TY  - JOUR
AU  - Liabeuf, Sophie
AU  - Pešić, Vesna
AU  - Spasovski, Goce
AU  - Maciulaitis, Romaldas
AU  - Bobot, Mickaël
AU  - Farinha, Ana
AU  - Wagner, Carsten A.
AU  - Unwin, Robert J.
AU  - Capasso, Giovambattista
AU  - Bumblyte, Inga Arune
AU  - Hafez, Gaye
PY  - 2023
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/5225
AB  - 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.
PB  - Oxford University Press ( Oxford Academic)
T2  - Clinical Kidney Journal
T1  - Drugs with a negative impact on cognitive function (Part 1): chronic kidney disease as a risk factor
VL  - 0
IS  - 0
SP  - 1
EP  - 13
DO  - 10.1093/ckj/sfad241
ER  - 

@article{
author = "Liabeuf, Sophie and Pešić, Vesna and Spasovski, Goce and Maciulaitis, Romaldas and Bobot, Mickaël and Farinha, Ana and Wagner, Carsten A. and Unwin, Robert J. and Capasso, Giovambattista and Bumblyte, Inga Arune and Hafez, Gaye",
year = "2023",
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.",
publisher = "Oxford University Press ( Oxford Academic)",
journal = "Clinical Kidney Journal",
title = "Drugs with a negative impact on cognitive function (Part 1): chronic kidney disease as a risk factor",
volume = "0",
number = "0",
pages = "1-13",
doi = "10.1093/ckj/sfad241"
}

Liabeuf, S., Pešić, V., Spasovski, G., Maciulaitis, R., Bobot, M., Farinha, A., Wagner, C. A., Unwin, R. J., Capasso, G., Bumblyte, I. A.,& Hafez, G.. (2023). Drugs with a negative impact on cognitive function (Part 1): chronic kidney disease as a risk factor. in Clinical Kidney Journal
Oxford University Press ( Oxford Academic)., 0(0), 1-13.
https://doi.org/10.1093/ckj/sfad241

Liabeuf S, Pešić V, Spasovski G, Maciulaitis R, Bobot M, Farinha A, Wagner CA, Unwin RJ, Capasso G, Bumblyte IA, Hafez G. Drugs with a negative impact on cognitive function (Part 1): chronic kidney disease as a risk factor. in Clinical Kidney Journal. 2023;0(0):1-13.
doi:10.1093/ckj/sfad241 .

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, "Drugs with a negative impact on cognitive function (Part 1): chronic kidney disease as a risk factor" in Clinical Kidney Journal, 0, no. 0 (2023):1-13,
https://doi.org/10.1093/ckj/sfad241 . .

TY  - JOUR
AU  - Bikbov, Boris
AU  - Soler, Maria Jose ́
AU  - Pešić, Vesna
AU  - Capasso, Giovambattista
AU  - Unwin, Robert
AU  - Endres, Matthias
AU  - Remuzzi, Giuseppe
AU  - Perico, Norberto
AU  - Gansevoort, Ron
AU  - Mattace-Raso, Francesco
AU  - Bruchfeld, Annette
AU  - Figurek, Andreja
AU  - Hafez, Gaye
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4031
AB  - 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.
PB  - Oxford University Press
T2  - Nephrology Dialysis Transplantation
T1  - Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?
VL  - 37
IS  - supplement 2
SP  - ii55
EP  - ii62
DO  - 10.1093/ndt/gfab261
ER  - 

@article{
author = "Bikbov, Boris and Soler, Maria Jose ́ and Pešić, Vesna and Capasso, Giovambattista and Unwin, Robert and Endres, Matthias and Remuzzi, Giuseppe and Perico, Norberto and Gansevoort, Ron and Mattace-Raso, Francesco and Bruchfeld, Annette and Figurek, Andreja and Hafez, Gaye",
year = "2022",
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.",
publisher = "Oxford University Press",
journal = "Nephrology Dialysis Transplantation",
title = "Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?",
volume = "37",
number = "supplement 2",
pages = "ii55-ii62",
doi = "10.1093/ndt/gfab261"
}

Bikbov, B., Soler, M. J. ́., Pešić, V., Capasso, G., Unwin, R., Endres, M., Remuzzi, G., Perico, N., Gansevoort, R., Mattace-Raso, F., Bruchfeld, A., Figurek, A.,& Hafez, G.. (2022). Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?. in Nephrology Dialysis Transplantation
Oxford University Press., 37(supplement 2), ii55-ii62.
https://doi.org/10.1093/ndt/gfab261

Bikbov B, Soler MJ́, Pešić V, Capasso G, Unwin R, Endres M, Remuzzi G, Perico N, Gansevoort R, Mattace-Raso F, Bruchfeld A, Figurek A, Hafez G. Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?. in Nephrology Dialysis Transplantation. 2022;37(supplement 2):ii55-ii62.
doi:10.1093/ndt/gfab261 .

