

Нервная система и почки. Перекрестные механизмы взаимодействия в норме и при патологии
https://doi.org/10.36485/1561-6274-2023-27-2-29-38
Аннотация
В физиологических состояниях нервная система и почки взаимодействуют друг с другом для поддержания нормального гомеостаза. Однако патологические состояния, такие как гипертоническая болезнь, патология самой почки как острое, так и хроническое, нарушают это взаимодействие. При остром повреждении почек (ОПП) различной этиологии и хронической болезни почек (ХБП) поврежденные почки могут оказывать существенное влияние на функцию центральной нервной системы. ХБП является независимым фактором риска развития цереброваскулярных заболеваний и когнитивных нарушений, обусловленны многими факторами, включая задержку уремических токсинов и фосфатов, были предложены в качестве специфических для ХБП факторов, ответственных за структурные и функциональные церебральные изменения у пациентов с ХБП, тем не менее необходимы дополнительные исследования для определения точного патогенеза. Наш обзор посвящается взаимодействию почки и нервной системы в физиологических условиях и при патофизиологических состояниях, пытаемся подробно раскрыть механизмы дисфункции нервной системы при патологиях почек.
Об авторах
Ф. А. ЮсуповКыргызстан
Юсупов Фуркат Абдулахатович, Проф. д-р мед наук, зав. кафедрой
714000, , г. Ош, ул. Ленина, д. 331
Тел.: (+996) 557202071
А. А. Юлдашев
Россия
Юлдашев Акмал Акбарович, Аспирант
714000, , г. Ош, ул. Ленина, д. 331
Тел.: (+996) 559062491
Список литературы
1. Coresh J, Selvin E, Stevens LA et al. Prevalence of chronic kidney disease in the United States. JAMA 2007 Nov 7;298(17):2038–2047. doi: 10.1001/jama.298.17.2038
2. Kurella M, Chertow GM, Fried LF et al. Chronic kidney disease and cognitive impairment in the elderly: the health, aging, and body composition study. J Am Soc Nephrol 2005;16(7):2127–2133. doi: 10.1681/ASN.2005010005
3. Yaffe K, Ackerson L, Kurella Tamura M et al. Chronic kidney disease and cognitive function in older adults: findings from the chronic renal insufficiency cohort cognitive study. J Am Geriatr Soc 2010;58(2):338–345. doi: 10.1111/j.1532-5415.2009.02670.x
4. Chertow GM, Burdick E, Honour M et al. Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol 2005;16(11):3365–3370. doi: 10.1681/ASN.2004090740
5. Susantitaphong P, Cruz DN, Cerda J et al. Clin J Am Soc Nephrol 2013;8(9):1482–1493. doi: 10.2215/CJN.00710113
6. Grams ME, Rabb H. The distant organ effects of acute kidney injury. Kidney Int 2012;81(10):942–948. doi: 10.1038/ki.2011.241
7. Wu VC, Wu PC, Wu CH, Huang TM, Chang CH, Tsai PR et al. The impact of acute kidney injury on the long-term risk of stroke. J Am Heart Assoc 2014;3(4):e000933. doi: 10.1161/JAHA.114.000933
8. Guerra C, Linde-Zwirble WT, Wunsch H. Risk factors for dementia after critical illness in elderly Medicare beneficiaries. Crit Care 2012;16(6):R233. doi: 10.1186/cc11901
9. Tsai HH, Yen RF, Lin CL, Kao CH. Increased risk of dementia in patients hospitalized with acute kidney injury: A nationwide population-based cohort study. PLoS One 2017;12(2):e017167. doi: 10.1371/journal.pone.0171671
10. Tanaka S, & Okusa, M.D. Crosstalk between the nervous system and the kidney. Kidney international 2020; 97(3): 466–476. doi: 10.1016/j.kint.2019.10.032
