37 results on '"Hafez, Gaye"'
Search Results
2. Efficacy of erythropoietin as a neuroprotective agent in CKD-associated cognitive dysfunction: A literature systematic review
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Barbieri, Michelangela, Chiodini, Paolo, Di Gennaro, Piergiacomo, Hafez, Gaye, Liabeuf, Sophie, Malyszko, Jolanta, Mani, Laila-Yasmin, Mattace-Raso, Francesco, Pepin, Marion, Perico, Norberto, Simeoni, Mariadelina, Zoccali, Carmine, Tortorella, Giovanni, Capuano, Annalisa, Remuzzi, Giuseppe, Capasso, Giovambattista, and Paolisso, Giuseppe
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- 2024
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3. Drugs with a negative impact on cognitive functions (part 3): antibacterial agents in patients with chronic kidney disease.
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Liabeuf, Sophie, Hafez, Gaye, Pešić, Vesna, Spasovski, Goce, Bobot, Mickaël, Mačiulaitis, Romaldas, Bumblyte, Inga Arune, Ferreira, Ana Carina, Farinha, Ana, Malyszko, Jolanta, Pépin, Marion, Massy, Ziad A, Unwin, Robert, Capasso, Giovambattista, Mani, Laila-Yasmin, and Target), CONNECT Action (Cognitive Decline in Nephro-Neurology European Cooperative
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The relationship between chronic kidney disease (CKD) and cognitive function has received increased attention in recent years. Antibacterial agents (ABs) represent a critical component of therapy regimens in patients with CKD due to increased susceptibility to infections. Following our reviewing work on the neurocognitive impact of long-term medications in patients with CKD, we propose to focus on AB-induced direct and indirect consequences on cognitive function. Patients with CKD are predisposed to adverse drug reactions (ADRs) due to altered drug pharmacokinetics, glomerular filtration decline, and the potential disruption of the blood–brain barrier. ABs have been identified as a major cause of ADRs in vulnerable patient populations. This review examines the direct neurotoxic effects of AB classes (e.g. beta-lactams, fluoroquinolones, aminoglycosides, and metronidazole) on the central nervous system (CNS) in patients with CKD. We will mainly focus on the acute effects on the CNS associated with AB since they are the most extensively studied effects in CKD patients. Moreover, the review describes the modulation of the gut microbiota by ABs, potentially influencing CNS symptoms. The intricate brain–gut–kidney axis emerges as a pivotal focus, revealing the interplay between microbiota alterations induced by ABs and CNS manifestations in patients with CKD. The prevalence of antibiotic-associated encephalopathy in patients with CKD undergoing intravenous AB therapy supports the use of therapeutic drug monitoring for ABs to reduce the number and seriousness of ADRs in this patient population. In conclusion, elucidating AB-induced cognitive effects in patients with CKD demands a comprehensive understanding and tailored therapeutic strategies that account for altered pharmacokinetics and the brain–gut–kidney axis. [ABSTRACT FROM AUTHOR]
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- 2024
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4. Animal models to study cognitive impairment of chronic kidney disease.
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Silva, Pedro H. Imenez, Pepin, Marion, Figurek, Andreja, Gutiérrez-Jiménez, Eugenio, Bobot, Mickaël, Iervolino, Anna, Mattace-Raso, Francesco, Hoorn, Ewout J., Bailey, Matthew A., Hénaut, Lucie, Nielsen, Rikke, Frische, Sebastian, Trepiccione, Francesco, Hafez, Gaye, Altunkaynak, Hande O., Endlich, Nicole, Unwin, Robert, Capasso, Giovambattista, Pesic, Vesna, and Massy, Ziad
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CHRONIC kidney failure ,COGNITION disorders ,EXECUTIVE function ,ACTIVITIES of daily living ,COGNITION - Abstract
Mild cognitive impairment (MCI) is common in people with chronic kidney disease (CKD), and its prevalence increases with progressive loss of kidney function. MCI is characterized by a decline in cognitive performance greater than expected for an individual age and education level but with minimal impairment of instrumental activities of daily living. Deterioration can affect one or several cognitive domains (attention, memory, executive functions, language, and perceptual motor or social cognition). Given the increasing prevalence of kidney disease, more and more people with CKD will also develop MCI causing an enormous disease burden for these individuals, their relatives, and society. However, the underlying pathomechanisms are poorly understood, and current therapies mostly aim at supporting patients in their daily lives. This illustrates the urgent need to elucidate the pathogenesis and potential therapeutic targets and test novel therapies in appropriate preclinical models. Here, we will outline the necessary criteria for experimental modeling of cognitive disorders in CKD. We discuss the use of mice, rats, and zebrafish as model systems and present valuable techniques through which kidney function and cognitive impairment can be assessed in this setting. Our objective is to enable researchers to overcome hurdles and accelerate preclinical research aimed at improving the therapy of people with CKD and MCI. [ABSTRACT FROM AUTHOR]
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- 2024
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5. Cognitive decline related to chronic kidney disease as an exclusion factor from kidney transplantation: results from an international survey.
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Farisco, Michele, Blumblyte, Inga A, Franssen, Casper, Nitsch, Dorothea, Zecchino, Irene, Capasso, Giovambattista, Hafez, Gaye, and Collaborators, COST CONNECT Action
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CHRONIC kidney failure ,KIDNEY transplantation ,COGNITION disorders ,PSYCHOSOCIAL factors ,CHRONICALLY ill - Abstract
Background and hypothesis There seems to be a lack of consensus on the necessity and the modality of psychological and specifically cognitive assessment of candidates for kidney transplantation. Both points are often delegated to individual hospitals/centres, whereas international guidelines are inconsistent. We think it is essential to investigate professionals' opinions to advance towards a consistent clinical practice. Methods This paper presents the results of an international survey among clinical professionals, mainly nephrologists from the CONNECT (Cognitive decline in Nephro-Neurology: European Cooperative Target) network and beyond (i.e. from personal contacts of CONNECT members). The survey investigated their opinions about the question of whether cognitive decline in patients with chronic kidney disease may affect their eligibility for kidney transplantation. Results Our results show that most clinicians working with patients affected by chronic kidney disease think that cognitive decline may challenge their eligibility for transplantation despite data that suggest that, in some patients, cognitive problems improve after kidney transplantation. Conclusion We conclude that three needs emerge as particularly pressing: defining agreed-on standards for a multifaceted and multifactorial assessment (i.e. including both clinical/medical and psychosocial factors) of candidates with chronic kidney disease to kidney transplantation; further investigating empirically the causal connection between chronic kidney disease and cognition; and further investigating empirically the possible partial reversibility of cognitive decline after kidney transplantation. [ABSTRACT FROM AUTHOR]
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- 2024
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6. Animal models to study cognitive impairment of chronic kidney disease
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Imenez Silva, Pedro H., Pepin, Marion, Figurek, Andreja, Gutiérrez-Jiménez, Eugenio, Bobot, Mickaël, Iervolino, Anna, Mattace-Raso, Francesco, Hoorn, Ewout J., Bailey, Matthew A., Hénaut, Lucie, Nielsen, Rikke, Frische, Sebastian, Trepiccione, Francesco, Hafez, Gaye, Altunkaynak, Hande O., Endlich, Nicole, Unwin, Robert, Capasso, Giovambattista, Pesic, Vesna, Massy, Ziad, and Wagner, Carsten A.
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- 2024
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7. The wear-off phenomenon of repeated botulinum toxin injection for chronic migraine treatment: A retrospective study.
