Researcher: Kanbay, Mehmet
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Kanbay, Mehmet
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Publication Metadata only Pathological features of COVID-19 infection from biopsy and autopsy series(Turkish Association of Tuberculosis and Thorax, 2020) Kanbay, Asiye; Afşar, Barış; Elsürer Afşar, Rengin; N/A; N/A; Çöpür, Sidar; Kanbay, Mehmet; Researcher; Faculty Member; School of Medicine; School of Medicine; 368625; 110580Novel coronavirus disease 2019 (COVID-19) which is caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) was first identified in December 2019 in Chinese town Wuhan and considered as a pandemic by World Health Organization. The disease has variety of symptoms including fever, shortness of breath, cough, fatigue, loss of smell and taste and diarrhea. While the majority of cases have mild symptoms, some progress to viral pneumonia, multi-organ failure, or cytokine storm and mortality is mostly caused by hypoxemic respiratory failure. Until now, more than 3.5 million people worldwide were infected and more than 240.000 mortality has been occurred. Thus, there is now evidence the disease may affect variety of organs according to accumulating biopsy and autopsy studies. Such pathological studies have potential role on the understanding of clinical outcomes and in the development of novel targeted therapeutic approaches. Given these aforementioned data, in the current manuscript we have summarized the pathological features of COVID-19 derived from biopsy and autopsy series.Publication Metadata only Prospective validation of a screening biomarker approach combining amino-terminal pro-brain natriuretic peptide with galectin-3 predicts death and cardiovascular events in asymptomatic hemodialysis patients(Sage Publications Inc, 2018) Voroneanu, Luminita; Siriopol, Dimitrie; Apetrii, Muğurel; Hogas, Simona; Onofriescu, Mihai; Nistor, Ionut; Dumea, Raluca; Cusai, Silvia; Cianga, Petru; Constantinescu, Daniela; Covic, Adrian; N/A; Kanbay, Mehmet; Faculty Member; School of Medicine; 110580Cardiovascular (CV) disease is a major cause of death in hemodialysis patients. Biomarkers used to identify high-risk asymptomatic patients would allow early evaluation of cardiac dysfunction and appropriate therapeutic intervention. Amino-terminal pro-brain natriuretic peptide (NT-proBNP) and galectin-3 (Gal-3) may serve this purpose. Plasma levels of NT-proBNP and Gal-3 were measured in 173 patients. Patients were prospectively followed for occurrences of major CV events or death. The association of NTproBNP and Gal-3 with outcome was analyzed. The prognostic abilities for the combined outcome of Gal-3 and/or NT-proBNP were evaluated. During a median follow-up of 36 months, there were 47 incident outcomes (death and CV events). In the univariable Cox analysis, age, hypertension, albumin, phosphorus levels, and combined elevation of NT-proBNP with Gal-3 above the median (hazard ratio [HR] ¼ 3.65, 95% confidence interval [CI] ¼ 1.45-9.21) were associated with outcomes. In multivariable Cox analysis, both NT-proBNP and Gal-3 values above the median remained associated with outcomes (HR ¼ 3.34, 95% CI ¼ 1.30-8.56). In clinically asymptomatic dialysis patients, combined use of NT-proBNP and Gal-3 may improve risk stratification for death and CV events. Keywords galectin-3, NT-proBNP, cardiovascular events, mortality, dialysisPublication Metadata only Uric acid in metabolic syndrome: does uric acid have a definitive role?(Elsevier, 2022) N/A; N/A; N/A; Çöpür, Sidar; Demiray, Atalay; Kanbay, Mehmet; Resercher; Master Student; Faculty Member; School of Medicine; Graduate School of Health Sciences; School of Medicine; 368625; N/A; 110580increased serum uric acid (SUa) levels are commonly seen in patients with metabolic syndrome and are widely accepted as risk factors for hypertension, gout, non-alcoholic fatty liver disease, chronic kidney disease (CKD), and cardiovascular diseases. although some ambiguity for the exact role of uric acid (Ua) in these diseases is still present, several pathophysiological mechanisms have been identified such as increased oxidative stress, inflammation, and apoptosis. accumulating evidence in genomics enlightens genetic variabilities and some epigenetic changes that can contribute to hyperuricemia. Here we discuss the role of Ua within metabolism and the consequences of asymptomatic hyperuricemia while providing newfound evidence for the associations between Ua and gut microbiota and vitamin D. increased SUa levels and beneficial effects of lowering SUa levels need to be elucidated more to understand its complicated function within different metabolic pathways and set optimal target levels for SUa for reducing risks for metabolic and cardiovascular diseases.Publication Metadata only Novel faces of fibroblast growth factor 23 (FGF23): iron deficiency, inflammation, insulin resistance, left ventricular hypertrophy, proteinuria and acute kidney injury(Springer, 