11. Robertson GL. Physiology of ADH secretion. Kidney Int Suppl 1987;21:S20–26
12. Antunes-Rodrigues J, de Castro M, Elias LL et al. Neuroendocrine control of body fluid metabolism. Physiol Rev 2004;84(1):169–208. doi: 10.1152/physrev.00017.2003
13. Agre P. Homer W. Smith award lecture. Aquaporin water channels in kidney. J Am Soc Nephrol 2000;11(4):764–777. doi: 10.1681/ASN.V114764
14. Kopp UC. Role of renal sensory nerves in physiological and pathophysiological conditions. Am J Physiol Regul Integr Comp Physiol 2015;308(2):R79–95. doi: 10.1152/ajpregu.00351.2014
15. Marfurt CF, Echtenkamp SF. Sensory innervation of the rat kidney and ureter as revealed by the anterograde transport of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) from dorsal root ganglia. J Comp Neurol 1991;311(3):389–404
16. Colindres RE, Spielman WS, Moss NG et al. Functional evidence for renorenal reflexes in the rat. Am J Physiol 1980;239(3):F265–270
17. Kopp UC, Smith LA. Role of prostaglandins in renal sensory receptor activation by substance P and bradykinin. Am J Physiol 1993;265(3 Pt 2):R544–551
18. Kopp UC, Cicha MZ, Smith LA et al. Dietary sodium modulates the interaction between efferent and afferent renal nerve activity by altering activation of alpha2-adrenoceptors on renal sensory nerves. Am J Physiol Regul Integr Comp Physiol 2011;300(2):R298–310. doi: 10.1152/ajpregu.00469.2010
19. Kopp UC, Cicha MZ, Smith LA et al. Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE2dependent activation of alpha1- and alpha2- adrenoceptors on renal sensory nerve fibers. Am J Physiol Regul Integr Comp Physiol 2007;293(4):R1561–1572. doi: 10.1152/ajpregu.00485.2007
20. Niijima A. The effect of efferent discharges in renal nerves on the activity of arterial mechanoreceptors in the kidney in rabbit. The Journal of physiology 1972;222(2):335–343
21. Kopp UC, Cicha MZ, Smith LA. Endogenous angiotensin modulates PGE(2)-mediated release of substance P from renal mechanosensory nerve fibers. Am J Physiol Regul Integr Comp Physiol 2002;282(1):R19–30. doi: 10.1152/ajpregu.2002.282.1.R19
22. Kopp UC, Cicha MZ, Smith LA. Angiotensin blocks substance P release from renal sensory nerves by inhibiting PGE2-mediated activation of cAMP. Am J Physiol Renal Physiol 2003;285(3):F472–483. doi: 10.1152/ajprenal.00399.2002
23. Kopp UC, Grisk O, Cicha MZ et al. Dietary sodium modulates the interaction between efferent renal sympathetic nerve activity and afferent renal nerve activity: role of endothelin. Am J Physiol Regul Integr Comp Physiol 2009;297(2):R337–351. doi: 10.1152/ajpregu.91029.2008
24. Kopp UC, Cicha MZ, Smith LA. Differential effects of endothelin on activation of renal mechanosensory nerves: stimulatory in high-sodium diet and inhibitory in low-sodium diet. Am J Physiol Regul Integr Comp Physiol 2006;291(5):R1545–1556. doi: 10.1152/ajpregu.00878.2005
25. Malpas SC. Sympathetic nervous system overactivity and its role in the development of cardiovascular disease. Physiol Rev 2010;90(2):513–557. doi: 10.1152/physrev.00007.2009
26. Johns EJ, Kopp UC, DiBona GF. Neural control of renal function. Compr Physiol 2011;1(2):731–767. doi: 10.1002/cphy.c100043
