Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease.

Pedro H Imenez Silva, Robert Unwin, Ewout J Hoorn, Alberto Ortiz, Francesco Trepiccione, Rikke Nielsen, Vesna Pesic, Gaye Hafez, Denis Fouque, Ziad A Massy, Chris I De Zeeuw, Giovambattista Capasso, Carsten A Wagner

Journal: Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2022;37(Suppl 2):ii4-ii12

PMID: 34718761

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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.

Address: Institute of Physiology, University of Zurich, Zürich, Switzerland.; National Center of Competence in Research NCCR Kidney.CH, Zürich, Switzerland.; Department of Renal Medicine, Royal Free Hospital, University College London, London, UK.; Department of Internal Medicine, Erasmus Medical Center, University Medical Center Rotterdam, Rotterdam, The Netherlands.; Department of Nephrology and Hypertension, IIS-Fundacion Jimenez Diaz, Universidad Autonoma de Madrid, Madrid, Spain.; Biogem Institute of Molecular Biology and Genetics, Ariano Irpino, Italy.; Department of Translational Medical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy.; Department of Biomedicine-Anatomy, University of Aarhus, Aarhus, Denmark.; Department of Physiology, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia.; Department of Pharmacology, Faculty of Pharmacy, Altinbas University, Istanbul, Turkey.; CarMeN, INSERM 1060, Université Claude Bernard Lyon 1, Lyon, France.; Service de Néphrologie, Lyon-Sud Hospital, Pierre-Bénite, France.; Department of Nephrology, Ambroise Paré University Hospital, Assistance Publique Hôpitaux de Paris, Boulogne-Billancourt, France.; Centre de Recherche en Epidémiologie et Santé des Populations, Institut National de la Santé et de la Recherche Médicale U1018-Team 5, Université de Versailles Saint-Quentin-en-Yvelines, University Paris Saclay, Villejuif, France.; Department of Neuroscience, Erasmus Medical Center, University Medical Center Rotterdam, Rotterdam, The Netherlands.; Netherlands Institute for Neuroscience, Royal Dutch Academy of Art and Science, Amsterdam, The Netherlands.

DOI: 10.1093/ndt/gfab216

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MeSH Terms: Acidosis, Bicarbonates, Cognitive Dysfunction, Humans, Motor Disorders, Renal Insufficiency, Chronic