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Öğe Ambulatory blood pressure monitoring: from old concepts to novel insights(SPRINGER, 2012) Kanbay, Mehmet; Turkmen, Kultigin; Ecder, Tevfik; Covic, AdrianAmbulatory blood pressure monitoring (ABPM) is an out-of-office technique for the assessment of 24-h blood pressure measurements. ABPM is indicated to diagnose many conditions, including white-coat hypertension, resistant hypertension, episodic hypertension, nocturnal hypertension, autonomic dysfunction, hypotension secondary to excessive usage of antihypertensive medication, and masked hypertension. ABPM gives a better prediction of clinical outcomes in patients with hypertension and cardiovascular diseases when compared to office blood pressure measurements. Recently, several new indices have been introduced with the aim of predicting various clinical end-points in several patient populations. In this review, we aimed to determine the clinical utility of 24-h ABPM and its potential implications for the management of hypertension in patients with a high risk of cardiovascular mortality and morbidity, as well as various novel indices that can predict clinical end-points in different patient populations.Öğe Association of serum calcitonin with coronary artery disease in individuals with and without chronic kidney disease(SPRINGER, 2012) Kanbay, Mehmet; Wolf, Myles; Selcoki, Yusuf; Solak, Yalcin; Ikizek, Mustafa; Uysal, Sema; Segall, LiviuCardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD). Recent data implicate disordered bone and mineral metabolism, including changes in serum levels of calcium, phosphate, parathyroid hormone (PTH), vitamin D, fibroblast growth factor-23 (FGF-23), and fetuin A, as novel risk factors for arterial calcification. The potential role of calcitonin, another hormonal regulator of mineral and bone metabolism, has not been studied in detail. We investigated the link between serum calcitonin and the total burden of coronary artery disease (CAD) using the validated Gensini score, in a cross-sectional study of 88 patients with estimated GFR (eGFR) between 46 and 87 ml/min/1.73 mA(2) who underwent coronary angiography. We evaluated the associations between serum calcitonin, minerals (calcium, phosphate), calcium x phosphate product, and other factors that regulate mineral metabolism (intact PTH, 25-OH-vitamin D, FGF-23, and fetuin A) and the severity of CAD. The mean serum calcitonin was 11.5 +/- A 7.8 pg/ml. In univariate analysis, the Gensini CAD severity score correlated significantly with male gender, eGFR, and serum levels of 25-OH-vitamin D, iPTH, FGF-23, fetuin A, and calcitonin (R = 0.474, P = 0.001 for the latter). In multivariate analysis adjusted for calcium, phosphate, 25-OH-vitamin D, iPTH, FGF 23, fetuin A, and calcitonin, only calcitonin (beta = 0.20; P = 0.03), FGF-23, fetuin A, and 25-OH-vitamin D emerged as independent predictors of Gensini score. In the second step, we adjusted for the presence of traditional risk factors, proteinuria, and GFR. After these adjustments, the FGF-23 and fetuin A remained statistically significant predictors of the Gensini score, while calcitonin did not. Our study suggests that, in addition to other well-known components of mineral metabolism, increased calcitonin levels are associated with greater severity of CAD. However, this relation was not independent of traditional and nontraditional cardiovascular risk factors. Longitudinal studies in larger populations including patients with more advanced CKD are needed.Öğe Mechanisms and consequences of salt sensitivity and dietary salt intake(LIPPINCOTT WILLIAMS & WILKINS, 2011) Kanbay, Mehmet; Chen, Yabing; Solak, Yalcin; Sanders, Paul W.Purpose of review Investigation into the underlying mechanisms of salt sensitivity has made important advances in recent years. This review examines in particular the effects of sodium and potassium on vascular function. Recent findings Sodium chloride (salt) intake promotes cutaneous lymphangiogenesis mediated through tissue macrophages and directly alters endothelial cell function, promoting increased production of transforming growth factor-beta (TGF-beta) and nitric oxide. In the setting of endothelial dysfunction, such as occurs with aging, diminished nitric oxide production exacerbates the vascular effects of TGF-beta, promoting decreased arterial compliance and hypertension. Dietary potassium intake may serve as an important countervailing influence on the effects of salt in the vasculature. Summary There is growing appreciation that, independently of alterations in blood pressure, dietary intake of sodium and potassium promotes functional changes in the vasculature and lymphatic system. These changes may protect against development of salt-sensitive hypertension. While salt sensitivity cannot be ascribed exclusively to these factors, perturbation of these processes promotes hypertension during high-salt intake. These studies add to the list of genetic and environmental factors that are associated with salt sensitivity, but in particular provide insight into adaptive mechanisms during high salt intake.