27. Kopp UC, Cicha MZ, Smith LA. Impaired interaction between efferent and afferent renal nerve activity in SHR involves increased activation of alpha2-adrenoceptors. Hypertension 2011 Mar;57(3):640–647. doi: 10.1161/HYPERTEN-SIONAHA.110.166595
28. Kopp UC, Cicha MZ. Impaired substance P release from renal sensory nerves in SHR involves a pertussis toxinsensitive mechanism. Am J Physiol Regul Integr Comp Physiol 2004;286(2):R326–333. doi: 10.1152/ajpregu.00493.2003
29. Kopp UC, Cicha MZ, Yorek MA. Impaired responsiveness of renal sensory nerves in streptozotocin-treated rats and obese Zucker diabetic fatty rats: role of angiotensin. Am J Physiol Regul Integr Comp Physiol 2008;294(3):R858–866. doi: 10.1152/ajpregu.00830.2007
30. Kopp UC, Cicha MZ, Smith LA. Impaired responsiveness of renal mechanosensory nerves in heart failure: role of endogenous angiotensin. Am J Physiol Regul Integr Comp Physiol 2003;284(1):R116–124. doi: 10.1152/ajpregu.00336.2002
31. Chien CT, Fu TC, Wu MS, Chen CF. Attenuated response of renal mechanoreceptors to volume expansion in chronically hypoxic rats. Am J Physiol 1997;273(5):F712–17
32. Ma MC, Huang HS, Chen CF. Impaired renal sensory responses after unilateral ureteral obstruction in the rat. J Am Soc Nephrol 2002;13(4):1008–1016. doi: 10.1681/ASN.V1341008
33. Ma MC, Huang HS, Chien CT, Wu MS, Chen CF. Temporal decrease in renal sensory responses in rats after chronic ligation of the bile duct. Am J Physiol Renal Physiol 2002;283(1):F164–172. doi: 10.1152/ajprenal.00231.2001
34. Ma MC, Huang HS, Wu MS, Chien CT, Chen CF. Impaired renal sensory responses after renal ischemia in the rat. J Am Soc Nephrol 2002;13(7):1872–1883. doi: 10.1097/01.asn.0000022009.44473.56
35. Kopp UC, Buckley-Bleiler RL. Impaired renorenal reflexes in two-kidney, one clip hypertensive rats. Hypertension 1989;14(4):445–452
36. Katholi RE, Hageman GR, Whitlow PL, Woods WT. Hemodynamic and afferent renal nerve responses to intrarenal adenosine in the dog. Hypertension 1983;5(2 Pt 2):I149–154
37. Katholi RE, Whitlow PL, Hageman GR, Woods WT. Intrarenal adenosine produces hypertension by activating the sympathetic nervous system via the renal nerves in the dog. J Hypertens 1984;2(4):349–359
38. Bhatt DL, Kandzari DE, O’Neill WW et al. A controlled trial of renal denervation for resistant hypertension. The New England journal of medicine 2014;370(15):1393–1401. doi: 10.1056/NEJMoa1402670
39. Esler MD, Krum H, Schlaich M et al. Renal sympathetic denervation for treatment of drug-resistant hypertension: one-year results from the Symplicity HTN-2 randomized, controlled trial. Circulation 2012;126(25):2976–2982. doi: 10.1161/CIRCULA-TIONAHA.112.130880
40. Kandzari DE, Bhatt DL, Brar S et al. Predictors of blood pressure response in the SYMPLICITY HTN-3 trial. Eur Heart J 2015;36(4):219–227. doi: 10.1093/eurheartj/ehu441
41. Symplicity HTNI. Catheter-based renal sympathetic denervation for resistant hypertension: durability of blood pressure reduction out to 24 months. Hypertension 2011;57(5):911–917. doi: 10.1161/HYPERTENSIONAHA.110.163014
42. Ito S, Nagasawa T, Abe M, Mori T. Strain vessel hypothesis: a viewpoint for linkage of albuminuria and cerebro-cardiovascular risk. Hypertens Res 2009;32(2):115–121. doi: 10.2215/CJN.00710113