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Ruşen, Emir, Hafez, Gaye, and Tunç, Yeşim
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CHRONIC pain , *PATIENT safety , *INTRAMUSCULAR injections , *VISUAL analog scale , *TREATMENT duration , *RETROSPECTIVE studies , *DESCRIPTIVE statistics , *BOTULINUM toxin , *DRUG efficacy , *HEALTH outcome assessment , *MIGRAINE , *DRUG tolerance , *EVALUATION - Abstract
Objectives: This study aimed to evaluate the efficacy, predictors of response, clinical considerations, and analysis of patient-reported wear-off events during injection periods of onabotulinumtoxinA (Onabot-A). Patients and methods: This retrospective study was conducted with 30 adult chronic migraine patients (26 females, 4 males; mean age: 37.9±9 3 years; range, 24 to 72 years) followed between January 2017 and December 2022. All patients received Onabot-A injections at different frequencies throughout their treatment and responded to Onabot-A. The duration between cycles was 3 months in 26 patients, and this period varied in four patients. The Visual Analog Scale scores were measured before and after the injection, all patients responded to Onabot-A. Results: Nine patients stated that they experienced wear-off at least once during their treatment cycles. In some patients, the duration of action lasted less than 12 weeks, resulting in a wear-off phenomenon. Although sex and age were not significant variables in terms of the presence or absence of wear-off phenomenon, the number of Onabot-A injections (Onabot-A treatment cycles) among patients was found to be a statistically significant variable in terms of the presence of wear-off (p<0.011). Conclusion: Repeated treatments using Onabot-A appear to be safe and well-tolerated, but the effectiveness of the drug appears to be affected by wear-off phases that may occur during long-term treatment with Onabot-A. [ABSTRACT FROM AUTHOR]
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- 2024
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8. Digital adherence technologies in tuberculosis
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Hafez, Gaye, primary and van Boven, Job F M, additional
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- 2023
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9. Methodological challenges and biases in the field of cognitive function among patients with chronic kidney disease
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Giannakou, Konstantinos, primary, Golenia, Aleksandra, additional, Liabeuf, Sophie, additional, Malyszko, Jolanta, additional, Mattace-Raso, Francesco, additional, Farinha, Ana, additional, Spasovski, Goce, additional, Hafez, Gaye, additional, Wiecek, Andrzej, additional, Capolongo, Giovanna, additional, Capasso, Giovambattista, additional, Massy, Ziad A., additional, and Pépin, Marion, additional
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- 2023
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10. Drugs with a negative impact on cognitive functions (Part 2): drug classes to consider while prescribing in CKD patients.
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Hafez, Gaye, Malyszko, Jolanta, Golenia, Aleksandra, Klimkowicz-Mrowiec, Aleksandra, Ferreira, Ana Carina, Arıcı, Mustafa, Bruchfeld, Annette, Nitsch, Dorothea, Massy, Ziad A, Pépin, Marion, Capasso, Giovambattista, Mani, Laila-Yasmin, Liabeuf, Sophie, and Target), CONNECT Action (Cognitive Decline in Nephro-Neurology European Cooperative
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DRUG side effects , *DRUG prescribing , *CHRONIC kidney failure , *COGNITIVE ability , *PSYCHIATRIC drugs - Abstract
There is growing evidence that chronic kidney disease (CKD) is an independent risk factor for cognitive impairment, especially due to vascular damage, blood–brain barrier disruption and uremic toxins. Given the presence of multiple comorbidities, the medication regimen of CKD patients often becomes very complex. Several medications such as psychotropic agents, drugs with anticholinergic properties, GABAergic drugs, opioids, corticosteroids, antibiotics and others have been linked to negative effects on cognition. These drugs are frequently included in the treatment regimen of CKD patients. The first review of this series described how CKD could represent a risk factor for adverse drug reactions affecting the central nervous system. This second review will describe some of the most common medications associated with cognitive impairment (in the general population and in CKD) and describe their effects. [ABSTRACT FROM AUTHOR]
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- 2023
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11. Drugs with a negative impact on cognitive function (Part 1): chronic kidney disease as a risk factor.
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Liabeuf, Sophie, Pešić, Vesna, Spasovski, Goce, Maciulaitis, Romaldas, Bobot, Mickaël, Farinha, Ana, Wagner, Carsten A, Unwin, Robert J, Capasso, Giovambattista, Bumblyte, Inga Arune, Hafez, Gaye, and Target), CONNECT Action (Cognitive Decline in Nephro-Neurology European Cooperative
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DISEASE risk factors ,DRUG side effects ,COGNITIVE ability ,CHRONIC kidney failure ,DRUGS - Abstract
People living with chronic kidney disease (CKD) frequently suffer from mild cognitive impairment and/or other neurocognitive disorders. This review in two parts will focus on adverse drug reactions resulting in cognitive impairment as a potentially modifiable risk factor in CKD patients. Many patients with CKD have a substantial burden of comorbidities leading to polypharmacy. A recent study found that patients seen by nephrologists were the most complex to treat because of their high number of comorbidities and medications. Due to polypharmacy, these patients may experience a wide range of adverse drug reactions. Along with CKD progression, the accumulation of uremic toxins may lead to blood–brain barrier (BBB) disruption and pharmacokinetic alterations, increasing the risk of adverse reactions affecting the central nervous system (CNS). In patients on dialysis, the excretion of drugs that depend on kidney function is severely reduced such that adverse and toxic levels of a drug or its metabolites may be reached at relatively low doses, unless dosing is adjusted. This first review will discuss how CKD represents a risk factor for adverse drug reactions affecting the CNS via (i) BBB disruption associated with CKD and (ii) the impact of reduced kidney function and dialysis itself on drug pharmacokinetics. [ABSTRACT FROM AUTHOR]
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- 2023
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12. Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?
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Liabeuf, Sophie, Pepin, Marion, Franssen, Casper, Viggiano, Davide, Carriazo, Sol, Gansevoort, Ron, Gesualdo, Loreto, Hafez, Gaye, Malyszko, Jolanta, Mayer, Christopher, Nitsch, Dorothea, Ortiz, Alberto, Pešić, Vesna, Wiecek, Andrzej, Massy, Ziad, Capasso, Giovambattista, Andrade, Alexandre, Bachmann, Maie, Bumblyte, Inga, Covic, Adrian Constantin, Delgado, Pilar, Endlich, Nicole, Engvig, Andreas, Fouque, Denis, Frische, Sebastian, Garneata, Liliana, Giannakou, Konstantinos, Goumenos, Dimitrios, Kartal, Ayşe Tuğba, Mani, Laila-Yasmin, Marti, Hans-Peter, Nielsen, Rikke, Rroji, Merita, Sakkas, Giorgos, Spasovski, Goce, Stevens, Kate, Vazelov, Evgueniy, Zacharia, Lefteris, Ferreira, Ana Carina, Hoorn, Ewout, Figurek, Andreja, Unwin, Robert, Wagner, Carsten, Wanner, Christoph, BRUCHFELD, Annette, Fridolin, Ivo, Romeo, Maria José Soler, Barbieri, Michelangela, Batinić, Bojan, Carrasco, Laura, Martino, Gianvito, Raso, Francesco Mattace, Nistor, Ionut, Paolisso, Giuseppe, Rastenytė, Daiva, Stefan, Gabriel, Tedeschi, Gioacchino, Bikbov, Boris, Endlich, Karl Hans, Godefroy, Olivier, Chillon, Jean-Marc, Kossioni, Anastassia, Kurganaite, Justina, Perico, Norberto, Remuzzi, Giuseppe, Grodzicki, Tomasz, Trepiccione, Francesco, Zoccali, Carmine, Arici, Mustafa, Blankestijn, Peter, Eckardt, Kai-Uwe, Fliser, Danilo, Jiménez, Eugenio Gutiérrez, Konig, Maximilian, Rychlik, Ivan, Deleidi, Michela, REUSZ, George, Mécanismes physiopathologiques et conséquences des calcifications vasculaires - UR UPJV 7517 (MP3CV), Université de Picardie Jules Verne (UPJV)-CHU Amiens-Picardie, Hôpital Ambroise Paré [AP-HP], Groningen University Medical Centre, Department of Nephrology [Groningue, Pays-Bas], University Medical Center Groningen [Groningen] (UMCG), CeRTA, Liabeuf, S., Pepin, M., Franssen, C. F. M., Viggiano, D., Carriazo, S., Gansevoort, R. T., Gesualdo, L., Hafez, G., Malyszko, J., Mayer, C., Nitsch, D., Ortiz, A., Pesic, V., Wiecek, A., and Massy, Z. A.