Bikbov, Boris, Soler, Maria Jose ́, Pešić, Vesna, Capasso, Giovambattista, Unwin, Robert, Endres, Matthias, Remuzzi, Giuseppe, Perico, Norberto, Gansevoort, Ron, Mattace-Raso, Francesco, Bruchfeld, Annette, Figurek, Andreja, Hafez, Gaye, "Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?" in Nephrology Dialysis Transplantation, 37, no. supplement 2 (2022):ii55-ii62,
https://doi.org/10.1093/ndt/gfab261 . .

TY  - JOUR
AU  - Viggiano, Davide
AU  - Bruchfeld, Annette
AU  - Carriazo, Sol
AU  - de Donato, Antonio
AU  - Endlich, Nicole
AU  - Ferreira, Ana Carina
AU  - Figurek, Andreja
AU  - Fouque, Denis
AU  - Franssen, Casper F.M.
AU  - Giannakou, Konstantinos
AU  - Goumenos, Dimitrios
AU  - Hoorn, Ewout J.
AU  - Nitsch, Dorothea
AU  - Ortiz, Alberto
AU  - Pešić, Vesna
AU  - Rastenyté, Daiva
AU  - Soler, Maria José
AU  - Rroji, Merita
AU  - Trepiccione, Francesco
AU  - Unwin, Robert J.
AU  - Wagner, Carsten A.
AU  - Wieçek, Andrzej
AU  - Zacchia, Miriam
AU  - Zoccali, Carmine
AU  - Capasso, Giovambattista
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4030
AB  - Kidney function has two important elements: glomerular filtration and tubular function (secretion and reabsorption). A persistent decrease in glomerular filtration rate (GFR), with or without proteinuria, is diagnostic of chronic kidney disease (CKD). While glomerular injury or disease is a major cause of CKD and usually associated with proteinuria, predominant tubular injury, with or without tubulointerstitial disease, is typically non-proteinuric. CKD has been linked with cognitive impairment, but it is unclear how much this depends on a decreased GFR, altered tubular function or the presence of proteinuria. Since CKD is often accompanied by tubular and interstitial dysfunction, we explore here for the first time the potential role of the tubular and tubulointerstitial compartments in cognitive dysfunction. To help address this issue we selected a group of primary tubular diseases with preserved GFR in which to review the evidence for any association with brain dysfunction. Cognition, mood, neurosensory and motor disturbances are not well characterized in tubular diseases, possibly because they are subclinical and less prominent than other clinical manifestations. The available literature suggests that brain dysfunction in tubular and tubulointerstitial diseases is usually mild and is more often seen in disorders of water handling. Brain dysfunction may occur when severe electrolyte and water disorders in young children persist over a long period of time before the diagnosis is made. We have chosen Bartter and Gitelman syndromes and nephrogenic diabetes insipidus as examples to highlight this topic. We discuss current published findings, some unanswered questions and propose topics for future research.
PB  - Oxford University Press
T2  - Nephrology Dialysis Transplantation
T1  - Brain dysfunction in tubular and tubulointerstitial kidney diseases
VL  - 37
IS  - supplement 2
SP  - ii46
EP  - ii55
DO  - 10.1093/ndt/gfab276
ER  - 

