AccScience Publishing / AN / Online First / DOI: 10.36922/an.314
Cite this article
457
Download
5864
Views
Journal Browser
Volume | Year
Issue
Search
News and Announcements
View All
REVIEW

Seizures and chronic kidney disease: An in-depth review

Henry H.L. Wu1* Claire C.Y. Wang2 Suresh K. Chhetri2 Arvind Ponnusamy3,4 Paul Warwicker3
Show Less
1 Department of Renal Research, Kolling Institute of Medical Research, Royal North Shore Hospital and The University of Sydney, Sydney, NSW, Australia
2 Department of Neurology, Lancashire Teaching Hospitals NHS Foundation Trust, Preston, United Kingdom
3 Department of Renal Medicine, Lancashire Teaching Hospitals NHS Foundation Trust, Preston, United Kingdom
4 Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom
Advanced Neurology 2023, 2(2), 314 https://doi.org/10.36922/an.314
Submitted: 27 December 2022 | Accepted: 3 April 2023 | Published: 12 April 2023
© 2023 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
Abstract

Seizures are not uncommon in patients with chronic kidney disease (CKD), with an approximate incidence of roughly 10%. There are two primary groups: Patients who develop acute provoked seizures in the setting of CKD and patients with pre-existing epilepsy who then develop CKD. The recognition of potential etiology and management of seizures in this patient population may be challenging for clinicians, particularly non-neurologists. Standard antiepileptic drug (AED) treatment is indicated for those with pre-existing epilepsy. The prescription of AED in CKD population requires careful consideration, due to potentially altered pharmacokinetics. Clinicians frequently encounter challenges in the selection, loading, titration, and maintenance of AEDs. There are few internationally recognized consensus recommendations for AED prescription in CKD and dialysis. Non-AED management aims at addressing factors that may have provoked the seizure. In this article, we provide an in-depth review of the potential etiologies and pathophysiological pathways of provoked seizures in CKD. We discuss strategies, including non-AED treatment options, which aim to prevent, and/or manage provoked seizures in the setting of CKD. We discuss the AEDs used in contemporary clinical practice and how their metabolism is affected by CKD, concurrent AED prescriptions, and dialysis.

Keywords
Seizures
Chronic kidney disease
Pathophysiology
Etiology
Management
Antiepileptic drugs
Funding
None.
Conflict of interest
The authors declare no conflicts of interest.
References
[1]

Fisher RS, Acevedo C, Arzimanoglou A, et al., 2014, ILAE official report: A practical clinical definition of epilepsy. Epilepsia, 55: 475–482. https://doi.org/10.1111/epi.12550

[2]

Ben-Ari Y, Dudek FE, 2010, Primary and secondary mechanisms of epileptogenesis in the temporal lobe: There is a before and an after. Epilepsy Curr, 10: 118–125. https://doi.org/10.1111/j.1535–7511.2010.01376.x 

[3]

McNamara JO, 1994, Cellular and molecular basis of epilepsy. J Neurosci, 14: 3413–3425.

[4]

Vezzani A, Fujinami RS, White HS, et al., 2016, Infections, inflammation and epilepsy. Acta Neuropathol, 131: 211–234. https://doi.org/10.1007/s00401–015–1481–5 

[5]

Dalmau J, Gleichman AJ, Hughes EG, et al., 2008, Anti- NMDA-receptor encephalitis: Case series and analysis of the effects of antibodies. Lancet Neurol, 7: 1091–1098. https://doi.org/10.1016/S1474-4422(08)70224-2

[6]

Titulaer MJ, McCracken L, Gabilondo I, et al., 2013, Treatment and prognostic factors for long-term outcome in patients with anti-NMDA receptor encephalitis: An observational cohort study. Lancet Neurol, 12: 157–165. https://doi.org/10.1016/S1474-4422(12)70310-1

[7]

Petit-Pedrol M, Armangue T, Peng X, et al., 2014, Encephalitis with refractory seizures, status epilepticus, and antibodies to the GABAA receptor: A case series, characterization of the antigen, and analysis of the effects of antibodies. Lancet Neurol, 13: 276–286. https://doi.org/10.1016/S1474-4422(13)70299-0 

[8]

Lancaster E, Dalmau J, 2012, Neuronal autoantigens-pathogenesis, associated disorders and antibody testing. Nat Rev Neurol, 8: 380–390. https://doi.org/10.1038/nrneurol.2012.99 

[9]

Sazgar M, 2021, Kidney disease and epilepsy. J Stroke Cerebrovasc Dis, 30: 105651. https://doi.org/10.1016/j.jstrokecerebrovasdis.2021.105651 

[10]

Levin A, Stevens PE, Bilous RW, et al., 2012, Kidney disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl, 3: 1–50. https://doi.org/10.1038/kisup.2012.73

[11]

Anders HJ, Huber TB, Isermann B, et al., 2018, CKD in diabetes: Diabetic kidney disease versus nondiabetic kidney disease. Nat Rev Nephrol, 14: 361–377. https://doi.org/10.1038/s41581-018-0001-y 

[12]

Foreman KJ, Marquez N, Dolgert A, et al., 2018, Forecasting life expectancy, years of life lost, and all-cause and cause-specific mortality for 250 causes of death: Reference and alternative scenarios for 2016-40 for 195 countries and territories. Lancet, 392: 2052–2090. https://doi.org/10.1016/S0140-6736(18)31694-5 

[13]

Kalantar-Zadeh K, Jafar TH, Nitsch D, et al., 2021, Chronic kidney disease. Lancet, 398: 786–802. https://doi.org/10.1016/S0140-6736(21)00519-5

[14]

Burn DJ, Bates D, 1998, Neurology and the kidney. J Neurol Neurosurg Psychiatry, 65: 810–821. http://dx.doi.org/10.1136/jnnp.65.6.810

[15]

Eknoyan G, Lameire N, Barsoum R, et al., 2004, The burden of kidney disease: Improving global outcomes. Kidney Int, 66: 1310–1314. https://doi.org/10.1111/j.1523-1755.2004.00894.x 

[16]

Títoff V, Moury HN, Títoff IB, et al., 2019, Seizures, antiepileptic drugs, and CKD. Am J Kidney Dis, 73: 90–101. https://doi.org/10.1053/j.ajkd.2018.03.021 

[17]

Barnett MW, Larkman PM, 2007, The action potential. Pract Neurol, 7: 192–197. 