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medicine.medical_specialty ,CLINICAL-OUTCOMES ,HEMODIALYSIS ,Movement disorders ,030232 urology & nephrology ,RENAL DYSFUNCTION ,URIC-ACID ,Review ,03 medical and health sciences ,0302 clinical medicine ,PARKINSONS-DISEASE ,Diabetes mellitus ,Internal medicine ,Epidemiology ,medicine ,CKD ,INDOXYL SULFATE ,AcademicSubjects/MED00340 ,Stroke ,Depression (differential diagnoses) ,RISK ,Transplantation ,Kidney ,COMPLICATIONS ,business.industry ,cardiovascular ,medicine.disease ,COGNITIVE FUNCTION ,indoxyl sulphate ,stroke ,3. Good health ,medicine.anatomical_structure ,Clinical research ,Nephrology ,[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology ,[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie ,medicine.symptom ,business ,030217 neurology & neurosurgery ,Kidney disease ,uraemic toxins - Abstract
Chronic kidney disease (CKD) perturbs the crosstalk with others organs, with the interaction between the kidneys and the heart having been studied most intensively. However, a growing body of data indicates that there is an association between kidney dysfunction and disorders of the central nervous system. In epidemiological studies, CKD is associated with a high prevalence of neurological complications, such as cerebrovascular disorders, movement disorders, cognitive impairment and depression. Along with traditional cardiovascular risk factors (such as diabetes, inflammation, hypertension and dyslipidaemia), non-traditional risk factors related to kidney damage (such as uraemic toxins) may predispose patients with CKD to neurological disorders. There is increasing evidence to show that uraemic toxins, for example indoxyl sulphate, have a neurotoxic effect. A better understanding of factors responsible for the elevated prevalence of neurological disorders among patients with CKD might facilitate the development of novel treatments. Here, we review (i) the potential clinical impact of CKD on cerebrovascular and neurological complications, (ii) the mechanisms underlying the uraemic toxins’ putative action (based on pre-clinical and clinical research) and (iii) the potential impact of these findings on patient care., Graphical Abstract Graphical Abstract
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- 2021
13. Medication Adherence Enhancing Interventions (MAEI) in patients with non-communicable chronic diseases: a protocol of systematic review and meta-analysis
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Treciokiene, Indre, Hafez, Gaye, Mala-Ladova, Katerina, Bago, Martina, Fernandez, Francisca, Kamusheva, Maria, Duborija-Kovacevic, Natasa, Smilkov, Katarina, Rogue, Fatima, SFAKIANAKIS, MICHAIL, Ioannidou, Elena, Tittmann, Judit, Drakul, Dragana, Qvarnstrom, Miriam, Cakmak, Seher, de Sousa, Jaime, Cretu, Aurelia, and Potocnjak, Ines
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Health and Medical Administration ,Medicine and Health Sciences ,Other Pharmacy and Pharmaceutical Sciences ,Pharmacy and Pharmaceutical Sciences ,Other Medicine and Health Sciences - Abstract
This is a protocol for systematic review and meta analysis. The objectives of this study are to identify which medication adherence enhancing interventions are effective in chronic health conditions and which of the methods are used to assess medication adherence in those studies. Additionally, facilitators and barriers in medication adherence enhancing interventions will be identified.
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- 2022
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14. Profiling of cardiac β-adrenoceptor subtypes in the cardiac left ventricle of rats with metabolic syndrome: comparison with streptozotocin-induced diabetic rats
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Okatan, Esma N., Tuncay, Erkan, Hafez, Gaye, and Turan, Belma
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Cardiac output -- Measurement ,Metabolic syndrome X -- Physiological aspects ,Beta adrenoceptors -- Health aspects ,Biological sciences - Abstract
Little is known about metabolic syndrome (MetS)-associated cardiomyopathy, especially in relation to the role and contribution of beta-adrenoceptor (β-AR) subtypes. Therefore, we examined the roles of β-AR subtypes in the cardiac function of rats with MetS (MetS group) and compared it with that of rats with streptozotocin (STZ)-induced diabetes (STZ group). Compared with the normal control rats, the protein levels of cardiac [β.sub.1]-and [β.sub.2]-AR in the MetS group were significantly decreased and with no changes in their mRNA levels, whereas the protein levels of [β.sub.3]-AR were similar to those of the controls. However, as shown previously, the protein levels of cardiac [β.sub.1]-and [β.sub.2]-AR in the STZ group were decreased, whereas the [β.sub.3]-AR levels were significantly increased by comparison with the controls. Additionally, the mRNA levels of [β.sub.2]-and [β.sub.3]-AR were increased, but [β.sub.1]-AR mRNA was decreased in the STZ group. Furthermore, left ventricular developed pressure responses to [β.sub.3]-AR agonist BRL37344 were increased in the STZ group but not in the MetS group, whereas for both groups, the responses to noradrenaline were not different from those of the controls. However, the response to stimulation with high concentrations of fenoterol was depressed in the MetS group, compared with the controls, but not in the STZ group. Consequently, our data suggest that the contribution of the β-AR system to cardiac dysfunction in the rats with MetS is not the same as that in the STZ group, although they have similar cardiac dysfunction with similar ultrastructural changes to the myocardium. Key words: sympathetic stimulation, high-sucrose diet, type 1 diabetes, cardiac dysfunction, intracellular calcium homeostasis. On sait peu de choses de la cardiomyopathie associee au syndrome metabolique, particulierement en ce qui concerne le role et la contribution des sous-types de recepteurs β-adrenergiques. En consequence, nous avons etudie le role de sous-types des recepteurs β-adrenergiques sur la fonction cardiaque chez des rats presentant un syndrome metabolique en les comparant a ceux de rats atteints de diabete induit par la streptozotocine. Comparativement a chez les temoins, les taux de proteines des recepteurs [β.sub.1]-et [β.sub.2]-adrenergiques etaient nettement diminues chez les rats presentant un syndrome metabolique alors que les taux de leurs ARNm demeuraient inchanges. Par contre, ces valeurs etaient similaires a celles des temoins pour les recepteurs [β.sub.3]-adrenergiques. Cependant, comme on l'a montre precedemment, dans le groupe streptozotocine, les taux de proteines des recepteurs [β.sub.1] et [β.sub.2]-adrenergiques cardiaques diminuaient et les taux de recepteurs [β.sub.3]-adrenergiques augmentaient par rapport a chez les temoins, et ce, de maniere notable. De plus, les taux d'ARNm des recepteurs [β.sub.2]-et [β.sub.3]-adrenergiques etaient augmentes et ceux des recepteurs β-adrenergiques etaient diminues dans le groupe streptozotocine. En outre, les reponses au BRL37344 (un agoniste [β.sub.3]-adrenergique), sur le plan de la pression ventriculaire gauche exercee, etaient augmentees dans le groupe streptozotocine, mais pas dans le groupe syndrome metabolique, alors que les reponses a la noradrenaline observees dans les deux groupes n'etaient pas differentes de celles des temoins. Cependant, comparativement aux temoins, les reponses a des stimulations par l'administration de fenoterol a concentration elevee etaient diminuees dans le groupe syndrome metabolique, mais pas dans le groupe streptozotocine. Par consequent, nos donnees laissent croire que la contribution du systeme β-adrenergique a la dysfonction cardiaque observee dans le syndrome metabolique ne correspond pas a celle que l'on observe avec la streptozotocine. Pourtant, la dysfonction cardiaque et les modifications observees dans les ultrastructures myocardiques leur sont semblables. [Traduit par la Redaction] Mots-cles: stimulation sympathique, regime a teneur elevee en glucose, diabete de type 1, dysfonction cardiaque, homeostasie du calcium intracellulaire., Introduction Beta-adrenoceptors (β-ARs) play important roles in the regulation of normal cardiac function under physiological conditions. Any abnormality in this pathway has been demonstrated to be an important determinant of [...]
