Researcher:
Hasbal, Nuri Barış

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Faculty Member

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Nuri Barış

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Hasbal

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Hasbal, Nuri Barış

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2022 - 20233

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    Abdominal compartment syndrome: an often overlooked cause of acute kidney injury
    (Springer Heidelberg, 2022) Basile, Carlo; N/A; N/A; N/A; N/A; Çöpür, Sidar; Berkkan, Metehan; Hasbal, Nuri Barış; Kanbay, Mehmet; Resercher; Undergraduate Student; Faculty Member; Faculty Member; School of Medicine; School of Medicine; School of Medicine; School of Medicine; 368625; N/A; 143778; 110580
    Abdominal compartment syndrome (ACS) is defined as any organ dysfunction caused by intra-abdominal hypertension (IAH), referred as intra-abdominal pressure (IAP) >= 12 mm Hg according to the World Society of Abdominal Compartment Syndrome. Abdominal compartment syndrome develops in most cases when IAP rises above 20 mmHg Abdominal compartment syndrome, while being a treatable and even preventable condition if detected early in the stage of intra-abdominal hypertension, is associated with high rates of morbidity and mortality if diagnosis is delayed: therefore, early detection is essential. Acute kidney injury (AKI) is a common comorbidity, affecting approximately one in every five hospitalized patients, with a higher incidence in surgical patients. AKI in response to intra-abdominal hypertension develops as a result of a decline in cardiac output and compression of the renal vasculature and renal parenchyma. In spite of the high incidence of intra-abdominal hypertension, especially in surgical patients, its potential role in the pathophysiology of AKI has been investigated in very few clinical studies and is commonly overlooked in clinical practice despite being potentially treatable and reversible. Aim of the present review is to illustrate the current evidence on the pathophysiology, diagnosis and therapy of intra-abdominal hypertension and abdominal compartment syndrome in the context of AKI. [GRAPHICS] .
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    The mitochondrion: a promising target for kidney disease
    (Multidisciplinary Digital Publishing Institute (MDPI), 2023) Soler, Maria Jose; N/A; Kanbay, Mehmet; Çöpür, Sidar; Tanrıöver, Cem; Uçku, Duygu; Çakır, Ahmet Berke; Hasbal, Nuri Barış; Faculty Member; Researcher; Undergraduate Student; Undergraduate Student; Undergraduate Student; Faculty Member; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; 110580; 368625; N/A; N/A; N/A; 143778
    Mitochondrial dysfunction is important in the pathogenesis of various kidney diseases and the mitochondria potentially serve as therapeutic targets necessitating further investigation. Alterations in mitochondrial biogenesis, imbalance between fusion and fission processes leading to mitochondrial fragmentation, oxidative stress, release of cytochrome c and mitochondrial DNA resulting in apoptosis, mitophagy, and defects in energy metabolism are the key pathophysiological mechanisms underlying the role of mitochondrial dysfunction in kidney diseases. Currently, various strategies target the mitochondria to improve kidney function and kidney treatment. The agents used in these strategies can be classified as biogenesis activators, fission inhibitors, antioxidants, mPTP inhibitors, and agents which enhance mitophagy and cardiolipin-protective drugs. Several glucose-lowering drugs, such as glucagon-like peptide-1 receptor agonists (GLP-1-RA) and sodium glucose co-transporter-2 (SGLT-2) inhibitors are also known to have influences on these mechanisms. In this review, we delineate the role of mitochondrial dysfunction in kidney disease, the current mitochondria-targeting treatment options affecting the kidneys and the future role of mitochondria in kidney pathology.
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    Immune checkpoints inhibitors and its link to acute kidney injury and renal prognosis
    (Springer) Siriopol, Dimitrie; Covic, Adrian; Perazella, Mark A.; N/A; Kanbay, Mehmet; Yıldız, Abdullah Burak; Vehbi, Sezan; Hasbal, Nuri Barış; Kesgin, Yavuz Erkam; Celayir, Özde Melisa; Selçukbiricik, Fatih; Faculty Member; Undergraduate Student; Undergraduate Student; Faculty Member; Researcher; Other; Faculty Member; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; N/A; School of Medicine; N/A; N/A; N/A; N/A; N/A; N/A; Koç University Hospital; 110580; N/A; N/A; 143778; 327622; N/A; 202015