[18]

Sokoloff L, 1999, Energetics of functional activation in neural tissues. Neurochem Res, 24: 321–329. https://doi.org/10.1023/a:1022534709672 

[19]

Dietzel I, Heinemann U, Lux HD, 1989, Relations between slow extracellular potential changes, glial potassium buffering, and electrolyte and cellular volume changes during neuronal hyperactivity in cat brain. Glia, 2: 25–44. https://doi.org/10.1002/glia.440020104

[20]

Kiernan MC, Walters RJ, Andersen KV, et al., 2002, Nerve excitability changes in chronic renal failure indicate membrane depolarization due to hyperkalaemia. Brain, 125: 1366–1378. https://doi.org/10.1093/brain/awf123

[21]

Lacerda G, Krummel T, Hirsch E, 2010, Neurologic presentations of renal diseases. Neurol Clin, 28: 45–59. https://doi.org/10.1016/j.ncl.2009.09.003

[22]

Rosner MH, Husain-Syed F, Reis T, et al., 2021, Uremic encephalopathy. Kidney Int, 101: 227–241. https://doi.org/10.1016/j.kint.2021.09.025

[23]

Abbott NJ, Patabendige AA, Dolman DE, et al., 2010, Structure and function of the blood-brain barrier. Neurobiol Dis, 37: 13–25. https://doi.org/10.1016/j.nbd.2009.07.030

[24]

Jing W, Jabbari B, Vaziri ND, 2018, Uremia induces upregulation of cerebral tissue oxidative/inflammatory cascade, down-regulation of Nrf2 pathway and disruption of blood brain barrier. Am J Transl Res, 10: 2137–2147. 

[25]

Heidland A, Sebekova K, Klassen A, et al., 2010, Mechanisms of acute uremic encephalopathy: Early activation of Fos and Fra-2 gene products in different nuclei/areas of the rat brain. J Ren Nutr, 20: S44–S50. https://doi.org/10.1053/j.jrn.2010.05.011

[26]

Kim DM, Lee IH, Song CJ, 2016, Uremic encephalopathy: MR imaging findings and clinical correlation. Am J Neuroradiol, 37: 1604–1609. https://doi.org/10.3174/ajnr.A4776

[27]

Malek M, 2018, Brain consequences of acute kidney injury: Focusing on the hippocampus. Kidney Res Clin Pract, 37: 315–322. https://doi.org/10.23876/j.krcp.18.0056

[28]

Zhang XM, Zhu J, 2011, Kainic acid-induced neurotoxicity: Targeting glial responses and glia-derived cytokines. Curr Neuropharmacol, 9: 388–398. https://doi.org/10.2174/157015911795596540

[29]

Büttner S, Stadler A, Mayer C, et al., 2020, Incidence, risk factors, and outcome of acute kidney injury in neurocritical care. J Intensive Care Med, 35: 338–346. https://doi.org/10.1177/0885066617748596 

[30]

Grams ME, Rabb H, 2012, The distant organ effects of acute kidney injury. Kidney Int, 81: 942–948. https://doi.org/10.1038/ki.2011.241

[31]

Brocker C, Thompson DC, Vasiliou V, 2012, The role of hyperosmotic stress in inflammation and disease. Biomol Concepts, 3: 345–364. https://doi.org/10.1515/bmc-2012-0001

[32]

Hamm LL, Nakhoul N, Hering-Smith KS, 2015, Acid-base homeostasis. Clin J Am Soc Nephrol, 10: 2232–2242. https://doi.org/10.2215/CJN.07400715 

[33]

Liu M, Liang Y, Chigurupati S, et al., 2008, Acute kidney injury leads to inflammation and functional changes in the brain. J Am Soc Nephrol, 19: 1360–1370. https://doi.org/10.1681/ASN.2007080901

[34]

Bramham K, Seed PT, Lightstone L, et al., 2016, Diagnostic and predictive biomarkers for pre-eclampsia in patients with established hypertension and chronic kidney disease. Kidney Int, 89: 874–885. https://doi.org/10.1016/j.kint.2015.10.012

[35]

Wiles K, Bramham K, Seed PT, et al., 2021, Placental and endothelial biomarkers for the prediction of superimposed pre-eclampsia in chronic kidney disease. Pregnancy Hypertens, 24: 58–64. https://doi.org/10.1016/j.preghy.2021.02.010

[36]

Szpera-Gozdziewicz A, Breborowicz GH, 2014, Endothelial dysfunction in the pathogenesis of pre-eclampsia. Front Biosci, 19: 734–746. https://doi.org/10.2741/4240 

[37]

Melchiorre K, Giorgione V, Thilaganathan B, 2021, The placenta and preeclampsia: Villain or victim? Am J Obstet Gynecol, 226: S954–S962. https://doi.org/10.1016/j.ajog.2020.10.024 

[38]

Clausen P, Ekbom P, Damm P, et al., 2007, Signs of maternal vascular dysfunction precede preeclampsia in women with Type 1 diabetes. J Diabetes Complications, 21: 288–293. https://doi.org/10.1016/j.jdiacomp.2006.03.004 

[39]

Dusse LM, Rios DR, Pinheiro MB, et al., 2011, Pre-eclampsia: Relationship between coagulation, fibrinolysis and inflammation. Clin Chim Acta, 412: 17–21. https://doi.org/10.1016/j.cca.2010.09.030 