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- 2015
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15. Post-Covid Era
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HAFEZ, Gaye
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Health Care Sciences and Services ,post-covid,era,editorial ,Sağlık Bilimleri ve Hizmetleri - Abstract
As Aurum Journal of Health Sciences, we are pleased to announce our new issue. We would like to thank all writers and reviewers for their valuable contributions.
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- 2021
16. Editorial- Impacts of Pandemic
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HAFEZ, Gaye
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Health Care Sciences and Services ,Editorial,pandemic,impact ,Sağlık Bilimleri ve Hizmetleri - Abstract
With the new academic year beginning in all countries, almost all of the universities have announced that they will provide online education in the fall semester. Besides the effects of the pandemic on education, it was inevitable that it would have unexpected consequences for research too, and from day one,researchers had to deal with these challenges. Laboratories have been closed, and all the non-critical experimental studies have been interrupted. The impacts of the pandemic on research studies are complex and multifaceted. Some of the problems we encounter in the short- term are related to publishing.The fact that there were retracted papers even in high-impact journals caused the spread of false information about Covid-19 and its treatment options. The disruption of the education of future researchers due to the laboratory lessons that cannot be done in all applied health sciences can be counted among these negative results. To prevent the long-term side effects of the pandemic, it is necessary to evaluate the sustainability and efficiency of online education and to discuss the development of new learning/teaching methods. Additionally, we need long-term plans for sustainable research systems. Although vaccination studies continue at a rapid pace, and the situation varies on a country basis, we cannot predict how long the Covid-19 pandemic will last. This period may take a long time, and it is important to recognize new strategies for research activities. As we continue to work from home due to social distancing measures, webinars, seminars, online courses, and virtual congresses offer us great opportunities. It is perhaps much easier to reach researchers anywhere in the world with increased online accessibility. It is possible to use these virtual environments to expand our scientific community and create new collaborations.And lastly, we are pleased to announce that we have recently published the new issue of our journal. Wewould like to thank all the esteemed authors and reviewers contributing to the issue.
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- 2020
17. Editorial – Covid-19 Outbreak
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HAFEZ, Gaye
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Health Care Sciences and Services ,Sağlık Bilimleri ve Hizmetleri ,Editorial,Covid-19 - Published
- 2020
18. Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?
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Liabeuf, Sophie, Pepin, Marion, Franssen, Casper F M, Viggiano, Davide, Carriazo, Sol, Gansevoort, Ron T, Gesualdo, Loreto, Hafez, Gaye, Malyszko, Jolanta, Mayer, Christopher, Nitsch, Dorothea, Ortiz, Alberto, Pešić, Vesna, Wiecek, Andrzej, Massy, Ziad A, and Target), CONNECT Action (Cognitive Decline in Nephro-Neurology European Cooperative
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NEUROLOGICAL disorders ,CHRONIC kidney failure ,TOXINS ,CEREBROVASCULAR disease ,CARDIOVASCULAR diseases risk factors ,CENTRAL nervous system ,MOVEMENT disorders - Abstract
Chronic kidney disease (CKD) perturbs the crosstalk with others organs, with the interaction between the kidneys and the heart having been studied most intensively. However, a growing body of data indicates that there is an association between kidney dysfunction and disorders of the central nervous system. In epidemiological studies, CKD is associated with a high prevalence of neurological complications, such as cerebrovascular disorders, movement disorders, cognitive impairment and depression. Along with traditional cardiovascular risk factors (such as diabetes, inflammation, hypertension and dyslipidaemia), non-traditional risk factors related to kidney damage (such as uraemic toxins) may predispose patients with CKD to neurological disorders. There is increasing evidence to show that uraemic toxins, for example indoxyl sulphate, have a neurotoxic effect. A better understanding of factors responsible for the elevated prevalence of neurological disorders among patients with CKD might facilitate the development of novel treatments. Here, we review (i) the potential clinical impact of CKD on cerebrovascular and neurological complications, (ii) the mechanisms underlying the uraemic toxins' putative action (based on pre-clinical and clinical research) and (iii) the potential impact of these findings on patient care. [ABSTRACT FROM AUTHOR]
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- 2022
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19. Albuminuria as a risk factor for mild cognitive impairment and dementia—what is the evidence?
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Bikbov, Boris, Soler, Maria José, Pešić, Vesna, Capasso, Giovambattista, Unwin, Robert, Endres, Matthias, Remuzzi, Giuseppe, Perico, Norberto, Gansevoort, Ron, Mattace-Raso, Francesco, Bruchfeld, Annette, Figurek, Andreja, Hafez, Gaye, and Target), the CONNECT Action (Cognitive Decline in Nephro-Neurology European Cooperative
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MILD cognitive impairment ,DEMENTIA ,ALBUMINURIA ,ENDOTHELIUM diseases ,DIABETIC nephropathies ,GLOMERULAR filtration rate ,CHRONIC kidney failure - Abstract
Kidney dysfunction can profoundly influence many organ systems, and recent evidence suggests a potential role for increased albuminuria in the development of mild cognitive impairment (MCI) or dementia. Epidemiological studies conducted in different populations have demonstrated that the presence of increased albuminuria is associated with a higher relative risk of MCI or dementia both in cross-sectional analyses and in studies with long-term follow-up. The underlying pathophysiological mechanisms of albuminuria's effect are as yet insufficiently studied, with several important knowledge gaps still present in a complex relationship with other MCI and dementia risk factors. Both the kidney and the brain have microvascular similarities that make them sensitive to endothelial dysfunction involving different mechanisms, including oxidative stress and inflammation. The exact substrate of MCI and dementia is still under investigation, however available experimental data indicate that elevated albuminuria and low glomerular filtration rate are associated with significant neuroanatomical declines in hippocampal function and grey matter volume. Thus, albuminuria may be critical in the development of cognitive impairment and its progression to dementia. In this review, we summarize the available evidence on albuminuria's link to MCI and dementia, point to existing gaps in our knowledge and suggest actions to overcome them. The major question of whether interventions that target increased albuminuria could prevent cognitive decline remains unanswered. Our recommendations for future research are aimed at helping to plan clinical trials and to solve the complex conundrum outlined in this review, with the ultimate goal of improving the lives of patients with chronic kidney disease. [ABSTRACT FROM AUTHOR]
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- 2022
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20. Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease.