43. Муркамилов ИТ и др. Диабетическая нефропатия: распространенность и факторы риска. Вестник Волгоградского государственного медицинского университета 2021;1(77)
44. Айтбаев КА, Му ркамилов ИТ, Фомин ВВ и др. Роль эпигенетических механизмов в патогенезе диабетической нефропатии. Нефрология 2021;25(2):35–42. https://doi.org/10.36485/1561-6274-2021-25-2-35-42 https://doi.org/10.36485/1561-6274-2021-25-2-35-42
45. Кинванлун ИГ и др. Клинико-функциональная характеристика допплерографической картины почек. The Scientific Heritage 2021;67(2):39–45
46. Муркамилов ИТ и др. Бета-2-микроглобулин как биомаркер при хронической болезни почек. The Scientific Heritage 2021;59(2)
47. Муркамилов ИТ и др. Вторичная профилактика хронической болезни почек: ренопротективный потенциал блокатора рецепторов ангиотензина II телмисартана. The Scientific Heritage 2021;63(2)
48. Муркамилов ИТ и др. Факторы риска развития инсульта у пациентов с терминальной стадией хронической болезни почек: современное состояние проблемы. Казанский медицинский журнал 2020;101(6):825–833
49. Муркамилова ЖА и др. Цистатин С и жесткость сосудов как маркеры нефро-и цереброваскулярных заболеваний у лиц пожилого и старческого возраста. Вестник Кыргызско- Российского Славянского университета 2020;20(5):34–44
50. Муркамилова ЖА и др. Структурно-функциональное состояние сосудов и эндотелиальная дисфункция при хронической болезни почек у больных пожилого и старческого возраста. The Scientific Heritage 2021;58(2):52–58
51. Муркамилов ИТ и др. Клинико-патогенетические аспекты формирования хронической болезни почек при хронической обструктивной болезни легких. The Scientific Heritage 2020;55(2):18–26
52. Debette S, Markus HS. The clinical importance of white matter hyperintensities on brain magnetic resonance imaging: systematic review and meta-analysis. BMJ 2010;341:c3666. doi: 10.1136/bmj.c3666
53. Khatri M, Wright CB, Nickolas TL et al. Chronic kidney disease is associated with white matter hyperintensity volume: the Northern Manhattan Study (NOMAS). Stroke 2007;38(12):3121–3126. doi: 10.1161/STROKEAHA.107.493593
54. Weiner DE, Bartolomei K, Scott T et al. Albuminuria, cognitive functioning, and white matter hyperintensities in homebound elders. Am J Kidney Dis 2009;53(3):438–447. doi: 10.1053/j.ajkd.2008.08.022
55. Seliger SL, Siscovick DS, Stehman-Breen CO et al. Moderate renal impairment and risk of dementia among older adults: the Cardiovascular Health Cognition Study. J Am Soc Nephrol 2004;15(7):1904–1911. doi: 10.1097/01.asn.0000131529.60019.fa
56. Watanabe K, Watanabe T, Nakayama M. Cerebro-renal interactions: impact of uremic toxins on cognitive function. Neurotoxicology 2014;44:184–193. doi: 10.1016/j.neuro.2014.06.014
57. De Deyn PP, Vanholder R, D’Hooge R. Nitric oxide in uremia: effects of several potentially toxic guanidino compounds. Kidney Int Suppl 2003(84):S25–28. doi: 10.1046/j.1523-1755.63.s84.9.x
58. D’Hooge R, Van de Vijver G, Van Bogaert PP et al. Involvement of voltage- and ligand-gated Ca2+ channels in the neuroexcitatory and synergistic effects of putative uremic neurotoxins. Kidney Int 2003;63(5):1764–1775. doi: 10.1046/j.1523-1755.2003.00912.x
59. Six I, Maizel J, Barreto FC et al. Effects of phosphate on vascular function under normal conditions and influence of the uraemic state. Cardiovasc Res 2012;96(1):130–139