[40]

Duley L, 2009, The global impact of pre-eclampsia and eclampsia. Semin Perinatol, 33: 130–137. https://doi.org/10.1053/j.semperi.2009.02.010

[41]

Usala RL, Verbalis JG, 2018, Disorders of water and sodium homeostasis and bone. Curr Opin Endocr Metab Res, 3: 83–92. https://doi.org/10.1016/j.coemr.2018.06.001

[42]

Halawa I, Andersson T, Tomson T, 2011, Hyponatremia and risk of seizures: A retrospective cross‐sectional study, Epilepsia, 52: 410–413. https://doi.org/10.1111/j.1528-1167.2010.02939.x 

[43]

Kengne FG, Decaux G, 2018, Hyponatremia and the brain. Kidney Int Rep, 3: 24–35. https://doi.org/10.1016/j.ekir.2017.08.015

[44]

Ayus JC, Krothapalli RK, Arieff AI, 1987, Treatment of symptomatic hyponatremia and its relation to brain damage. New Engl J Med, 317: 1190–1195. https://doi.org/10.1056/NEJM198711053171905

[45]

George JC, Zafar W, Bucaloiu ID, et al., 2018, Risk factors and outcomes of rapid correction of severe hyponatremia. Clin J Am Soc Nephrol, 13: 984–992. https://doi.org/10.2215/CJN.13061117

[46]

DeLorenzo RJ, Sun DA, Deshpande LS, 2006, Erratum to “Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintenance of epilepsy”. [Pharmacol Ther, 105: (2005) 229–266]. Pharmacol Ther, 111: 288–325. https://doi.org/10.1016/j.pharmthera.2004.10.004

[47]

Isaev D, Ivanchick G, Khmyz V, et al., 2012, Surface charge impact in low-magnesium model of seizure in rat hippocampus. J Neurophysiol, 107: 417–423. https://doi.org/10.1152/jn.00574.2011 

[48]

Sinert R, Zehtabchi S, Desai S, et al., 2007, Serum ionized magnesium and calcium levels in adult patients with seizures. Scand J Clin Lab Invest, 67: 317–326. https://doi.org/10.1080/00365510601051441

[49]

Yuen AW, Sander JW, 2012, Can magnesium supplementation reduce seizures in people with epilepsy? A hypothesis. Epilepsy Res, 100: 152–156. https://doi.org/10.1016/j.eplepsyres.2012.02.004 

[50]

Tombini M, Palermo A, Assenza G, et al., 2018, Calcium metabolism serum markers in adult patients with epilepsy and the effect of vitamin D supplementation on seizure control. Seizure, 58: 75–81. https://doi.org/10.1016/j.seizure.2018.04.008

[51]

Ureña-Torres PA, Vervloet M, Mazzaferro S, et al., 2019, Novel insights into parathyroid hormone: Report of the

[52]

Bühler G, Balabanova S, Milowski S, et al., 1997, Detection of immunoreactive parathyroid hormone-related protein in human cerebrospinal fluid. Exp Clin Endocrinol Diabetes, 105: 336–340. https://doi.org/10.1055/s-0029-1211775

[53]

Weinstein R, 2001, Hypocalcemic toxicity and atypical reactions in therapeutic plasma exchange. J Clin Apher, 16: 210–211. https://doi.org/10.1002/jca.10000

[54]

Gibbs R, Macnaughton P, 2007, Electrolyte and metabolic disturbances in critically ill patients. Anaesth Intensive Care, 8: 529–533. https://doi.org/10.1016/j.mpaic.2007.09.015

[55]

Gungor O, Aydin Z, Inci A, et al., 2021, Seizures in patients with kidney diseases: A neglected problem? Nephrol Dial Transplant, 38: 291–299. https://doi.org/10.1093/ndt/gfab283 

[56]

Abdelmalik PA, Shannon P, Yiu A, et al., 2007, Hypoglycemic seizures during transient hypoglycemia exacerbate hippocampal dysfunction. Neurobiol Dis, 26: 646–660. https://doi.org/10.1016/j.nbd.2007.03.002 

[57]

Halawa I, Zelano J, Kumlien E, 2015, Hypoglycemia and risk of seizures: A retrospective cross-sectional study. Seizure, 25: 147–149. https://doi.org/10.1016/j.seizure.2014.10.005 

[58]

Hahr AJ, Molitch ME, 2015, Management of diabetes mellitus in patients with chronic kidney disease. Clin Diabetes Endocrinol, 1: 2. https://doi.org/10.1186/s40842-015-0001-9 

[59]

Brick JF, Gutrecht JA, Ringel RA, 1989, Reflex epilepsy and nonketotic hyperglycemia in the elderly: A specific neuroendocrine syndrome. Neurology, 39: 394. https://doi.org/10.1212/WNL.39.3.394

[60]

Santos PC, Krieger JE, Pereira AC, 2012, Renin-angiotensin system, hypertension, and chronic kidney disease: Pharmacogenetic implications. J Pharmacol Sci, 120: 77–88. https://doi.org/10.1254/jphs.12r03cr

[61]

Kopecky C, Lytvyn Y, Domenig O, et al., 2019, Molecular regulation of the renin-angiotensin system by sodium-glucose cotransporter 2 inhibition in Type 1 diabetes mellitus. Diabetologia, 62: 1090–1093. https://doi.org/10.1007/s00125-019-4871-8 

[62]

Zhou L, Liu Y, 2016, Wnt/β-catenin signaling and renin-angiotensin system in chronic kidney disease. Curr Opin Nephrol Hypertens, 25: 100–106. https://doi.org/10.1097/MNH.0000000000000205 

[63]