    Background Immunotherapy with immune checkpoint inhibitors (ICPi) may cause acute kidney injury (AKI) and their use is increasing. Materials and methods This is a single-center retrospective cohort study of patients receiving ICPi drugs for solid organ malignancies. ICPi-related AKI, the need for renal replacement therapy during or following ICPi treatment, and the associated mortality was studied. Results Two hundred thirty five patients were included in the final analysis. Patients with (N = 40) and without (n = 195) AKI had similar age, sex, type of ICPi, baseline serum creatinine levels, comorbidities and mortality; while patients with AKI were more likely to be receiving a nephrotoxic agent or be treated for genitourinary malignancy. 18 patients had ICPi-related AKI; 7 of these patients underwent kidney biopsy, which showed acute interstitial nephritis while the remaining 11 were diagnosed on clinical parameters. 18 (45%) patients recovered kidney function after AKI. No differences were observed between patients with and without kidney function recovery, although patients without recovery had a numerical, but not statistically significant, higher mortality. Patients with biopsy-confirmed ICPi-induced AKI had an increased risk of mortality, as compared with the rest of the population-HR 1.83, 95% CI 1.22-2.74, p = 0.003. Conclusion Use of nephrotoxic drugs and the location of malignancy appear to be common drivers of AKI in patients receiving ICPis for solid organ malignancy. Whether nephrotoxic agents or urinary tract obstruction may favor ICPi-related autoimmunity should be further studied.
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    Dietary protein and muscle wasting in chronic kidney disease: new insights
    (Lippincott Williams and Wilkins (LWW), 2023) Güngör, Özkan; Kara, Ali Veysel; Kalantar Zadeh, Kamyar; N/A; Hasbal, Nuri Barış; Faculty Member; School of Medicine; Koç University Hospital; 143778
    Purpose of review: muscle wasting is an important health problem in chronic kidney disease (CKD) patients. Protein restriction in the diet can be one of the main causes of muscle wasting in this population. In this review, we aimed to investigate the relationship between dietary protein intake and muscle wasting in CKD patients according to recent literature. Recent findings: The one of the main mechanisms responsible for the muscle wasting is the disturbances in skeletal muscle protein turnover. Muscle wasting primarily occurs when the rates of muscle protein breakdown exceed the muscle protein synthesis. Dietary protein intake represents an important role by causing a potent anabolic stimulus resulting a positive muscle protein balance. Compared to studies made in healthy populations, there are very limited studies in the literature about the relationship between dietary protein intake and muscle wasting in the CKD population. Majority of the studies showed that a more liberal protein intake is beneficial for muscle wasting in especially advanced CKD and hemodialysis population. Summary : Although evaluating muscle wasting in CKD patients, the amount of protein in the diet of patients should also be reviewed. Although excessive protein intake has some negative consequences on this patient group, a more liberated dietary protein intake should be taken into account in this patient group with muscle wasting and especially in dialysis patients.
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    PublicationOpen Access
    The association between acute kidney injury and outcomes in cancer patients receiving immune checkpoint inhibitor therapy: a systematic review and meta-analysis
    (Oxford University Press (OUP)) Siriopol, Dimitrie; Popa, Raluca; Ortiz, Alberto; Perazella, Mark A.; Kanbay, Mehmet; Çöpür, Sidar; Yıldız, Abdullah Burak; Berkkan, Metehan; Hasbal, Nuri Barış; Faculty Member; Researcher; School of Medicine; Koç University Hospital; 110580; 368625; N/A; N/A; N/A
    Lay summary: immune checkpoint inhibitors are a novel therapeutic approach to cancer treatment that have changed the landscape of cancer therapy but also have some considerable drawbacks. Acute kidney injury (AKI) is one of these potential complications that may have effects on patient outcomes. In this review, development of AKI in patients with cancer receiving immune checkpoint inhibitors is associated with increased risk of mortality. Background: immune checkpoint inhibitors (ICPIs) are a novel therapeutic approach to cancer treatment that have changed the landscape of cancer therapy but also have some considerable drawbacks. Acute kidney injury (AKI) is one of these potential complications that may have effects on patient outcomes. In this review, we assessed the effect of AKI on mortality outcomes in cancer patients receiving this immunotherapy. Methods: we performed a systematic review and meta-analysis of prospective, retrospective, randomized and non-randomized studies, which examined the effects of AKI in cancer patients receiving immune checkpoint inhibitors. We searched through PubMed, Medline, Web of Science, Scopus, and Cochrane Library databases. Results: seven studies were included in the final analysis, with a total number of patients of 761. Overall, the risk of death was higher in patients that developed AKI during ICPI treatment [hazard ratio (HR) 1.42, 95% confidence interval (CI) 1.05-1.92, P = 0.02; heterogeneity chi(2) = 11.68, I-2 = 66%, P = 0.02] compared with patients that did not develop AKI. In addition, there was a trend to a better survival in those with less severe AKI patients compared with those with more severe AKI (HR 1.35, 95% CI 0.99-1.83, P = 0.05). Lastly, it was seen that patients with persistent kidney dysfunction (non-recovery) had an increased risk for all-cause mortality (HR 2.93, 95% CI 1.41-6.08, P = 0.004; heterogeneity chi(2) = 0.53, I-2 = 0%, P = 0.47). Conclusions: development of AKI in patients with cancer receiving immune checkpoint inhibitors is associated with increased risk of mortality.