Öğe Microvascular disease and its role in the brain and cardiovascular system: a potential role for uric acid as a cardiorenal toxin(OXFORD UNIV PRESS, 2011) Kanbay, Mehmet; Sanchez-Lozada, Laura-Gabriela; Franco, Martha; Madero, Magdalena; Solak, Yalcin; Rodriguez-Iturbe, Bernardo; Covic, AdrianArteriolosclerosis (microvascular disease) may have a key role not only in driving salt-sensitive hypertension but also in mediating the development of chronic kidney disease, vascular dementia, stroke and coronary heart disease. In this paper, we review the evidence that these latter conditions result from the altered autoregulation that occurs when arterioles become diseased. We also discuss the increasing evidence that dietary intake of sugars rich in fructose may be driving the development of microvascular disease as a consequence of raising intracellular uric acid. We hypothesize that the treatment of microvascular disease may require a multifaceted approach by utilizing agents which aim at blocking of the renin-angiotensin system, reducing oxidative stress, stimulating endothelial nitric oxide production and lowering uric acid levels. Paradoxically, agents that only stimulate nitric oxide, such as oestrogens, may increase the risk of poor outcomes if microvascular disease is not reversed.Öğe A Randomized Study of Allopurinol on Endothelial Function and Estimated Glomular Filtration Rate in Asymptomatic Hyperuricemic Subjects with Normal Renal Function(AMER SOC NEPHROLOGY, 2011) Kanbay, Mehmet; Huddam, Bulent; Azak, Alper; Solak, Yalcin; Kadioglu, Gulay Kocak; Kirbas, Ismail; Duranay, MuratBackground and objectives Endothelial dysfunction is an early manifestation of vascular injury and contributes to the development of atherosclerotic cardiovascular disease. Recent studies have implicated hyperuricemia as a risk factor for cardiovascular disease. We hypothesized that lowering uric acid in subjects with asymptomatic hyperuricemia with allopurinol might improve endothelial dysfunction, BP, estimated GFR (eGFR), and inflammatory markers. Design, setting, participants, & measurements Subjects with asymptomatic hyperuricemia and no history of gout and 30 normouricemic control subjects were enrolled in this 4-month randomized prospective study. Thirty hyperuricemic patients received 300 mg/d allopurinol and were compared with 37 hyperuricemic patients and 30 normouricemic subjects in matched control groups. Flow-mediated dilation (FMD), eGFR, ambulatory BP monitoring, spot urine protein-creatine ratio, and highly sensitive C-reactive protein were measured at baseline and at 4 months. Results Age, gender, lipid profile, eGFR, hemoglobin, glucose, and level of proteinuria were similar in hyperuricemic subjects and controls at baseline. As expected, hyperuricemic patients had higher levels of highly sensitive C-reactive protein and lower FMD compared with normouricemic patients. Allopurinol treatment resulted in a decrease in serum uric acid, a decrease in systolic BP, an increase in FMD, and an increase in eGFR compared with baseline. No significant difference was observed in the control hyperuricemic and normouricemic groups. In a multiple regression analysis, FMD levels were independently related to uric acid both before (beta = -0.55) and after (beta = -0.40) treatment. Conclusions Treatment of hyperuricemia with allopurinol improves endothelial dysfunction and eGFR in subjects with asymptomatic hyperuricemia. Clin J Am Soc Nephrol 6: 1887-1894, 2011. doi: 10.2215/CJN.11451210Öğe The relationship between weight, height and body mass index with hemodynamic parameters is not same in patients with and without chronic kidney disease(SPRINGER, 2016) Afşar, Barış; Elsürer, Rengin; Soypaçacı, Zeki; Kanbay, MehmetAlthough anthropometric measurements are related with clinical outcomes; these relationships are not universal and differ in some disease states such as in chronic kidney disease (CKD). The current study was aimed to analyze the relationship between height, weight and BMI with hemodynamic and arterial stiffness parameters