Petrea RE, O’Donnell A, Beiser AS, et al., 2020, Mid to late life hypertension trends and cerebral small vessel disease in the Framingham Heart Study. Hypertension, 76: 707–714. https://doi.org/10.1161/HYPERTENSIONAHA.120.15073

[64]

Biose IJ, Dewar D, Macrae IM, et al., 2020, Impact of stroke co-morbidities on cortical collateral flow following ischaemic stroke. J Cereb Blood Flow Metab, 40: 978–990. https://doi.org/10.1177/0271678X19858532

[65]

Sprick JD, Nocera JR, Hajjar I, et al., 2020, Cerebral blood flow regulation in end-stage kidney disease. Am J Physiol Ren Physiol, 319: F782–F791. https://doi.org/10.1152/ajprenal.00438.2020

[66]

Claassen JA, Thijssen DH, Panerai RB, et al., 2021, Regulation of cerebral blood flow in humans: Physiology and clinical implications of autoregulation. Physiol Rev, 101: 1487–1559. https://doi.org/10.1152/physrev.00022.2020

[67]

Mauritz M, Hirsch LJ, Camfield P, et al., 2022, Acute symptomatic seizures: An educational, evidence‐based review. Epileptic Disord, 24: 26–49. https://doi.org/10.1684/epd.2021.1376 

[68]

Fugate JE, Rabinstein AA, 2015, Posterior reversible encephalopathy syndrome: Clinical and radiological manifestations, pathophysiology, and outstanding questions. Lancet Neurol, 14: 914–925. https://doi.org/10.1016/S1474-4422(15)00111-8

[69]

Fugate JE, Claassen DO, Cloft HJ, et al., 2010, Posterior reversible encephalopathy syndrome: Associated clinical and radiologic findings. Mayo Clin Proc, 85: 427–432. https://doi.org/10.4065/mcp.2009.0590

[70]

Fischer M, Schmutzhard E, 2017, Posterior reversible encephalopathy syndrome. J Neurol, 264: 1608–1616. https://doi.org/10.1007/s00415-016-8377-8

[71]

Agarwal R, 2018, Mechanisms and mediators of hypertension induced by erythropoietin and related molecules. Nephrol Dial Transplant, 33: 1690–1698. https://doi.org/10.1093/ndt/gfx324

[72]

Strippoli GF, Craig JC, Manno C, et al., 2004, Hemoglobin targets for the anemia of chronic kidney disease: A meta-analysis of randomized, controlled trials. J Am Soc Nephrol, 15: 3154–3165. https://doi.org/10.1097/01.ASN.0000145436.09176.A7 

[73]

Mahmoud SH, Zhou XY, Ahmed SN, 2020, Managing the patient with epilepsy and renal impairment. Seizure, 76: 143–152. https://doi.org/10.1016/j.seizure.2020.02.006

[74]

Hitchings AW, 2016, Drugs that lower the seizure threshold. Adverse Drug React Bull, 298: 1151–1154. https://doi.org/10.1097/FAD.0000000000000016

[75]

Sahani MM, Daoud TM, Sam R, et al., 2001, Dialysis disequilibrium syndrome revisited. Hemodial Int, 5: 92–96. https://doi.org/10.1111/hdi.2001.5.1.92 

[76]

Mistry K, 2019, Dialysis disequilibrium syndrome prevention and management. Int J Nephrol Renovasc Dis, 12: 69–77. https://doi.org/10.2147/IJNRD.S165925

[77]

Zepeda-Orozco D, Quigley R, 2012, Dialysis disequilibrium syndrome. Pediatr Nephrol, 27: 2205–2211. https://doi.org/10.1007/s00467-012-2199-4

[78]

Trinh-Trang-Tan MM, Cartron JP, Bankir L, 2005, Molecular basis for the dialysis disequilibrium syndrome: Altered aquaporin and urea transporter expression in the brain. Nephrol Dial Transplant, 20: 1984–1988. https://doi.org/10.1093/ndt/gfh877

[79]

Wong SS, Kwaan HC, Ing TS, 2017, Venous air embolism related to the use of central catheters revisited: With emphasis on dialysis catheters. Clin Kidney J, 10: 797–803. https://doi.org/10.1093/ckj/sfx064 

[80]

Brull SJ, Prielipp RC, 2017, Vascular air embolism: A silent hazard to patient safety. J Crit Care, 42: 255–263. https://doi.org/10.1016/j.jcrc.2017.08.010

[81]

Sprague SM, Corwin HL, Wilson RS, et al., 1986, Encephalopathy in chronic renal failure responsive to deferoxamine therapy: Another manifestation of aluminum neurotoxicity. Arch Intern Med, 146: 2063–2064. https://doi.org/10.1001/archinte.1986.00360220245039

[82]

Coulson JM, Hughes BW, 2022, Dose-response relationships in aluminum toxicity in humans. Clin Toxicol, 60: 415–428. https://doi.org/10.1080/15563650.2022.2029879 

[83]

Sadakane Y, Kawahara M, 2018, Implications of metal binding and asparagine deamidation for amyloid formation. Int J Mol Sci, 19: 2449. https://doi.org/10.3390/ijms19082449

[84]

Ahmed GA, Khalil SK, Abbas L, et al., 2020, ATR-IR and EPR spectroscopy for detecting the alterations in cortical synaptosomes induced by aluminium stress. Spectrochim Acta A Mol Biomol Spectrosc, 228: 117535. https://doi.org/10.1016/j.chemphyslip.2020.104931

[85]

Bechstein WO, 2000, Neurotoxicity of calcineurin inhibitors: Impact and clinical management. Transplant Int, 13: 313–326. https://doi.org/10.1007/s001470050708

[86]

Tan TC, Robinson PJ, 2006, Mechanisms of calcineurin inhibitor-induced neurotoxicity. Transplant Rev, 20: 49–60. https://doi.org/10.1016/j.trre.2006.02.005

[87]

Anghel D, Tanasescu R, Campeanu A, et al., 2013, Neurotoxicity of immunosuppressive therapies in organ transplantation. Maedica, 8: 170–175. 