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Silva, Pedro H Imenez, Unwin, Robert, Hoorn, Ewout J, Ortiz, Alberto, Trepiccione, Francesco, Nielsen, Rikke, Pesic, Vesna, Hafez, Gaye, Fouque, Denis, Massy, Ziad A, Zeeuw, Chris I De, Capasso, Giovambattista, Wagner, Carsten A, and Target), CONNECT Action (Cognitive Decline in Nephro-Neurology European Cooperative
- Subjects
COGNITION disorders ,KIDNEY diseases ,ACIDOSIS ,CHRONIC kidney failure ,MEMORY disorders - Abstract
Metabolic acidosis, defined as a plasma or serum bicarbonate concentration <22 mmol/L, is a frequent consequence of chronic kidney disease (CKD) and occurs in ~10–30% of patients with advanced stages of CKD. Likewise, in patients with a kidney transplant, prevalence rates of metabolic acidosis range from 20% to 50%. CKD has recently been associated with cognitive dysfunction, including mild cognitive impairment with memory and attention deficits, reduced executive functions and morphological damage detectable with imaging. Also, impaired motor functions and loss of muscle strength are often found in patients with advanced CKD, which in part may be attributed to altered central nervous system (CNS) functions. While the exact mechanisms of how CKD may cause cognitive dysfunction and reduced motor functions are still debated, recent data point towards the possibility that acidosis is one modifiable contributor to cognitive dysfunction. This review summarizes recent evidence for an association between acidosis and cognitive dysfunction in patients with CKD and discusses potential mechanisms by which acidosis may impact CNS functions. The review also identifies important open questions to be answered to improve prevention and therapy of cognitive dysfunction in the setting of metabolic acidosis in patients with CKD. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
21. Effect of urothelium on bladder contractility in diabetic rats
- Author
-
KOŞAN, MURAT, HAFEZ, GAYE, ÖZTÜRK, BÜLENT, ÖZGÜNES, OZAN, GÜR, SERAP, and ÇETINKAYA, MESUT
- Published
- 2005
22. The Effect of Diabetes Mellitus on α1-Adrenergic Receptor Subtypes in the Bladder of Rats
- Author
-
Gonulalan, Umut, Kosan, Murat, Hafez, Gaye, Arıoglu, Ebru, Akdemir, Ozgur, Ozturk, Bulent, Gur, Serap, and Cetinkaya, Mesut
- Published
- 2012
- Full Text
- View/download PDF
23. Profiling Of Cardiac Beta-Adrenoceptor Subtypes In The Cardiac Left Ventricle Of Rats With Metabolic Syndrome: Comparison With Streptozotocin-Induced Diabetic Rats
- Author
-
Okatan, Esma N., Tuncay, Erkan, Hafez, Gaye, and Turan, Belma
- Abstract
Little is known about metabolic syndrome (MetS)-associated cardiomyopathy, especially in relation to the role and contribution of beta-adrenoceptor (beta-AR) subtypes. Therefore, we examined the roles of beta-AR subtypes in the cardiac function of rats with MetS (MetS group) and compared it with that of rats with streptozotocin (STZ)-induced diabetes (STZ group). Compared with the normal control rats, the protein levels of cardiac beta(1)-and beta(2)-AR in the MetS group were significantly decreased and with no changes in their mRNA levels, whereas the protein levels of beta(3)-AR were similar to those of the controls. However, as shown previously, the protein levels of cardiac beta(1)-and beta(2)-AR in the STZ group were decreased, whereas the beta(3)-AR levels were significantly increased by comparison with the controls. Additionally, the mRNA levels of beta(2)-and beta(3)-AR were increased, but beta(1)-AR mRNA was decreased in the STZ group. Furthermore, left ventricular developed pressure responses to beta(3)-AR agonist BRL37344 were increased in the STZ group but not in the MetS group, whereas for both groups, the responses to noradrenaline were not different from those of the controls. However, the response to stimulation with high concentrations of fenoterol was depressed in the MetS group, compared with the controls, but not in the STZ group. Consequently, our data suggest that the contribution of the beta-AR system to cardiac dysfunction in the rats with MetS is not the same as that in the STZ group, although they have similar cardiac dysfunction with similar ultrastructural changes to the myocardium.
- Published
- 2015
24. The Role of Cross‐links Between Endoplasmic Reticulum Stress, Oxidative stress and Mitochondrial dysfunction in Cardiomyocytes and H9c2 Cells under Hyperglycemia
- Author
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HAFEZ, GAYE, primary, TUNCAY, ERKAN, additional, TOY, Aysegul, additional, and TURAN, Belma, additional
- Published
- 2015
- Full Text
- View/download PDF
25. Diabetes mellitus'un yol açtığı erektil disfonksiyonda asetilsalisilik asit kullanımının koruyucu rolü olup olmadığının araştırılması
- Author
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Hafez, Gaye, Gür, Serap, and Farmakoloji Anabilim Dalı
- Subjects
Erection ,Aspirin ,Pharmacy and Pharmacology ,Diabetes mellitus-type 1 ,Cavernous sinus ,Eczacılık ve Farmakoloji - Abstract
Bu çalışmanın amacı, diabetes mellitus gibi son organ komplikasyonunun çok olduğu bir patolojide, aspirin gibi bilinen, ulaşımı kolay ve vasküler sistemde etkileri sıkça tartışılan bir ilacın, erektil disfonksiyonda da koruyucu rolü olup olmadığının araştırılmasıdır.8 haftalık diabet oluşturulmuş erkek Sprague-Dawley cinsi sıçanlara, kuyruk veninden verilen 40 mg/kg STZ ile diabet indüksiyonundan 4 gün sonra 100 mg/kg/gün dozda asetilsalisilik asit (ASA, aspirin süspansiyonu), 8 hafta boyunca her gün oral yolla verilmiştir. Denekler, kontrol (K), aspirin tedavili (K-ASA), diabetik (D) ve diabetik aspirin tedavili (D-ASA) olmak üzere dört gruba ayrılmış, in vivo ve in vitro çalışma sonuçları bu gruplar arasında karşılaştırılmıştır. In vivo deneylere alınan sıçanlarda, intrakavernozal basınç ölçümü, ortalama sistolik arteriyal basınca bölünerek hesaplanmıştır (ICP/MAP). D-ASA grubuna ait sıçanlarda elde edilen artmış intrakavernozal basınç değerleri istatistiksel olarak anlamlı bulunmuştur. In vitro çalışmalar dahilindeki elektriksel alan stimülasyonu, sodyum nitroprussit gevşeme yanıtlarında anlamlı fark gözlenmemiştir. Fenilefrin kasılma yanıtlarında da anlamlı farktan sözedilmemiştir. Moleküler çalışmalarda COX-1 ve nNOS mRNA ekspresyonları, PCR ile hesaplanmış, beta-aktine oranlarında anlamlı sonuç elde edilmemiştir.Sonuç olarak değerlendirmemiz, oral yolla verilen aspirinin, kavernoz sinir üzerinde diabetin oluşturabileceği geri dönüşümsüz patolojilerden önce koruyucu etkisinin olabileceği, ASA tedavisi ile erektil fonksiyonların bozulmasının önlenebileceğini yönündedir. Ancak sonraki çalışmalarda yapılması gereken adımlar, gruplara ait n sayısının artırılması, NOS ve COX enzimlerine ait detaylı mekanizmalara yönelik in vitro ve in vivo çalışmaların yapılmasıdır. The aim of this study is, to investigate the possible protective effects of acetylsalicylic acid called Aspirin in generic, which is the most discussed drug on vascular system, on erectile