both in normal and CKD patients separately. This cross-sectional study included 381 patients with (N 226) and without CKD (N 155) with hypertension. Routine laboratory and 24-h urine collection were performed. Augmentation index (Aix) which is the ratio of augmentation pressure to pulse pressure was calculated from the blood pressure waveform after adjusted heart rate at 75 [Aix@75 (%)]. Pulse wave velocity (PWV) is a simple measure of the time taken by the pressure wave to travel over a specific distance. Both [Aix@75 (%)] and PWV which are measures of arterial stiffness were measured by validated oscillometric methods using mobil-O-Graph device. In patients without CKD, height is inversely correlated with [Aix@75 (%)]. Additionally, weight and BMI were positively associated with PWV in multivariate analysis. However, in patients with CKD, weight and BMI were inversely and independently related with PWV. In CKD patients, as weight and BMI increased stiffness parameters such as Aix@75 (%) and PWV decreased. While BMI and weight are positively associated with arterial stiffness in normal patients, this association is negative in patients with CKD. In conclusion, height, weight and BMI relationship with hemodynamic and arterial stiffness parameters differs in patients with and without CKD.Öğe Renal Anemia of Inflammation: The Name Is Self-Explanatory(KARGER, 2011) Yilmaz, Mahmut Ilker; Solak, Yalcin; Covic, Adrian; Goldsmith, David; Kanbay, MehmetBackground: Anemia is inevitable as chronic kidney disease (CKD) advances. With the advent of erythropoietin-stimulating agents (ESAs), considerable improvement has been achieved in the management of anemia. However, some patients show a reduced response to ESAs. Methods: Many factors affect the response to ESA treatment. CKD is now considered as an inflammatory disorder and this understanding led to the recognition of the central role of inflammation in ESA resistance. Inflammation is related to untoward outcomes, including atherosclerosis and anemia, in the CKD population. Furthermore, recognition of deleterious effects of proinflammatory markers at different levels of erythropoiesis led to a change in the name of 'anemia of chronic disease' to anemia of inflammation. Results: The discovery of hepcidin as the major controller of iron metabolism in anemia of inflammation answered many questions regarding the interaction of erythropoietin, iron and bone marrow. Hepcidin production in the liver is driven by three major factors: inflammation, iron overload and anemia/hypoxia. Hepcidin levels are increased in patients with CKD due to the interaction of many factors; a comprehensive understanding of these pathways is thus critical in the effort to alleviate anemia of inflammation and ESA resistance. Conclusion: In this review, we discussed the epidemiology, determinants and consequences of anemia of inflammation in CKD patients with special emphasis on the central role of hepcidin along with molecular pathways driving its production. Copyright (C) 2011 S. Karger AG, BaselÖğe Sudden Cardiac Death in Patients with Chronic Kidney Disease: Prevention Is the sine qua non(KARGER, 2011) Kanbay, Mehmet; Solak, Yalcin; Covic, Adrian; Goldsmith, DavidDespite developments in the technology of dialysis procedures and improvements in the understanding of systemic derangements related to chronic kidney disease (CKD), cardiovascular disease is the major cause of death. Unfortunately, the leading subset of cardiovascular disease death is sudden cardiac death (SCD). To date much effort has been exerted to figure out the clues pointing to the risk of future development of SCD in patients with CKD. However, none of these factors satisfactorily detects a truly vulnerable dialysis patient. Thus, recently, it has been advocated that a combination of noninvasive risk assessment methods, carefully chosen to reflect the different aspects of the underlying pathology and changes in the myocardial substrate in CKD, could help to identify patients at high risk of SCD within the CKD. In this review, we aimed to summarize what is known about risk stratification of patients with CKD and appropriate prevention strategies with a special emphasis on recent developments and the use of complimentary tests perhaps as a risk prediction rule. Copyright (C) 2011 S. Karger AG, BaselÖğe Uric Acid and Pentraxin-3 Levels Are Independently Associated with Coronary Artery Disease Risk in Patients with Stage 2 and 3 Kidney Disease(KARGER, 2011) Kanbay, Mehmet; Ikizek, Mustafa; Solak, Yalcin; Selcoki, Yusuf; Uysal, Sema; Armutcu, Ferah; Eryonucu, BeyhanBackground