[88]

De Castro JT, Appenzeller S, Colella MP, et al., 2022, Neurological manifestations in thrombotic microangiopathy: Imaging features, risk factors and clinical course. PLoS One, 17: e0272290. https://doi.org/10.1371/journal.pone.0272290

[89]

Mohammadi MH, Salarzaei M, Parooie F, 2019, Neurological complications after renal transplantation: A systematic review and meta‐analysis. Ther Aph Dial, 23: 518–528. https://doi.org/10.1111/1744-9987.12838

[90]

Faravelli I, Velardo D, Podestà MA, et al., 2021, Immunosuppression-related neurological disorders in kidney transplantation. J Nephrol, 34: 539–555. https://doi.org/10.1007/s40620-020-00956-1

[91]

Bayer G, von Tokarski F, Thoreau B, et al., 2019, Etiology and outcomes of thrombotic microangiopathies. Clin J Am Soc Nephrol, 14: 557–566. https://doi.org/10.2215/CJN.11470918 

[92]

Sakhuja V, Sud K, Kalra OP, et al., 2001, Central nervous system complications in renal transplant recipients in a tropical environment. J Neurol Sci, 183: 89–93. https://doi.org/10.1016/s0022-510x(00)00485-8

[93]

Mahale P, Shiels MS, Lynch CF, et al., 2018, Incidence and outcomes of primary central nervous system lymphoma in solid organ transplant recipients. Am J Transplant, 18: 453–461. https://doi.org/10.1111/ajt.14465

[94]

Snanoudj R, Durrbach A, Leblond V, et al., 2003, Primary brain lymphomas after kidney transplantation: Presentation and outcome. Transplantation, 76: 930–937. https://doi.org/10.1097/01.TP.0000079253.06061.52

[95]

DeAngelis LM, 1999, Primary central nervous system lymphoma. J Neurol Neurosurg Psychiatry, 66: 699–701. https://doi.org/10.1136/jnnp.66.6.699

[96]

Power A, Chan K, Singh SK, et al., 2012, Appraising stroke risk in maintenance hemodialysis patients: A large single-center cohort study. Am J Kidney Dis, 59: 249–257. https://doi.org/10.1053/j.ajkd.2011.07.016

[97]

Toyoda K, Ninomiya T, 2014, Stroke and cerebrovascular diseases in patients with chronic kidney disease. Lancet Neurol, 13: 823–833. https://doi.org/10.1016/S1474-4422(14)70026-2

[98]

Conrad J, Pawlowski M, Dogan M, et al., 2013, Seizures after cerebrovascular events: Risk factors and clinical features. Seizure, 22: 275–282. https://doi.org/10.1016/j.seizure.2013.01.014

[99]

Tietjen DP, Moore J Jr., Gouge SF, 1987, Hemodialysis-associated acute subdural hematoma. Am J Nephrol, 7: 478–481. https://doi.org/10.1159/000167526 

[100]

Kumar A, Cage A, Dhar R, 2015, Dialysis-induced worsening of cerebral edema in intracranial hemorrhage: A case series and clinical perspective. Neurocrit Care, 22: 283–287. https://doi.org/10.1007/s12028-014-0063-z 

[101]

Chen J, Ye H, Zhang J, et al., 2022, Pathogenesis of seizures and epilepsy after stroke. Acta Epileptologica, 4: 2. https://doi.org/10.1186/s42494-021-00068-8

[102]

Baumgaertel MW, Kraemer M, Berlit P, 2014, Neurologic complications of acute and chronic renal disease. Handb Clin Neurol, 119: 383–393. https://doi.org/10.1016/B978-0-7020-4086-3.00024-2

[103]

Hart LA, Sibai BM, 2013, Seizures in pregnancy: Epilepsy, eclampsia, and stroke. Semin Perinatol, 37: 207–224. https://doi.org/10.1053/j.semperi.2013.04.001

[104]

Sterns RH, 2015, Disorders of plasma sodium-causes, consequences, and correction. N Engl J Med, 372: 55–65. https://doi.org/10.1056/NEJMra1404489

[105]

Nardonea R, Brigoc F, Trinkaa E, 2016, Acute symptomatic seizures caused by electrolyte disturbances. J Clin Neurol, 12: 21–33. https://doi.org/10.3988/jcn.2016.12.1.21

[106]

Chen BB, Prasad C, Kobrzynski M, et al., 2016, Seizures related to hypomagnesemia: A case series and review of the literature. Child Neurol Open, 3: 2329048X16674834. https://doi.org/10.1177/2329048X1667483 

[107]

Gasparini S, Ferlazzo E, Sueri C, et al., 2019, Hypertension, seizures, and epilepsy: A review on pathophysiology and management. Neurol Sci, 40: 1775–1783. https://doi.org/10.1007/s10072-019-03913-4

[108]

Miller JB, Suchdev K, Jayaprakash N, et al., 2018, New developments in hypertensive encephalopathy. Curr Hypertens Rep, 20(2): 13. https://doi.org/10.1007/s11906-018-0813-y

[109]

Unger T, Borghi C, Charchar F, et al., 2020, 2020 International Society of Hypertension global hypertension practice guidelines. Hypertension, 75: 1334–1357. https://doi.org/10.1161/HYPERTENSIONAHA.120.15026 

[110]

Alhilali LM, Reynolds AR, Fakhran S, 2014, A multidisciplinary model of risk factors for fatal outcome in posterior reversible encephalopathy syndrome. J Neurol Sci, 347: 59–65. https://doi.org/10.1016/j.jns.2014.09.019 

[111]