dysfunction, one of the end-organ pathologies of diabetes mellitus.Male Spraque Dawley rats were diabetic by injection of 40mg/kg streptozotocin via tail vein. The duration was 8 weeks. After 4 days of the incubation of diabetes, 100 mg/kg/day acetylsalicylic acid (ASA, as aspirin suspension) were given by orally during 8 weeks. Rats were divided into 4 groups as control (K), diabetic (D), aspirin treated (K-ASA), and diabetic aspirin treated (D-ASA), and all in vivo and in vitro studies were compared in these groups. For in vivo studies, intracavernosal pressure was measured and calculated by division into mean arterial blood pressure (ICP/MAP). ICP/MAP results of D-ASA group were found significantly higher when compared with diabetics.We did not find any significant results in in vitro studies as EFS, SNP relaxant responses and phenylephrine contractile responses. In molecular studies COX-1 and nNOS mRNA levels did not change compared with controls when divided into betaactin mRNA levels.As result, we thought that orally given 100mg/kg/day aspirin, may protect cavernosal nerve from irreversible possible pathologies of diabetes, as a possible protective effect of ASA, before the dysfunction of erection. The next steps must be to increase the n number of experiments, and to study on the detailed mechanisms of NOS and COX enzymes in vivo and in vitro. 78
- Published
- 2009
26. Diabetik ve non-diabetik sıçanlardan alınan idrar kesesi preparatlarında kolinerjik ve pürinerjik sistem yanıtlarına parsiyel obstrüksiyonun etkileri
- Author
-
Hafez, Gaye, Gür, Serap, and Farmakoloji Anabilim Dalı
- Subjects
Pharmacy and Pharmacology ,Eczacılık ve Farmakoloji - Abstract
76 ÖZET Diabetik ve Non-Diabetik Sıçanlardan Alınan İdrar Kesesi Preparatlarında Kolinerjik ve Pürinerjik Sistem Yanıtlarına Parsiyel Obstrüksiyonun Etkileri Bu çalışmanın amacı, diabetik ve non-diabetik sıçanlardan alınan detrusorlerde, kontraktilite üzerine parsiyel obstrüksiyonun etkilerini araştırmaktır. Deney hayvanları olarak, ortalama vücut ağırlıkları 250-300 g olan erkek Wistar sıçanlar kullanılmış ve kontrol, obstrüktif, diabetik, diabetik obstrüktif olmak üzere 4 gruba ayrılmıştır. Diabet, 35 mg/kg streptozotosin (STZ)' in kuyruk veninden i.v. olarak verilmesi ile oluşturulmuştur. Diabetin oluşumundan 8 hafta sonra, kontrol ve diabetik hayvanlara cerrahi girişimle, parsiyel obstrüksiyon oluşturulmuştur. Parsiyel obstrüksiyon, mesane boynuna yerleştirilen 5F üreter kateteri (1.65 mm) etrafından nonabsorbabl 4/0 prolen (monofilament polypropylene) stür kullanılarak oluşturulmuştur. 4- hafta obstrüksiyondan sonra, 12. haftada, hayvanlar deneye alınmışlardır. Ortalama mesane ağırlıkları, elektriksel stimulasyon (EFS), karbakol, adenozin trifosfat, p,v-metilen-ATP ve KCI ile elde edilen maksimum kontraktil yanıtlar hesaplanmıştır. Obstrüktif ve diabetik obstrüktif grupta, mesane ağırlığının, kontrollerle karşılaştırıldığında 2 kat artmasına karşın, diabetik mesane ağırlıklarında bir değişme gözlenmemiştir. Obstrüktif ve diabetik grupta, EFS ve karbakolle elde edilen kontraksiyon yanıtları, kontrol grupla karşılaştırıldığında, oldukça artmış görülmektedir. Buna karşın, diabetik obstrüktif grupta, kontraktil yanıtlar, kontrol seviyelerine dek77 düşmektedir. Tüm gruplarda, kolinerjik ve pürinerjik sistemin, artan yanıtlara ne derece katkıda bulunduğu ortaya konulmaya çalışılmıştır. Tüm gruplardan alınan striplerdeki kontraktil yanıtlar arasında, kolinerjik, pürinerjik ve henüz tam olarak bilinmeyen non-kolinerjik non-pürinerjik nörotransmitterlere bağlı olarak, belirgin değişiklikler gözlenmiştir. Bu çalışmanın esas bulgusu, pürinerjik fonksiyonun, parsiyel obstrüksiyon, diabet, diabet ve obstrüksiyonun bir arada bulunduğu durumlarda değiştiğini göstermektedir. Bu yüzden anormal pürinerjik iletim, bu tip bireylerde bozulan mesane motilitesini açıklayabilir. Böylece, P2X reseptörlerini hedefleyen ilaçlar, bu hastalıkların tedavilerinde yeni ve etkin rol oynayabilir. Anahtar Sözcükler: Diabet, kolinerjik, pürinerjik, parsiyel obstrüksiyon, sıçan mesanesi 78 SUMMARY The Effects of Partial Obstruction on The Cholinergic and Purinergic System Responses in Diabetic and Non-Diabetic Rat Bladder The aim of this study to determine the effects of partial obstruction (PO) on the detrusor contractility of diabetic and non-diabetic rats. Male Wistar rats with average weight of 250-300 g were divided randomized into four groups as control, obstructed, diabetic (D) and diabetic-obstructed (DO). Intraperitoneal injection of 35 mg/kg streptozotocin was performed to achieve diabetes mellitus. After 8-week of diabetes, partial obstruction was created surgically by replacing the catheter from outside, around the bladder neck with a 1,65 mm feeding tube. They lived with obstruction for 4 weeks. Totally, after 12 weeks, the experiments were done. Mean detrusor weights were measured and the maximal contractile responses to electrical field stimulation (EFS), carbachol, adenosine-5'triphosphate (ATP), p,y- methylene-ATP and KCI of detrusor strips in all groups were studied in vitro. Although bladder mass was two-fold in obstructed and diabetic-obstructed groups compared to the control group., there was no change in diabetic bladder weight compared to controls. The responses to EFS and carbachol in the obstructed and DO groups were significantly higher than the controls. In the DO group however, the responses were reaching almost similar levels with the controls. The negative effects of PO on detrusor muscle contractility is masked by diabetes mellitus. It is concluded that there is a markedly difference between in all groups about the percentage of contribution of79 cholinergic, purinergic and unknown contractile neurotransmitter(s). The principal finding of our experiments is that purinergic function is altered in obstructed, diabetic and diabetic-obstructed groups. Therefore, abnormal purinergic transmission may explain the altered bladder motility in patients with these diseases. Thus drug targeting P2X receptors may represent a novel and effective way of treating these diseases. Key Words: Diabetes, cholinergic, rat bladder, partial obstruction, purinergic 10102
- Published
- 2003
27. Alteration in Contractile Responses in Human Detrusor Smooth Muscle from Obstructed Bladders with Overactivity
- Author
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Kosan, Murat, primary, Tul, Mesut, additional, Ozturk, Bulent, additional, Hafez, Gaye, additional, Inal, Gurdal, additional, and Cetinkaya, Mesut, additional
- Published
- 2008
- Full Text
- View/download PDF
28. Short-Term Effects of Arsenic Sulfur in Deficits of Contractile and Relaxant Responses on Urinary Bladder: Pharmacological and Structural Changes
- Author
-
Gür, Serap, primary, Dogan, A. Umran, additional, Dogan, Meral, additional, Karahan, S. Tuna, additional, Can, Belgin, additional, Hafez, Gaye, additional, Ozgunes, Ozan, additional, and Kendirci, Muammer, additional
