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 . .

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 . .