Li R, Mitchell P, Dowling R, et al., 2013, Is hypertension predictive of clinical recurrence in posterior reversible encephalopathy syndrome? J Clin Neurosci, 20: 248–252. https://doi.org/10.1016/j.jocn.2012.02.023

[112]

Winkelmayer WC, Mehta J, Wang PS, 2007, Benzodiazepine use and mortality of incident dialysis patients in the United States. Kidney Int, 72: 1388–1393. https://doi.org/10.1038/sj.ki.5002548 

[113]

Canavese C, Morellini V, Lazzarich E, et al., 2005, Seizures and renal failure: Is there a link? Nephrol Dial Transplant, 20: 2855–2857. https://doi.org/10.1093/ndt/gfi140

[114]

Barbour T, Johnson S, Cohney S, et al., 2012, Thrombotic microangiopathy and associated renal disorders. Nephrol Dial Transplant, 27: 2673–2685. https://doi.org/10.1093/ndt/gfs279

[115]

Hodzic E, Brcic M, Atic M, et al., 2014, Posterior reversible encephalopathy syndrome (PRES) as a complication of immunosuppressive therapy in renal transplantation in children. Med Arch, 68: 218–220. https://doi.org/10.5455/medarh.2014.68.218-220 

[116]

Piotrowski PC, Lutkowska A, Tsibulski A, et al., 2017, Neurologic complications in kidney transplant recipients. Folia Neuropathol, 55: 86–109. https://doi.org/10.5114/fn.2017.68577 

[117]

Delanty N, Vaughan CJ, French JA, 1998, Medical causes of seizures. Lancet, 352: 383–390. https://doi.org/10.1016/S0140-6736(98)02158-8

[118]

Fugate JE, Kalimullah EA, Hocker SE, et al., 2013, Cefepime neurotoxicity in the intensive care unit: A cause of severe, underappreciated encephalopathy. Crit Care, 17: R264. https://doi.org/10.1186/cc13094 

[119]

Nalesnik MA, 2001, The diverse pathology of post-transplant lymphoproliferative disorders: The importance of a standardized approach. Transpl Infect Dis, 3: 88–96. https://doi.org/10.1034/j.1399-3062.2001.003002088.x

[120]

Cavaliere R, Petroni G, Lopes MB, et al., 2010, Primary central nervous system post‐transplantation lymphoproliferative disorder: An international primary central nervous system lymphoma collaborative group report. Cancer, 116: 863–870. https://doi.org/10.1002/cncr.24834

[121]

Hughes S, Szeki I, Nash MJ, et al., 2014, Anticoagulation in chronic kidney disease patients-the practical aspects. Clin Kidney J, 7: 442–449. https://doi.org/10.1093/ckj/sfu080 

[122]

Malhotra K, Ishfaq MF, Goyal N, et al., 2019, Oral anticoagulation in patients with chronic kidney disease: A systematic review and meta-analysis. Neurology, 92: e2421–e2431. https://doi.org/10.1212/WNL.0000000000007534 

[123]

Vinters HV, Magaki SD, Williams CK, 2021, Neuropathologic findings in chronic kidney disease (CKD). J Stroke Cerebrovasc Dis, 30: 105657. https://doi.org/10.1016/j.jstrokecerebrovasdis.2021.105657 

[124]

Lionaki S, Hogan SL, Jennette CE, et al., 2009, The clinical course of ANCA small-vessel vasculitis on chronic dialysis. Kidney Int, 76: 644–651. https://doi.org/10.1038/ki.2009.218 

[125]

Nayak-Rao S, Shenoy MP, 2017, Stroke in patients with chronic kidney disease: How do we approach and manage it? Indian J Nephrol, 27: 167–171. https://doi.org/10.4103/0971-4065.202405 

[126]

Kerr PG, Toussaint ND, 2013, KHA‐CARI guideline: Dialysis adequacy (haemodialysis): Dialysis membranes. Nephrology, 18: 485–488. https://doi.org/10.1111/nep.12096

[127]

Jin DC, Yun SR, Lee SW, et al., 2018, Current characteristics of dialysis therapy in Korea: 2016 registry data focusing on diabetic patients. Kidney Res Clin Pract, 37: 20–29. https://doi.org/10.23876/j.krcp.2018.37.1.20

[128]

Peixoto AJ, 2019, Acute severe hypertension. New Engl J Med, 381: 1843–1852. https://doi.org/10.1056/NEJMcp1901117

[129]

Diaz A, Deliz B, Benbadis SR, 2012, The use of newer antiepileptic drugs in patients with renal failure. Expert Rev Neurother, 12: 99–105. https://doi.org/10.1586/ern.11.181

[130]

Ashley C, Dunleavy A. 2018. The Renal Drug Handbook: The Ultimate Prescribing Guide for Renal Practitioners. 5th ed. Boca Raton, Florida, United States: CRC Press. p1–1108. 

[131]

Asconapé JJ, 2014, Use of antiepileptic drugs in hepatic and renal disease. Handb Clin Neurol, 119: 417–432. https://doi.org/10.1016/B978-0-7020-4086-3.00027-8 

[132]

Mintzer S, Skidmore CT, Abidin CJ, et al., 2009, Effects of antiepileptic drugs on lipids, homocysteine, and C‐reactive protein. Ann Neurol, 65: 448–456. https://doi.org/10.1002/ana.21615 

[133]

Vyas MV, Davidson BA, Escalaya L, et al., 2015, Antiepileptic drug use for treatment of epilepsy and dyslipidemia: Systematic review. Epilepsy Res, 113: 44–67. https://doi.org/10.1016/j.eplepsyres.2015.03.002

[134]

Hesselink JM, Kopsky DJ, 2017, Phenytoin: 80 years young, from epilepsy to breast cancer, a remarkable molecule with multiple modes of action. J Neurol, 264: 1617–1621. https://doi.org/10.1007/s00415-017-8391-5 

[135]

Bansal AD, Hill CE, Berns JS, 2015, Use of antiepileptic drugs in patients with chronic kidney disease and end stage renal disease. Semin Dial, 28: 404–412. https://doi.org/10.1111/sdi.12385

[136]

Roberts WL, De BK, Coleman JP, et al., 1999, Falsely increased immunoassay measurements of total and unbound phenytoin in critically ill uremic patients receiving fosphenytoin. Clin Chem, 45: 829–837.

