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  - Liabeuf, Sophie
AU  - Pepin, , Marion
AU  - Franssen, Casper F.M.
AU  - Viggiano, Davide
AU  - Carriazo, Sol
AU  - Gansevoort, Ron T.
AU  - Gesualdo, Loreto
AU  - Hafez, Gaye
AU  - Malyszko, Jolanta
AU  - Mayer, Christopher
AU  - Nitsch, Dorothea
AU  - Ortiz, Alberto
AU  - Pešić, Vesna
AU  - Wiecek, Andrzej
AU  - Massy, Ziad
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4029
AB  - 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.
PB  - Oxford University Press
T2  - Nephrology Dialysis Transplantation
T1  - Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?
VL  - 37
IS  - supplement 2
SP  - ii33
EP  - ii44
DO  - 10.1093/ndt/gfab223
ER  - 

@article{
author = "Liabeuf, Sophie and Pepin, , Marion and Franssen, Casper F.M. and Viggiano, Davide and Carriazo, Sol and Gansevoort, Ron T. and Gesualdo, Loreto and Hafez, Gaye and Malyszko, Jolanta and Mayer, Christopher and Nitsch, Dorothea and Ortiz, Alberto and Pešić, Vesna and Wiecek, Andrzej and Massy, Ziad",
year = "2022",
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.",
publisher = "Oxford University Press",
journal = "Nephrology Dialysis Transplantation",
title = "Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?",
volume = "37",
number = "supplement 2",
pages = "ii33-ii44",
doi = "10.1093/ndt/gfab223"
}

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., Pešić, V., Wiecek, A.,& Massy, Z.. (2022). Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?. in Nephrology Dialysis Transplantation
Oxford University Press., 37(supplement 2), ii33-ii44.
https://doi.org/10.1093/ndt/gfab223

Liabeuf S, Pepin ,M, Franssen CF, Viggiano D, Carriazo S, Gansevoort RT, Gesualdo L, Hafez G, Malyszko J, Mayer C, Nitsch D, Ortiz A, Pešić V, Wiecek A, Massy Z. Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?. in Nephrology Dialysis Transplantation. 2022;37(supplement 2):ii33-ii44.
doi:10.1093/ndt/gfab223 .

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, "Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?" in Nephrology Dialysis Transplantation, 37, no. supplement 2 (2022):ii33-ii44,
https://doi.org/10.1093/ndt/gfab223 . .

TY  - JOUR
AU  - Imenez Silva, Pedro H.
AU  - Unwin, Robert
AU  - Hoorn, Ewout J.
AU  - Ortiz, Alberto
AU  - Trepiccione, Francesco
AU  - Nielsen, Rikke
AU  - Pešić, Vesna
AU  - Hafez, Gaye
AU  - Fouque, , Denis
AU  - Massy, Ziad A.
AU  - De Zeeuw, Chris I.
AU  - Capasso, Giovambattist
AU  - Wagner, Carsten
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4028
AB  - 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.
PB  - Oxford University Press
T2  - Nephrology Dialysis Transplantation
T1  - Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease
VL  - 37
IS  - supplement 2
SP  - ii4
EP  - ii12
DO  - 10.1093/ndt/gfab216
ER  - 

@article{
author = "Imenez Silva, Pedro H. and Unwin, Robert and Hoorn, Ewout J. and Ortiz, Alberto and Trepiccione, Francesco and Nielsen, Rikke and Pešić, Vesna and Hafez, Gaye and Fouque, , Denis and Massy, Ziad A. and De Zeeuw, Chris I. and Capasso, Giovambattist and Wagner, Carsten",
year = "2022",
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.",
publisher = "Oxford University Press",
journal = "Nephrology Dialysis Transplantation",
title = "Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease",
volume = "37",
number = "supplement 2",
pages = "ii4-ii12",
doi = "10.1093/ndt/gfab216"
}

Imenez Silva, P. H., Unwin, R., Hoorn, E. J., Ortiz, A., Trepiccione, F., Nielsen, R., Pešić, V., Hafez, G., Fouque, ,. D., Massy, Z. A., De Zeeuw, C. I., Capasso, G.,& Wagner, C.. (2022). Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease. in Nephrology Dialysis Transplantation
Oxford University Press., 37(supplement 2), ii4-ii12.
https://doi.org/10.1093/ndt/gfab216

Imenez Silva PH, Unwin R, Hoorn EJ, Ortiz A, Trepiccione F, Nielsen R, Pešić V, Hafez G, Fouque ,D, Massy ZA, De Zeeuw CI, Capasso G, Wagner C. Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease. in Nephrology Dialysis Transplantation. 2022;37(supplement 2):ii4-ii12.
doi:10.1093/ndt/gfab216 .

Imenez Silva, Pedro H., Unwin, Robert, Hoorn, Ewout J., Ortiz, Alberto, Trepiccione, Francesco, Nielsen, Rikke, Pešić, Vesna, Hafez, Gaye, Fouque, , Denis, Massy, Ziad A., De Zeeuw, Chris I., Capasso, Giovambattist, Wagner, Carsten, "Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease" in Nephrology Dialysis Transplantation, 37, no. supplement 2 (2022):ii4-ii12,
https://doi.org/10.1093/ndt/gfab216 . .