60. Jono S, McKee MD, Murry CE, Shioi A, Nishizawa Y, Mori K et al. Phosphate regulation of vascular smooth muscle cell calcification. Circ Res 2000;87(7):E10–17. doi: 10.1161/01.res.87.7.e10
61. Steitz SA, Speer MY, Curinga G et al. Smooth muscle cell phenotypic transition associated with calcification: upregulation of Cbfa1 and downregulation of smooth muscle lineage markers. Circ Res 2001;89(12):1147–1154. doi: 10.1161/hh2401.101070
62. Speer MY, Yang HY, Brabb T et al. Smooth muscle cells give rise to osteochondrogenic precursors and chondrocytes in calcifying arteries. Circ Res 2009;104(6):733–741. doi: 10.1161/CIRCRESAHA.108.183053
63. Tyson KL, Reynolds JL, McNair R et al. Osteo/chondrocytic transcription factors and their target genes exhibit distinct patterns of expression in human arterial calcification. Arterioscler Thromb Vasc Biol 2003;23(3):489–494. doi: 10.1161/01.ATV.0000059406.92165.31
64. Li X, Yang HY, Giachelli CM. Role of the sodium-dependent phosphate cotransporter, Pit-1, in vascular smooth muscle cell calcification. Circ Res 2006;98(7):905–912. doi: 10.1161/01.RES.0000216409.20863.e7
65. Crouthamel MH, Lau WL, Leaf EM et al. Sodium-dependent phosphate cotransporters and phosphate-induced calcification of vascular smooth muscle cells: redundant roles for PiT-1 and PiT-2. Arterioscler Thromb Vasc Biol 2013;33(11):2625–2632. doi: 10.1161/ATVBAHA.113.302249
66. Marebwa BK, Adams RJ, Magwood GS et al. Fibroblast growth factor23 is associated with axonal integrity and neural network architecture in the human frontal lobes. PLoS One 2018;13(9):e0203460. doi: 10.1371/journal.pone.0203460
67. Wright CB, Dong C, Stark M et al. Plasma FGF23 and the risk of stroke: the Northern Manhattan Study (NOMAS). Neurology 2014;82(19):1700–1706. doi: 10.1212/WNL.0000000000000410
68. Wright CB, Shah NH, Mendez AJ et al. Fibroblast Growth Factor 23 Is Associated With Subclinical Cerebrovascular Damage: The Northern Manhattan Study. Stroke 2016;47(4):923–928. doi: 10.1161/STROKEAHA.115.012379
69. Muteliefu G, Enomoto A, Jiang P et al. Indoxyl sulphate induces oxidative stress and the expression of osteoblast-specific proteins in vascular smooth muscle cells. Nephrol Dial Transplant 2009;24(7):2051–2058. doi: 10.1186/2050-6511-14-60
70. Adijiang A, Goto S, Uramoto S et al. Indoxyl sulphate promotes aortic calcification with expression of osteoblastspecific proteins in hypertensive rats. Nephrol Dial Transplant 2008;23(6):1892–1901. doi: 10.1093/ndt/gfm861
71. Stinghen AE, Chillon JM, Massy ZA, Boullier A. Differential effects of indoxyl sulfate and inorganic phosphate in a murine cerebral endothelial cell line (bEnd.3). Toxins (Basel) 2014;6(6):1742–1760. doi: 10.3390/toxins6061742
72. Shroff R, Speer T, Colin S et al. HDL in children with CKD promotes endothelial dysfunction and an abnormal vascular phenotype. J Am Soc Nephrol 2014;25(11):2658–2668. doi: 10.1681/ASN.2013111212
73. Zewinger S, Speer T, Kleber ME et al. HDL cholesterol is not associated with lower mortality in patients with kidney dysfunction. J Am Soc Nephrol 2014;25(5):1073–1082. doi: 10.1681/ASN.2013050482