[137]

Czapinski P, Blaszczyk B, Czuczwar SJ, 2005, Mechanisms of action of antiepileptic drugs. Curr Top Med Chem, 5: 3–14. https://doi.org/10.2174/1568026053386962

[138]

Patsalos PN, Berry DJ, Bourgeois BF, et al., 2008, Antiepileptic drugs--best practice guidelines for therapeutic drug monitoring: A position paper by the subcommission on therapeutic drug monitoring, ILAE Commission on Therapeutic Strategies. Epilepsia, 49: 1239–1276. https://doi.org/10.1111/j.1528-1167.2008.01561.x

[139]

Israni RK, Kasbekar N, Haynes K, et al., 2006, Use of antiepileptic drugs in patients with kidney disease. Semin Dial, 19: 408–416. https://doi.org/10.1111/j.1525-139X.2006.00195.x

[140]

Lee CS, Marbury TC, Perchalski RT, et al., 1982, Pharmacokinetics of primidone elimination by uremic patients. J Clin Pharmacol, 22: 301–308. https://doi.org/10.1002/j.1552-4604.1982.tb02679.x

[141]

Streete JM, Berry DJ, Jones JA, et al., 1990, Clearance of phenylethylmalonamide during haemodialysis of a patient with renal failure. Ther Drug Monit, 12: 281–283. https://doi.org/10.1097/00007691-199005000-00012

[142]

Dichter MA, Brodie MJ, 1996, New antiepileptic drugs. New Engl J Med, 334: 1583–1590. https://doi.org/10.1056/NEJM199606133342407

[143]

Ambrósio AF, Soares-da-Silva P, Carvalho CM, et al., 2002, Mechanisms of action of carbamazepine and its derivatives, oxcarbazepine, BIA 2-093, and BIA 2-024. Neurochem Res, 27: 121–130. https://doi.org/10.1023/a:1014814924965

[144]

Guerreiro CA, Guerreiro MM, Mintzer S, 2015, Carbamazepine, oxcarbazepine, and eslicarbazepine. In: The Treatment of Epilepsy: Principles and Practice. 6th ed. Philadelphia, PA: Wolters Kluwer. p615–625.

[145]

Almeida L, Soares-da-Silva P, 2007, Eslicarbazepine acetate (BIA 2-093). Neurotherapeutics, 4: 88–96. https://doi.org/10.1016/j.nurt.2006.10.005

[146]

Kandrotas RJ, Love JM, Gal P, et al., 1990, The effect of hemodialysis and hemoperfusion on serum valproic acid concentration. Neurology, 40: 1456. https://doi.org/10.1212/wnl.40.9.1456

[147]

Gillard M, Chatelain P, Fuks B, 2006, Binding characteristics of levetiracetam to synaptic vesicle protein 2A (SV2A) in human brain and in CHO cells expressing the human recombinant protein. Eur J Pharmacol, 536: 102–108. https://doi.org/10.1016/j.ejphar.2006.02.022

[148]

Lynch BA, Lambeng N, Nocka K, et al., 2004, The synaptic vesicle protein SV2A is the binding site for the antiepileptic drug levetiracetam. Proc Natl Acad Sci, 101: 9861–9866. https://doi.org/10.1073/pnas.0308208101

[149]

Chang WP, Südhof TC, 2009, SV2 renders primed synaptic vesicles competent for Ca2+-induced exocytosis. J Neurosci, 29: 883–897. https://doi.org/10.1523/JNEUROSCI.4521-08.2009

[150]

Deshpande LS, DeLorenzo RJ, 2014, Mechanisms of levetiracetam in the control of status epilepticus and epilepsy. Front Neurol, 5: 11. https://doi.org/10.3389/fneur.2014.00011

[152]

Carunchio I, Pieri M, Ciotti MT, et al., 2007, Modulation of AMPA receptors in cultured cortical neurons induced by the antiepileptic drug levetiracetam. Epilepsia, 48: 654–662. https://doi.org/10.1111/j.1528-1167.2006.00973.x

[153]

Zona C, Pieri M, Carunchio I, et al., 2010, Brivaracetam (ucb 34714) inhibits Na+current in rat cortical neurons in culture. Epilepsy Res, 88: 46–54. https://doi.org/10.1016/j.eplepsyres.2009.09.024

[154]

Klitgaard H, Matagne A, Nicolas JM, et al., 2016, Brivaracetam: Rationale for discovery and preclinical profile of a selective SV 2A ligand for epilepsy treatment. Epilepsia, 57: 538–548. https://doi.org/10.1111/epi.13340

[155]

Nicolas JM, Hannestad J, Holden D, et al., 2016, Brivaracetam, a selective high‐affinity synaptic vesicle protein 2A (SV 2A) ligand with preclinical evidence of high brain permeability and fast onset of action. Epilepsia, 57: 201–209. https://doi.org/10.1111/epi.13267

[156]

Rolan P, Sargentini‐Maier ML, Pigeolet E, et al., 2008, The pharmacokinetics, CNS pharmacodynamics and adverse event profile of brivaracetam after multiple increasing oral doses in healthy men. Br J Clin Pharmacol, 66: 71–75. https://doi.org/10.1111/j.1365-2125.2008.03158.x

[157]

Rosenfeld WE, 1997, Topiramate: A review of preclinical, pharmacokinetic, and clinical data. Clin Ther, 19: 1294–1308. https://doi.org/10.1016/s0149-2918(97)80006-9