and Objectives: Cardiovascular disease is prevalent in chronic kidney disease (CKD). Uric acid is increased in subjects with CKD and has been linked with cardiovascular mortality in this population. However, no study has evaluated the relationship of uric acid with angiographically proven coronary artery disease (CAD) in this population. We therefore investigated the link between serum uric acid (SUA) levels and (i) extent of CAD assessed by the Gensini score and (ii) inflammatory parameters, including C-reactive protein (CRP) and pentraxin-3, in patients with mild-to-moderate CKD. Material and Methods: In an unselected population of 130 patients with estimated glomerular filtration rate (eGFR) between 90 and 30 ml/min/1.73 m(2), we measured SUA, serum pentraxin-3, CRP, urinary protein-to-creatinine ratio, lipid parameters and the severity of CAD as assessed by coronary angiography and quantified by the Gensini lesion severity score. Results: The mean serum values for SUA, pentraxin-3 and CRP in the entire study population were 5.5 +/- 1.5 mg/dl, 6.4 +/- 3.4 ng/ml and 3.5 +/- 2.6 mg/dl, respectively. The Gensini scores significantly correlated in univariate analysis with gender (R = -0.379, p = 0.02), uric acid (R = 0.42, p = 0.001), pentraxin-3 (R = 0.54, p = 0.001), CRP (R = 0.29, p = 0.006) levels, eGFR (R = -0.33, p = 0.02), proteinuria (R = 0.21, p = 0.01), and presence of hypertension (R = 0.37, p = 0.001), but not with smoking status, diabetes mellitus, and lipid parameters. After adjustments for traditional cardiovascular risk factors, only uric acid (R = 0.21, p = 0.02) and pentraxin-3 (R = 0.28, p = 0.01) remained significant predictors of the Gensini score. Conclusions: SUA and pentraxin-3 levels are independent determinants of severity of CAD in patients with mild-to-moderate CKD. We recommend a clinical trial to determine whether lowering uric acid could prevent progression of CAD in patients with CKD. Copyright (C) 2011 S. Karger AG, BaselÖğe Uric Acid in Hypertension and Renal Disease: The Chicken or the Egg?(KARGER, 2010) Kanbay, Mehmet; Solak, Yalcin; Dogan, Ekrem; Lanaspa, Miguel A.; Covic, AdrianAfter uric acid was recognized as the causative factor in gout, increased prevalence of renal disease and hypertension in this patient population caught the attention of the medical community. Thus, it has been proposed that uric acid might have caused these disorders. However, uric acid suffered a long period of ignorance in which it was considered a metabolically inert substance. However, recent years has witnessed a resurrection of interest. Experimental studies showed an association between increased uric acid and renal arteriolar disease and hypertension. These preliminary results were supported with clinical studies. However, controversy regarding the precise pathophysiologic role of uric acid in inducing hypertension and renal disease remains to be elucidated. Despite being limited at this time, a few randomized intervention studies showed that even treatment of asymptomatic hyperuricemia was beneficial in terms of blood pressure regulation and kidney function. In this review, we focus on the pathophysiologic role of uric acid in the development and progression of renal disease and hypertension. We also discuss recent clinical evidence suggesting a causal role of uric acid in these disease states. Copyright (C) 2010 S. Karger AG, BaselÖğe Urinary Sodium Excretion and Ambulatory Blood Pressure Findings in Patients With Hypertension(WILEY, 2015) Afşar, Barış; Elsürer, Rengin; Kırkpantur, Alper; Kanbay, MehmetUse of ambulatory blood pressure (BP) monitoring (ABPM) allows for identification of dipping, nondipping, extreme dipping, and reverse dipping of BP. Using office BP and ABPM, hypertension subtypes can be identified: sustained normotension (SNT), white-coat hypertension, masked hypertension, and sustained hypertension. The comparison of hemodynamic parameters and salt intake has not been investigated among these patient groups. Office BP, ABPM, augmentation index (AIx), pulse wave velocity (PWV), cardiac output (CO), and total peripheral resistance (TPR) were automatically measured. Estimation of salt intake was assessed by 24-hour urinary sodium excretion. Urinary sodium excretion was not different among groups. AIx, PWV, CO, and TPR were lowest in patients with SNT. CO was lowest while AIx adjusted for a heart rate of 75 beats per minute, PWV, and TPR were highest in the extreme dipper group. No relationship was detected between hypertension subtypes and urinary sodium excretion. (C) 2015 Wiley Periodicals, Inc.