74. Speer T, Rohrer L, Blyszczuk P et al. Abnormal high-density lipoprotein induces endothelial dysfunction via activation of Tolllike receptor-2. Immunity 2013;38(4):754–768. doi: 10.1016/j.immuni.2013.02.009
75. Holzer M, Birner-Gruenberger R, Stojakovic T et al. Uremia alters HDL composition and function. J Am Soc Nephrol 2011;22(9):1631–1641. doi: 10.1681/ASN.2010111144
76. Liu M, Liang Y, Chigurupati S et al. Acute kidney injury leads to inflammation and functional changes in the brain. J Am Soc Nephrol 2008;19(7):1360–1370. doi: 10.1681/ASN.2007080901
77. Salama M, Farrag SM, Abulasrar S et al. Up-regulation of TLR-4 in the brain after ischemic kidney-induced encephalopathy in the rat. CNS Neurol Disord Drug Targets 2013;12(5):583–586. doi: 10.2174/1871527311312050006
78. Doi K, Ishizu T, Tsukamoto-Sumida M et al. The highmobility group protein B1-Toll-like receptor 4 pathway contributes to the acute lung injury induced by bilateral nephrectomy. Kidney Int 2014;86(2):316–326. doi: 10.1038/ki.2014.62
79. Adachi N, Lei B, Deshpande G et al. Uraemia suppresses central dopaminergic metabolism and impairs motor activity in rats. Intensive Care Med 2001;27(10):1655–1660. doi: 10.1007/s001340101067
80. Kim J, Padanilam BJ. Renal nerves drive interstitial fibrogenesis in obstructive nephropathy. J Am Soc Nephrol 2013;24(2):229–242. doi: 10.1681/ASN.2012070678
81. Kim J, Padanilam BJ. Renal denervation prevents longterm sequelae of ischemic renal injury. Kidney Int 2015;87(2):350–358. doi: 10.1038/ki.2014.300
82. Bernik TR, Friedman SG, Ochani M et al. Pharmacological stimulation of the cholinergic antiinflammatory pathway. J Exp Med 2002;195(6):781–788. doi: 10.1084/jem.20011714
83. Kramer AA, Postler G, Salhab KF et al. Renal ischemia/reperfusion leads to macrophage-mediated increase in pulmonary vascular permeability. Kidney Int 1999;55(6):2362–2367
84. Abe C, Inoue T, Inglis MA et al. C1 neurons mediate a stress-induced anti-inflammatory reflex in mice. Nat Neurosci 2017;20(5):700–707. doi: 10.1038/nn.4526
85. Guyenet PG, Stornetta RL, Bochorishvili G et al. C1 neurons: the body’s EMTs. Am J Physiol Regul Integr Comp Physiol 2013;305(3):R187–204. doi: 10.1152/ajpregu.00054.2013
86. Doi K, Rabb H. Impact of acute kidney injury on distant organ function: recent findings and potential therapeutic targets. Kidney Int 2016;89(3):555–564. doi: 10.1016/j.kint.2015.11.019
87. Gigliotti JC, Okusa MD. The spleen: the forgotten organ in acute kidney injury of critical illness. Nephron Clin Pract 2014;127(1–4):153–157. doi: 10.1159/000363255
88. Inoue T, Abe C, Kohro T et al. Non-canonical cholinergic anti-inflammatory pathway-mediated activation of peritoneal macrophages induces Hes1 and blocks ischemia/reperfusion injury in the kidney. Kidney Int 2019;95(3):563–576. doi: 10.1016/j.kint.2018.09.020
Рецензия
Для цитирования:
Юсупов Ф.А., Юлдашев А.А. Нервная система и почки. Перекрестные механизмы взаимодействия в норме и при патологии. Нефрология. 2023;27(2):29-38. https://doi.org/10.36485/1561-6274-2023-27-2-29-38
For citation:
Yusupov F.A., Yuldashev A.A. Nervous system and kidneys. Cross-mechanisms of interaction in normal and pathological conditions. Nephrology (Saint-Petersburg). 2023;27(2):29-38. (In Russ.) https://doi.org/10.36485/1561-6274-2023-27-2-29-38