[157]

Lamb EJ, Stevens PE, Nashef L, 2004, Topiramate increases biochemical risk of nephrolithiasis. Ann Clin Biochem, 41: 166–169. https://doi.org/10.1258/000456304322880104

[158]

Leppik IE, 2004, Zonisamide: Chemistry, mechanism of action, and pharmacokinetics. Seizure, 13: S5-S9. https://doi.org/10.1016/j.seizure.2004.04.016 

[159]

Ijiri Y, Inoue T, Fukuda F, et al., 2004, of the antiepileptic drug zonisamide in patients undergoing hemodialysis. Epilepsia, 45: 924–927. https://doi.org/10.1111/j.0013-9580.2004.30603.x 

[160]

Rogawski MA, Tofighy A, White HS, et al., 2015, Current understanding of the mechanism of action of the antiepileptic drug lacosamide. Epilepsy Res, 110: 189–205. https://doi.org/10.1016/j.eplepsyres.2014.11.021

[161]

Jo S, Bean BP, 2017, Lacosamide inhibition of Nav1. 7 voltage-gated sodium channels: Slow binding to fast-inactivated states. Mol Pharmacol, 91: 277–286. https://doi.org/10.1124/mol.116.106401

[162]

Cawello W, Fuhr U, Hering U, et al., 2013, Impact of impaired renal function on the pharmacokinetics of the antiepileptic drug lacosamide. Clin Pharmacokinet, 52: 897–906. https://doi.org/10.1007/s40262-013-0080-7

[163]

Goa KL, Ross SR, Chrisp P, 1993, Lamotrigine. Drugs, 46: 152–176. https://doi.org/10.2165/00003495-199346010-00009 

[164]

Wootton R, Soul‐Lawton J, Rolan PE, et al., 1997, Comparison of the pharmacokinetics of lamotrigine in patients with chronic renal failure and healthy volunteers. Br J Pharmacol, 43: 23–27. https://doi.org/10.1111/j.1365-2125.1997.tb00028.x

[165]

Smetana KS, Cook AM, Bastin ML, et al., 2016, Antiepileptic dosing for critically ill adult patients receiving renal replacement therapy. J Crit Care, 36: 116–124. https://doi.org/10.1016/j.jcrc.2016.06.023

[166]

Perucca P, Dopp JM, editors. 2015, Gabapentin and pregabalin. In: Wyllie’s Treatment of Epilepsy: Principles and Practice. Philadelphia, PA: Lippincott Williams and Wilkins. p647–657. 

[167]

Ochs HR, Greenblatt DJ, Kaschell HJ, et al., 1981, Diazepam kinetics in patients with renal insufficiency or hyperthyroidism. Br J Pharmacol, 12: 829–832. https://doi.org/10.1111/j.1365-2125.1981.tb01315.x

[168]

Sankar R, 2012, GABAA receptor physiology and its relationship to the mechanism of action of the 1, 5-benzodiazepine clobazam. CNS Drugs, 26: 229–244. https://doi.org/10.2165/11599020-000000000-00000 

[169]

Kuo CC, Lin BJ, Chang HR, et al., 2004, Use-dependent inhibition of the N-methyl-D-aspartate currents by felbamate: A gating modifier with selective binding to the desensitized channels. Mol Pharmacol, 65: 370–380. https://doi.org/10.1124/mol.65.2.370

[170]

McCabe RT, Wasterlain CG, Kucharczyk NO, et al., 1993, Evidence for anticonvulsant and neuroprotectant action of felbamate mediated by strychnine-insensitive glycine receptors. J Pharmacol Exp Ther, 264: 1248–1252.

[171]

Sparagana SP, Strand WR, Adams RC, 2001, Felbamate urolithiasis. Epilepsia, 42: 682–685. https://doi.org/10.1046/j.1528-1157.2001.32500.x 

[172]

White HS, 1999, Comparative anticonvulsant and mechanistic profile of the established and newer antiepileptic drugs. Epilepsia, 40: S2–S10. https://doi.org/10.1111/j.1528-1157.1999.tb00913.x

[173]

Marbury TC, Lee CS, Perchalski RJ, et al., 1981, Hemodialysis clearance of ethosuximide in patients with chronic renal disease. Am J Hosp Pharm, 38: 1757–1760. 

[174]

Marquardt ED, Ishisaka DY, Batra KK, et al., 1992, Removal of ethosuximide and phenobarbital by peritoneal dialysis in a child. Clin Pharm, 11: 1030–1031.

[175]

Adkins JC, Noble S, 1998, Tiagabine. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in the management of epilepsy. Drugs, 55: 437–460. https://doi.org/10.2165/00003495-199855030-00013

[176]

Grant SM, Heel RC, 1991, Vigabatrin. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in epilepsy and disorders of motor control. Drugs, 41: 889–926. https://doi.org/10.2165/00003495-199141060-00007

[177]

McLean MJ, Schmutz M, Pozza M, et al., 2005, The influence of rufinamide on sodium currents and action potential firing in rodent neurons. Epilepsia, 46: 296. 

[178]

Rogawski MA, Hanada T, 2013, Preclinical pharmacology of perampanel, a selective non‐competitive AMPA receptor antagonist. Acta Neurol Scand Suppl, 127: 19–24. https://doi.org/10.1111/ane.12100 

[179]

Hanada T, Hashizume Y, Tokuhara N, et al., 2011, Perampanel: A novel, orally active, noncompetitive AMPA‐receptor antagonist that reduces seizure activity in rodent models of epilepsy. Epilepsia, 52: 1331–1340. https://doi.org/10.1111/j.1528-1167.2011.03109.x

Share
Back to top
Advanced Neurology, Electronic ISSN: 2810-9619 Print ISSN: 3060-8589, Published by AccScience Publishing