2017) Vervloet, Marc; Cozzolino, Mario; Siriopol, Dimitrie; Covic, Adrian; Goldsmith, David; Solak, Yalçın; N/A; Kanbay, Mehmet; Faculty Member; School of Medicine; 110580FGF23 is a hormone that appears as the core regulator of phosphate metabolism. Great deal of data has accumulated to demonstrate increased FGF23 secretion from the bone to compensate for even subtle increases in serum phosphorus long before intact PTH. However, recent evidence points to the fact that actions and interactions of FGF23 are not limited solely to phosphate metabolism. FGF23 may be implicated in iron metabolism and erythropoiesis, inflammation, insulin resistance, proteinuria, acute kidney injury and left ventricular hypertrophy. In this review, we will summarize latest experimental and clinical data examining impact of FGF23 on aforementioned pathophysiologic pathways/disorders.Publication Metadata only The role of uric acid in mineral bone disorders in chronic kidney disease(Springer, 2019) Afsar, Baris; Sag, Alan A.; Kuwabara, Masanari; Cozzolino, Mario; Covic, Adrian; N/A; Öztosun, Çınar; Kanbay, Mehmet; Undergraduate Student; Faculty Member; School of Medicine; School of Medicine; N/A; 110580Increasing survival in the chronic kidney disease (CKD) population exposes the bone to the cumulative detrimental sequelae of CKD, now defined physiologically and histopathologically as chronic kidney disease mineral bone disorder (CKD-BMD). This disorder is increasingly recognized as a "nontraditional" driver of morbidity and mortality and presents an opportunity to improve CKD outcomes via research. However, recent advances in the literature on this topic have not yet been collected into a single review. Therefore, this report aims to discuss the disordered renal-bone axis in CKD-BMD, molecular and hormonal drivers, novel treatment strategies, and forthcoming research in a clinician-directed format. A key novel topic will be the unique impact of uric acid on CKD-BMD, which is poised to apply extensive existing research in the uric acid domain to benefit the CKD-BMD population.Publication Metadata only Intravenous fluid therapy in accordance with kidney injury risk: when to prescribe what volume of which solution(Oxford University Press (OUP), 2023) Ortiz, Alberto; Soler, Maria Jose; N/A; Kanbay, Mehmet; Çöpür, Sidar; Mızrak, Berk; Faculty Member; Researcher; Undergraduate Student; School of Medicine; School of Medicine; School of Medicine; 110580; 368625; N/AAcute kidney injury (AKI) is common in hospitalized patients while common risk factors for the development of AKI include postoperative settings, patients with baseline chronic kidney disease (CKD) or congestive heart failure. Intravenous (IV) fluid therapy is a crucial component of care for prevention and treatment of AKI. In this narrative review, we update the approach to IV fluid therapy in hospitalized patients including the timing of fluid prescription, and the choice of fluid type, amount and infusion rate along with the potential adverse effects of various crystalloid and colloid solutions, addressing specifically their use in patients with acute kidney disease, CKD or heart failure, and their potential impact on the risk of hospital-acquired AKI.Publication Metadata only Therapeutic implications of shared mechanisms in non-alcoholic fatty liver disease and chronic kidney disease(Springer, 2021) Afsar, Baris; Sag, Alan A.; Siriopol, Dimitrie; Kuwabara, Masanari; Badarau, Silvia; Covic, Adrian; Ortiz, Alberto; N/A; Kanbay, Mehmet; Çöpür, Sidar; Bülbül, Mustafa Cem; Faculty Member; Researcher; Researcher; School of Medicine; School of Medicine; School of Medicine; 110580; 368625; 327626The most common cause of liver disease worldwide is now non-alcoholic fatty liver disease (NAFLD). NAFLD refers to a spectrum of disease ranging from steatosis to non-alcoholic steatohepatitis, causing cirrhosis, and ultimately hepatocellular carcinoma. However, the impact of NAFLD is not limited to the liver. NAFLD has extra-hepatic consequences, most notably, cardiovascular and renal disease. NAFLD and chronic kidney disease share pathogenic mechanisms including insulin resistance, lipotoxicity, inflammation and oxidative stress. Not surprisingly, there has been a recent surge in efforts to manage NAFLD in an integrated way that not only protects the liver but also delays comorbidities such as chronic kidney disease. This concept of simultaneously addressing the main disease target and comorbidities is key to improve outcomes, as recently demonstrated by clinical trials of SGLT2 inhibitors and GLP1 receptor agonists in diabetes. HIF activators, already marketed in China, also have the potential to protect both liver and kidney, as suggested by preclinical data. This review concisely discusses efforts at identifying common pathogenic pathways between NAFLD and chronic kidney disease with an emphasis on potential paradigm shifts in diagnostic workup and therapeutic management.Publication Metadata only Protein convertase subtilisin/kexin type 9 biology in nephrotic syndrome: