic patients with CKD stages 3 and 4. Nephrol Dial Transplant 2010; 25: 1853-1858.
Smith ER, Cai MM, McMahon LP et al.: Serum fetuin-A concentration and fetuin-A-containing calciprotein particles in patients with chronic inflammatory disease and renal failure. Nephrology (Carlton) 2013; 18: 215-221.
Krzanowski M, Janda K, Dumnicka P et al.: Relationship between aortic pulse wave velocity, selected proinflammatory cytokines, and vascular calcification parameters in peritoneal dialysis patients. J Hypertens 2014; 32: 142-148.
Metry G, Stenvinkel P, Qureshi AR et al.: Low serum fetuin-A concentration predicts poor outcome only in the presence of inflammation in prevalent haemodialysis patients. Eur J Clin Invest 2008; 38: 804-811.
Ix JH, Chertow GM, Shlipak MG et al.: Association of fetuin-A with mitral annular calcification and aortic stenosis among persons with coronary heart disease data from the heart and soul study. Circulation 2007; 115: 2533-2539.
Coen G, De Paolis P, Ballanti P et al.: Peripheral artery calcifications evaluated by histology correlate to those detected by CT: relationships with fetuin-A and FGF-23. J Nephrol 2011; 24: 313-321.
Szweras M, Liu D, Partridge EA et al.: α2-HS Glycoprotein/Fetuin, a Transforming Growth Factor – β/Bone Morphogenetic Protein antagonist, regulates postnatal bone growth and remodeling. J Biol Chem 2002; 277: 19991-19997.
Coen G, Ballanti P, Balducci A et al.: Renal osteodystrophy: α-Heremans Schid Glycoprotein/Fetuin A, Matrix Gla Protein serum levels, and bone histomorphometry. Am J Kidney Dis 2006; 48: 106-113.
Fiore CE, Celotta G, Politi GG et al.: Association of high alpha2-Heremans-Schmid glycoprotein/fetuin concentration in serum and intima-media thickness in patients with atherosclerotic vascular disease and low bone mass. Atherosclerosis 2007; 195: 110-115.
Porożka T, Huźniar J, Kusztal M et al.: Increased aortic wall stiffness associated with low circulating fetuin A and high C-reactive protein in predialysis patients. Nephron Clin Pract 2009; 113: 1-87.
Mann A, Makkar V, Mann S et al.: Fetuin-A and vascular calcification in Indian end-stage renal disease population. Indian J Nephrol 2016; 26: 33-38.
Ix JH, Katz R, de Boer HI et al.: Fetuin-A is inversely associated with coronary artery calcification in community-living persons: The multi-ethnic study of atherosclerosis. Clin Chem 2012; 58: 887-895.
El-Shehaby AM, Zakaria A, El-Khatib M, Mostafa N: Association of fetuin-A and cardiac calcification and inflammation levels in hemodialysis patients. Scand J Clin Lab Invest 2010; 70: 575-582.
Chen HY, Chiu YL, Hsu SP et al.: Low serum fetuin A levels and incident stroke in patients with maintenance haemodialysis. Eur J Clin Invest 2013; 43: 387-396.
Ravn P, Fledelius C, Rosenquist C et al.: High bone turnover is associated with low bone mass in both pre- and postmenopausal women. Bone 1996; 19: 291-298.
Hruska KA, Mathew S, Lund RJ et al.: The pathogenesis of vascular calcification in the chronic kidney disease mineral bone disorder: the links between bone and the vasculature. Semin Nephrol 2009; 29: 156-165.
Rasul S, Ilhan A, Reiter MH et al.: Levels of fetuin-A relate to the levels of bone turnover biomarkers in male and female patients with type 2 diabetes. Clin Endocrinol (Oxf) 2012; 76: 499-505.
Honda H, Qureshi AR, Heimbürger O et al.: Serum albumin, C-reactive protein, interleukin 6, and fetuin A as predictors of malnutrition, cardiovascular disease, and mortality in patients with ESRD. Am J Kidney Dis 2006; 47: 139-148.
Chailurkit L, Kruavit A, Rajatanavin R et al.: The relationship of fetuin-A and lactoferrin with bone mass in elderly women. Osteopor Internat 2011; 22: 2159-2164.
Marshall LA, Cain DF, Dmowski WP et al.: Urinary N-telopeptides to monitor bone resorption while on GnRH agonist therapy. Obstetr Gynecol 1996; 87: 350-354.
Barengolts EI, Berman M, Kukreja SC et al.: Osteoporosis and coronary atherosclerosis in asymptomatic postmenopausal women. Calcif Tissue Int 1998; 62: 209-213.
Jie KS, Bots ML, Vermeer C et al.: Vitamin K status and bone mass in women with and without aortic atherosclerosis: A population based study. Calcif Tissue Int 1996; 59: 352-356.
Nishizawa Y, Morii H: Osteoporosis and atherosclerosis in chronic renal failure. Osteoporos Int 1997; 7: S188-S192.
Özkan E, Özkan H, Bilgiç S et al.: Serum fetuin-A levels in postmenopausal women with osteoporosis. Turk J Med Sci 2014; 44: 985-988.
Smith ER, Ford ML, Tomlinson LA et al.: Poor agreement between commercial ELISAs for plasma fetuin-A: An effect of protein glycosylation? Clin Chim Acta 2010; 411: 1367-1370.
Hamano T, Matsui I, Mikami S et al.: Fetuin-mineral complex reflects extraosseous calcification stress in CKD. J Am Soc Nephrol 2010; 21: 1998-2007.
otrzymano: 2016-08-04
zaakceptowano do druku: 2016-08-25

Adres do korespondencji:
*Władysław Sułowicz
Chair and Department of Nephrology Jagiellonian University Medical College
ul. Kopernika 15 c, 31-501 Kraków
tel. +48 (12) 424-78-92
wladsul@mp.pl

Postępy Nauk Medycznych 9/2016
Strona internetowa czasopisma Postępy Nauk Medycznych