- Published
- 2005
- Full Text
- View/download PDF
29. Pan‐European survey on medication adherence management by healthcare professionals.
- Author
-
Kamusheva, Maria, Aarnio, Emma, Qvarnström, Miriam, Hafez, Gaye, Mucherino, Sara, Potočnjak, Ines, Trečiokiene, Indre, Mihajlović, Jovan, Ekenberg, Marie, Boven, Job F. M., and Leiva‐Fernandez, Francisca
- Subjects
- *
MEDICAL personnel , *PATIENT compliance , *MEDICATION therapy management , *CHI-squared test , *DIGITAL technology , *MEDICATION reconciliation - Abstract
Aims Methods Results Conclusions While medication adherence (MA) is a key prerequisite for achieving optimal clinical and economic outcomes, nonadherence is highly prevalent. Assessing how healthcare professionals (HCPs) in Europe manage MA, focusing on measurement, reporting and interventions, is the subject of this study.A cross‐sectional study was conducted among 40 European countries and quantitative analysis was conducted via an online survey. The multi‐language online survey was created using Webropol 3.0 survey and reporting tool. Descriptive statistics and chi‐squared tests were applied.In total, 2875 HCPs (pharmacists: 39.9%; physicians: 36.7%; nurses: 16.4%) from 37 European countries participated. The most used methods for MA assessment were direct communication with patients (86.4%) and referring to personal patient records (56.7%) (
P < 0.0001). Physicians (74.9%) and nurses (58.8%) were more aware of problems related to MA in contrast to pharmacists (48.6%) (P < 0.001). Almost all HCPs (92.6%) indicated that MA‐enhancing interventions involved mainly direct communication with nonadherent patients (93.3%) and their caregivers (55.7%). Medication review and related optimization of therapy were mainly performed in Western European countries (46.8%). Technological solutions were ranked as one of the less applied approaches (10–15%) (P < 0.001).HCPs in all European regions recognize MA management as an integral element of overall patient‐centred care. More efforts are needed to ensure timely, adequate and relevant MA assessment, reporting and improvement and involvement of all HCPs, especially among pharmacists who were generally less aware of MA issues. Promotion and use of digital technological solutions should be the focus of current and future clinical practice to optimize MA management processes. [ABSTRACT FROM AUTHOR]- Published
- 2024
- Full Text
- View/download PDF
30. Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease
- Author
-
Imenez Silva, Pedro H, Unwin, Robert, Hoorn, Ewout J, Ortiz, Alberto, Trepiccione, Francesco, Nielsen, Rikke, Pesic, Vesna, Hafez, Gaye, Fouque, Denis, Massy, Ziad A, De Zeeuw, Chris I, Capasso, Giovambattista, and Wagner, Carsten A
- Subjects
3. Good health - Abstract
Metabolic acidosis, defined as a plasma or serum bicarbonate concentration
31. Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?
- Author
-
Liabeuf, Sophie, Pepin, Marion, Franssen, Casper F M, Viggiano, Davide, Carriazo, Sol, Gansevoort, Ron T, Gesualdo, Loreto, Hafez, Gaye, Malyszko, Jolanta, Mayer, Christopher, Nitsch, Dorothea, Ortiz, Alberto, Pe��i��, Vesna, Wiecek, Andrzej, and Massy, Ziad A
- Subjects
3. Good health - Abstract
Chronic kidney disease (CKD) perturbs the crosstalk with others organs, with the interaction between the kidneys and the heart having been studied most intensively. However, a growing body of data indicates that there is an association between kidney dysfunction and disorders of the central nervous system. In epidemiological studies, CKD is associated with a high prevalence of neurological complications, such as cerebrovascular disorders, movement disorders, cognitive impairment and depression. Along with traditional cardiovascular risk factors (such as diabetes, inflammation, hypertension and dyslipidaemia), non-traditional risk factors related to kidney damage (such as uraemic toxins) may predispose patients with CKD to neurological disorders. There is increasing evidence to show that uraemic toxins, for example indoxyl sulphate, have a neurotoxic effect. A better understanding of factors responsible for the elevated prevalence of neurological disorders among patients with CKD might facilitate the development of novel treatments. Here, we review (i) the potential clinical impact of CKD on cerebrovascular and neurological complications, (ii) the mechanisms underlying the uraemic toxins' putative action (based on pre-clinical and clinical research) and (iii) the potential impact of these findings on patient care.
32. Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?
- Author
-
Bikbov, Boris, Soler, Maria Jos��, Pe��i��, Vesna, Capasso, Giovambattista, Unwin, Robert, Endres, Matthias, Remuzzi, Giuseppe, Perico, Norberto, Gansevoort, Ron, Mattace-Raso, Francesco, Bruchfeld, Annette, Figurek, Andreja, and Hafez, Gaye
- Subjects
mental disorders ,3. Good health - Abstract
Kidney dysfunction can profoundly influence many organ systems, and recent evidence suggests a potential role for increased albuminuria in the development of mild cognitive impairment (MCI) or dementia. Epidemiological studies conducted in different populations have demonstrated that the presence of increased albuminuria is associated with a higher relative risk of MCI or dementia both in cross-sectional analyses and in studies with long-term follow-up. The underlying pathophysiological mechanisms of albuminuria's effect are as yet insufficiently studied, with several important knowledge gaps still present in a complex relationship with other MCI and dementia risk factors. Both the kidney and the brain have microvascular similarities that make them sensitive to endothelial dysfunction involving different mechanisms, including oxidative stress and inflammation. The exact substrate of MCI and dementia is still under investigation, however available experimental data indicate that elevated albuminuria and low glomerular filtration rate are associated with significant neuroanatomical declines in hippocampal function and grey matter volume. Thus, albuminuria may be critical in the development of cognitive impairment and its progression to dementia. In this review, we summarize the available evidence on albuminuria's link to MCI and dementia, point to existing gaps in our knowledge and suggest actions to overcome them. The major question of whether interventions that target increased albuminuria could prevent cognitive decline remains unanswered. Our recommendations for future research are aimed at helping to plan clinical trials and to solve the complex conundrum outlined in this review, with the ultimate goal of improving the lives of patients with chronic kidney disease.
33. Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease
- Author
-
Giovambattista Capasso, Francesco Trepiccione, Gaye Hafez, Ewout J. Hoorn, Robert J. Unwin, Denis Fouque, Alberto Ortiz, Chris I. De Zeeuw, Rikke Nielsen, Vesna Pešić, Pedro Henrique Imenez Silva, Carsten A. Wagner, Ziad A. Massy, University of Zurich, Internal Medicine, Neurosciences, Netherlands Institute for Neuroscience (NIN), Imenez Silva, Pedro H, Unwin, Robert, Hoorn, Ewout J, Ortiz, Alberto, Trepiccione, Francesco, Nielsen, Rikke, Pesic, Vesna, Hafez, Gaye, Fouque, Deni, Massy, Ziad A, De Zeeuw, Chris I, Capasso, Giovambattista, and Wagner, Carsten A
- Subjects
medicine.medical_specialty ,klotho ,Central nervous system ,030232 urology & nephrology ,610 Medicine & health ,acidosi ,Review ,10052 Institute of Physiology ,03 medical and health sciences ,0302 clinical medicine ,cognitive dysfunction ,Internal medicine ,medicine ,In patient ,AcademicSubjects/MED00340 ,Klotho ,030304 developmental biology ,Acidosis ,0303 health sciences ,Transplantation ,business.industry ,motor function ,Metabolic acidosis ,Cognition ,medicine.disease ,Executive functions ,3. Good health ,medicine.anatomical_structure ,Nephrology ,Cardiology ,570 Life sciences ,biology ,acidosis ,medicine.symptom ,business ,chronic kidney disease ,Kidney disease - Abstract
Metabolic acidosis, defined as a plasma or serum bicarbonate concentration, Graphical Abstract Graphical Abstract