implications for use as therapy(Oxford University Press (OUP), 2020) Busuioc, Ruxandra Mihaela; Covic, Adrian; Banach, Maciej; Burlacu, Alexandru; Mircescu, Gabriel; N/A; Kanbay, Mehmet; Faculty Member; School of Medicine; 110580Low-density lipoprotein cholesterol (LDL-C) levels almost constantly increased in patients with nephrotic syndrome (NS). Protein convertase subtilisin/kexin type 9 (PCSK9) [accelerates LDL-receptor (LDL-R) degradation] is overexpressed by liver cells in NS. Their levels, correlated inversely to LDL-R expression and directly to LDL-C, seem to play a central role in hypercholesterolaemia in NS. Hypersynthesis resulting from sterol regulatory element-binding protein dysfunction, hyperactivity induced by c-inhibitor of apoptosis protein expressed in response to stimulation by tumour necrosis factor-a produced by damaged podocytes and hypoclearance are the main possible mechanisms. Increased LDLC may damage all kidney cell populations (podocytes, mesangial and tubular cells) in a similar manner. Intracellular cholesterol accumulation produces oxidative stress, foam cell formation and apoptosis, all favoured by local inflammation. The cumulative effect of cellular lesions is worsened proteinuria and kidney function loss. Accordingly, NS patients should be considered high risk and treated by lowering LDLC. However, there is still not enough evidence determining whether lipid-lowering agents are helpful in managing dyslipidaemia in NS. Based on good efficacy and safety proved in the general population, therapeutic modulation of PCSK9 via antibody therapy might be a reasonable solution. This article explores the established and forthcoming evidence implicating PCSK9 in LDL-C dysregulation in NS.Publication Metadata only Noninvasive optical coherence tomography imaging correlates with anatomic and physiologic end-organ changes in healthy normotensives with systemic blood pressure variability(Lippincott Williams & Wilkins, 2020) Afşar, Barış; Sağ, Alan A.; N/A; Dağel, Tuncay; Derin, Gözde; Kesim, Cem; Taş, Ayşe Yıldız; Şahin, Afsun; Dinçer, Neris; Kanbay, Mehmet; Doctor; Undergraduate Student; Teaching Faculty; Faculty Member; Faculty Member; Undergraduate Student; Faculty Member; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; Koç University Hospital; N/A; N/A; 387367; 200905; 171267; 349025; 110580Objective: Blood pressure variability (BPV) is considered as a novel risk factor for cardiovascular disease including left ventricular hypertrophy, vascular stiffness, and renal dysfunction. In this study, we aimed to determine the relationship between ambulatory BPV with subclinical organ damage and vascular stiffness parameters in normotensive healthy subjects. Methods: A total of 100 healthy subjects over 18 years of age were included in this cross-sectional study. We divided the participants into two groups according to the median value of the SD of mean 24-h blood pressure (BP) (Group 1: SD of mean 24-h BP 10.15). BPs of these subjects were recorded over a 24-h period using ambulatory BP monitoring. Mobil-O-Graph device was used to estimate the augmentation index (AIx), pulse wave velocity (PWV), and ambulatory BP measurement. The choroidal thickness was measured by using optical coherence tomography device. Results: The mean age of the patients was 25.4 +/- 5.0 years. Choroidal thickness was correlated with PWV, AIx, protein excretion, and SD of systolic and diastolic BP (P < 0.05). Additionally, participants with higher BP variability have lower choroidal thickness and higher AIx. Conclusion: We showed that even in normotensive subjects, BPV correlates with choroid thickness. Thus, BPV can be an early prognostic parameter for pathologic vascular changes.Publication Metadata only Intensive blood pressure control on dementia in patients with chronic kidney disease: potential reduction in disease burden(Elsevier, 2022) Berkkan, Metehan; Sarafidis, Pantelis; N/A; N/A; Çöpür, Sidar; Kanbay, Mehmet; Researcher; Faculty Member; School of Medicine; School of Medicine; 368625; 110580Chronic kidney disease (CKD) and dementia are both common comorbidities creating considerable morbidity and mortality, especially in the elderly population with potential interactions. Even though various hypothetical mechanisms underlying the pathophysiology of increased risk of dementia and cognitive impairment in CKD patients have been implicated, no consensus has been reached so far. Recent clinical trials have investigated the therapeutic role of intensive blood pressure control on the risk of dementia in CKD patients with potentially improved outcomes. However, such trials have significant limitations that may influence the outcome and lack specific management guidelines. We reviewed the role of blood pressure and other factors on the risk of dementia in CKD patients which is an issue with high potential for clinical implications that may improve morbidity, mortality, and health expenditures along with its' potential pathophysiological mechanisms and future guidance.