@article{
author = "Viggiano, Davide and Bruchfeld, Annette and Carriazo, Sol and de Donato, Antonio and Endlich, Nicole and Ferreira, Ana Carina and Figurek, Andreja and Fouque, Denis and Franssen, Casper F.M. and Giannakou, Konstantinos and Goumenos, Dimitrios and Hoorn, Ewout J. and Nitsch, Dorothea and Ortiz, Alberto and Pešić, Vesna and Rastenyté, Daiva and Soler, Maria José and Rroji, Merita and Trepiccione, Francesco and Unwin, Robert J. and Wagner, Carsten A. and Wieçek, Andrzej and Zacchia, Miriam and Zoccali, Carmine and Capasso, Giovambattista",
year = "2022",
abstract = "Kidney function has two important elements: glomerular filtration and tubular function (secretion and reabsorption). A persistent decrease in glomerular filtration rate (GFR), with or without proteinuria, is diagnostic of chronic kidney disease (CKD). While glomerular injury or disease is a major cause of CKD and usually associated with proteinuria, predominant tubular injury, with or without tubulointerstitial disease, is typically non-proteinuric. CKD has been linked with cognitive impairment, but it is unclear how much this depends on a decreased GFR, altered tubular function or the presence of proteinuria. Since CKD is often accompanied by tubular and interstitial dysfunction, we explore here for the first time the potential role of the tubular and tubulointerstitial compartments in cognitive dysfunction. To help address this issue we selected a group of primary tubular diseases with preserved GFR in which to review the evidence for any association with brain dysfunction. Cognition, mood, neurosensory and motor disturbances are not well characterized in tubular diseases, possibly because they are subclinical and less prominent than other clinical manifestations. The available literature suggests that brain dysfunction in tubular and tubulointerstitial diseases is usually mild and is more often seen in disorders of water handling. Brain dysfunction may occur when severe electrolyte and water disorders in young children persist over a long period of time before the diagnosis is made. We have chosen Bartter and Gitelman syndromes and nephrogenic diabetes insipidus as examples to highlight this topic. We discuss current published findings, some unanswered questions and propose topics for future research.",
publisher = "Oxford University Press",
journal = "Nephrology Dialysis Transplantation",
title = "Brain dysfunction in tubular and tubulointerstitial kidney diseases",
volume = "37",
number = "supplement 2",
pages = "ii46-ii55",
doi = "10.1093/ndt/gfab276"
}

Viggiano, D., Bruchfeld, A., Carriazo, S., de Donato, A., Endlich, N., Ferreira, A. C., Figurek, A., Fouque, D., Franssen, C. F.M., Giannakou, K., Goumenos, D., Hoorn, E. J., Nitsch, D., Ortiz, A., Pešić, V., Rastenyté, D., Soler, M. J., Rroji, M., Trepiccione, F., Unwin, R. J., Wagner, C. A., Wieçek, A., Zacchia, M., Zoccali, C.,& Capasso, G.. (2022). Brain dysfunction in tubular and tubulointerstitial kidney diseases. in Nephrology Dialysis Transplantation
Oxford University Press., 37(supplement 2), ii46-ii55.
https://doi.org/10.1093/ndt/gfab276

Viggiano D, Bruchfeld A, Carriazo S, de Donato A, Endlich N, Ferreira AC, Figurek A, Fouque D, Franssen CF, Giannakou K, Goumenos D, Hoorn EJ, Nitsch D, Ortiz A, Pešić V, Rastenyté D, Soler MJ, Rroji M, Trepiccione F, Unwin RJ, Wagner CA, Wieçek A, Zacchia M, Zoccali C, Capasso G. Brain dysfunction in tubular and tubulointerstitial kidney diseases. in Nephrology Dialysis Transplantation. 2022;37(supplement 2):ii46-ii55.
doi:10.1093/ndt/gfab276 .

Viggiano, Davide, Bruchfeld, Annette, Carriazo, Sol, de Donato, Antonio, Endlich, Nicole, Ferreira, Ana Carina, Figurek, Andreja, Fouque, Denis, Franssen, Casper F.M., Giannakou, Konstantinos, Goumenos, Dimitrios, Hoorn, Ewout J., Nitsch, Dorothea, Ortiz, Alberto, Pešić, Vesna, Rastenyté, Daiva, Soler, Maria José, Rroji, Merita, Trepiccione, Francesco, Unwin, Robert J., Wagner, Carsten A., Wieçek, Andrzej, Zacchia, Miriam, Zoccali, Carmine, Capasso, Giovambattista, "Brain dysfunction in tubular and tubulointerstitial kidney diseases" in Nephrology Dialysis Transplantation, 37, no. supplement 2 (2022):ii46-ii55,
https://doi.org/10.1093/ndt/gfab276 . .