- Published
- 2021
34. Albuminuria as a risk factor for mild cognitive impairment and dementia—what is the evidence?
- Author
-
Bikbov, Boris, Jose´ Soler, Maria, Pesic, Vesna, Capasso, Giovambattista, Unwin, Robert, Endres, Matthias, Remuzzi, Giuseppe, Perico, Norberto, Gansevoort, Ron, Mattace-Raso, Francesco, Bruchfeld, Annette, Figurek, Andreja, and Hafez, Gaye
- Subjects
mental disorders ,Chronic Kidney Disease ,Mild Cognitive İmpairment ,Albuminuria ,Dementia ,Glomerular Filtration Rate - Abstract
Kidney dysfunction can profoundly influence many organ systems, and recent evidence suggests a potential role for increased albuminuria in the development of mild cognitive impairment (MCI) or dementia. Epidemiological studies conducted in different populations have demonstrated that the presence of increased albuminuria is associated with a higher relative risk of MCI or dementia both in cross-sectional analyses and in studies with long-term follow-up. The underlying pathophysiological mechanisms of albuminuria’s effect are as yet insufficiently studied, with several important knowledge gaps still present in a complex relationship with other MCI and dementia risk factors. Both the kidney and the brain have microvascular similarities that make them sensitive to endothelial dysfunction involving different mechanisms, including oxidative stress and inflammation. The exact substrate of MCI and dementia is still under investigation, however available experimental data indicate that elevated albuminuria and low glomerular filtration rate are associated with significant neuroanatomical declines in hippocampal function and grey matter volume. Thus, albuminuria may be critical in the development of cognitive impairment and its progression to dementia. In this review, we summarize the available evidence on albuminuria’s link to MCI and dementia, point to existing gaps in our knowledge and suggest actions to overcome them. The major question of whether interventions that target increased albuminuria could prevent cognitive decline remains unanswered. Our recommendations for future research are aimed at helping to plan clinical trials and to solve the complex conundrum outlined in this review, with the ultimate goal of improving the lives of patients with chronic kidney disease.
- Published
- 2021
35. Animal models to study cognitive impairment of chronic kidney disease.
- Author
-
Imenez Silva PH, Pepin M, Figurek A, Gutiérrez-Jiménez E, Bobot M, Iervolino A, Mattace-Raso F, Hoorn EJ, Bailey MA, Hénaut L, Nielsen R, Frische S, Trepiccione F, Hafez G, Altunkaynak HO, Endlich N, Unwin R, Capasso G, Pesic V, Massy Z, and Wagner CA
- Subjects
- Animals, Humans, Mice, Zebrafish, Cognition, Rats, Kidney physiopathology, Kidney metabolism, Renal Insufficiency, Chronic physiopathology, Renal Insufficiency, Chronic psychology, Renal Insufficiency, Chronic complications, Disease Models, Animal, Cognitive Dysfunction etiology, Cognitive Dysfunction physiopathology, Cognitive Dysfunction psychology
- Abstract
Mild cognitive impairment (MCI) is common in people with chronic kidney disease (CKD), and its prevalence increases with progressive loss of kidney function. MCI is characterized by a decline in cognitive performance greater than expected for an individual age and education level but with minimal impairment of instrumental activities of daily living. Deterioration can affect one or several cognitive domains (attention, memory, executive functions, language, and perceptual motor or social cognition). Given the increasing prevalence of kidney disease, more and more people with CKD will also develop MCI causing an enormous disease burden for these individuals, their relatives, and society. However, the underlying pathomechanisms are poorly understood, and current therapies mostly aim at supporting patients in their daily lives. This illustrates the urgent need to elucidate the pathogenesis and potential therapeutic targets and test novel therapies in appropriate preclinical models. Here, we will outline the necessary criteria for experimental modeling of cognitive disorders in CKD. We discuss the use of mice, rats, and zebrafish as model systems and present valuable techniques through which kidney function and cognitive impairment can be assessed in this setting. Our objective is to enable researchers to overcome hurdles and accelerate preclinical research aimed at improving the therapy of people with CKD and MCI.
- Published
- 2024
- Full Text
- View/download PDF
36. Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease.
- Author
-
Imenez Silva PH, Unwin R, Hoorn EJ, Ortiz A, Trepiccione F, Nielsen R, Pesic V, Hafez G, Fouque D, Massy ZA, De Zeeuw CI, Capasso G, and Wagner CA
- Subjects
- Bicarbonates, Humans, Acidosis etiology, Cognitive Dysfunction etiology, Motor Disorders complications, Renal Insufficiency, Chronic
- Abstract
Metabolic acidosis, defined as a plasma or serum bicarbonate concentration <22 mmol/L, is a frequent consequence of chronic kidney disease (CKD) and occurs in ~10-30% of patients with advanced stages of CKD. Likewise, in patients with a kidney transplant, prevalence rates of metabolic acidosis range from 20% to 50%. CKD has recently been associated with cognitive dysfunction, including mild cognitive impairment with memory and attention deficits, reduced executive functions and morphological damage detectable with imaging. Also, impaired motor functions and loss of muscle strength are often found in patients with advanced CKD, which in part may be attributed to altered central nervous system (CNS) functions. While the exact mechanisms of how CKD may cause cognitive dysfunction and reduced motor functions are still debated, recent data point towards the possibility that acidosis is one modifiable contributor to cognitive dysfunction. This review summarizes recent evidence for an association between acidosis and cognitive dysfunction in patients with CKD and discusses potential mechanisms by which acidosis may impact CNS functions. The review also identifies important open questions to be answered to improve prevention and therapy of cognitive dysfunction in the setting of metabolic acidosis in patients with CKD., (© The Author(s) 2021. Published byOxford University Press on behalf of ERA.)
- Published
- 2021
- Full Text
- View/download PDF
37. Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?
- Author
-
Bikbov B, Soler MJ, Pešić V, Capasso G, Unwin R, Endres M, Remuzzi G, Perico N, Gansevoort R, Mattace-Raso F, Bruchfeld A, Figurek A, and Hafez G
- Subjects
- Albuminuria complications, Cross-Sectional Studies, Disease Progression, Humans, Risk Factors, Cognitive Dysfunction etiology, Dementia complications, Dementia etiology
- Abstract
Kidney dysfunction can profoundly influence many organ systems, and recent evidence suggests a potential role for increased albuminuria in the development of mild cognitive impairment (MCI) or dementia. Epidemiological studies conducted in different populations have demonstrated that the presence of increased albuminuria is associated with a higher relative risk of MCI or dementia both in cross-sectional analyses and in studies with long-term follow-up. The underlying pathophysiological mechanisms of albuminuria's effect are as yet insufficiently studied, with several important knowledge gaps still present in a complex relationship with other MCI and dementia risk factors. Both the kidney and the brain have microvascular similarities that make them sensitive to endothelial dysfunction involving different mechanisms, including oxidative stress and inflammation. The exact substrate of MCI and dementia is still under investigation, however available experimental data indicate that elevated albuminuria and low glomerular filtration rate are associated with significant neuroanatomical declines in hippocampal function and grey matter volume. Thus, albuminuria may be critical in the development of cognitive impairment and its progression to dementia. In this review, we summarize the available evidence on albuminuria's link to MCI and dementia, point to existing gaps in our knowledge and suggest actions to overcome them. The major question of whether interventions that target increased albuminuria could prevent cognitive decline remains unanswered. Our recommendations for future research are aimed at helping to plan clinical trials and to solve the complex conundrum outlined in this review, with the ultimate goal of improving the lives of patients with chronic kidney disease., (© The Author(s) 2021. Published byOxford University Press on behalf of ERA.)
- Published
- 2021
- Full Text
- View/download PDF
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