The mechanisms of chronic kidney disease progression: evolution of views


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详细

Chronic kidney disease is an important medical and social problem that has a significant impact on disability and mortality worldwide. Progressive tubulointerstitial fibrosis is the heart of this pathology. it does not depend on the type of nephropathy. According to multiple studies, there is a strong correlation between tubulointerstitial fibrosis and decrease of glomerular filtration rate. The question about chronic kidney disease progression has been occupying one of the leading positions for several decades, because there is an urgent need to develop new diagnostic and treatment methods for management of CKD. This article discusses possible mechanisms for the progression of chronic kidney diseases, namely hemodynamic factors, proteinuria, the effects of hypoxia, the renin-angiotensin-aldosterone system, the epithelial-mesenchymal transition, as well as a number of growth factors.

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作者简介

L. Plenkina

Kirov State Medical University

Email: lidia.plenkina@gmail.com
postgraduate student in the field of clinical medicine Kirov, Russia

O. Simonova

Kirov State Medical University

Email: simonova043@mail.ru
Doctor of Medical Sciences, Head of the Department of Hospital Therapy Kirov, Russia

V. Rozinova

Kirov State Medical University

Email: kolobok_503@mail.ru
postgraduate student in the field of clinical medicine Kirov, Russia

参考

  1. Национальныерекомендации.Хроническаяболезньпочек:основныепринципы скрининга, диагностики, профилактики и подходы к лечению. Нефрология. 2012; 16(1):89-115
  2. Takaori K., Nakamura J., Yamamoto S., Nakata H., Sato Y., Takase M., Nameta M., Yamamoto T., Economides A.N., et al. Severity and frequency of proximal tubule injury determines renal prognosis. J. Am. Soc. Nephrol 2016;27(8):2393-2406. doi: 10.1681/ASN.2015060647.
  3. Shimamura T., Morrison A.B. A progressive glomerulosclerosis occurring in partial five-sixths nephrectomized rats. Am. J. Pathol. 1975;79(1):95-106.
  4. Brenner B.M., Meyer T.W., Hostetter T.H. Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease. N. Engl. J. Med.1982;307(11):652- 659. doi: 10.1056/NEJM198209093071104.
  5. Higashihara E., Horie S., Takeuchi T., Nutahara K., Aso Y.: Long-term consequence of nephrectomy. J. Urol. 1990;143(2):239-243. Doi: 10.1016/ s0022-5347(17)39922-6.
  6. Cravedi1 P., Remuzzi G. Pathophysiology of proteinuria and its value as an outcome measure in chronic kidney disease. Br. J. Clin. Pharmacol. 2013;76(4):516-523. doi: 10.1111/bcp.12104.
  7. Fine L.G., Bandy op adhay D., Norman J.T. Is there a common mechanism for the progression of different types of renal diseases other than proteinuria ? Towards the unifying theme of chronic hypoxia. Kidney Int. 2000;57(75):22-26. Doi: https://doi.org/10.1046/j.1523-1755.2000.07512.x.
  8. Loeffler I., Wolf G. Transforming growth factor-в and the progression of renal disease. Nephrol. Dial. Transplant. 2014;29(1):37-45. doi: 10.1093/ndt/gft267.
  9. Tan R.J., Zhou D., Zhou L, Liu Y. Wnt/e-catenin signaling and kidney fibrosis. Kidney Int. 2014;4(1):84-90. doi: 10.1038/kisup.2014.16.
  10. Liu M, Ning X., Li R., Yang Z., Yang X., Sun S., Qian Q. Signalling pathways involved in hypoxia-induced renal fibrosis. J. Cell. Mol. Med. 2017;21(7):1248- 1259. doi: 10.1111/jcmm.13060.
  11. Stetler-Stevenson W.G. Dynamics of matrix turnover during pathologic remodeling of the extracellular matrix. Am. J. Pathol. 1996;148 (5):1345-1350.
  12. Fu Q., Colgan S.P, Shelley C.S. Hypoxia: The force that drives chronic kidney disease. Clin. Med. Res. 2016;14:15-39. doi: 10.3121/cmr.2015.1282.
  13. Hirakawa Y., Tanaka T., Nangaku M. Renal hypoxia in CKD; Pathophysiology and detecting methods. Front. Physiol. 2017;8:99. Doi: 10.3389/ fphys.2017.00099.
  14. Tanaka T. A mechanistic link between renal ischemia and fibrosis. Med. Mol. Morphol. 2017;50:1-8. doi: 10.1007/s00795-016-0146.
  15. Vio C.P., Jeanneret V.A. Local induction of angiotensin-converting enzyme in the kidney as a mechanism of progressive renal diseases. Kidney Int. Suppl. 2003;86:57-63.
  16. Anderson S., Jung F.F., Ingelfinge J.R. Renal renin angiotensin system in diabetes: functional, immunohistochemical, and molecular biological correlations. Am. J. Physiol. 1993;265(2):477-486. doi: 10.1152/ajprenal.1993.265.4.F477.
  17. Lombardi D.M., Viswanathan M., Vio C.P., et al. Renal and vascular injury induced by exogenous angiotensin II is AT1 receptor-dependent. Nephron. 2001;87(1):66-74. doi: 10.1159/000045886.
  18. Johnson R.J., Gordon K.L., Suga S., et al. Renal injury and salt-sensitive hypertension after exposure to catecholamines. Hypertension. 1999;34(1):151-159. doi: 10.1161/01.hyp.34.1.151.
  19. Mezzano S.A., Ruiz-Ortega M., Egido J. Angiotensin II and renal fibrosis. Hypertens. 2001;38(2):635-638. doi: 10.1161/hy09t1.094234.
  20. Wolf G. Renal injury due to renin-angiotensin-aldosterone system activation of the transforming growth factor-в pathway. Kidney Int. 2006;70(11):1914-1919. doi: 10.1038/sj.ki.5001846.
  21. Suga S.I., Phillips M.I., Ray P.E., et al. Hypokalemia induces renal injury and alterations in intrarenal vasoactive mediators that favor salt-sensitivity. Am. J. Physiol. Renal. Physiol. 2001;281(4):620-629. Doi: 10.1152/ ajprenal.2001.281.4.F620.
  22. Iwano M., Plieth D., Danoff T.M., Xue C., Okada H., Neilson E.G. Evidence that fibroblasts derive from epithelium during tissue fibrosis. J. Clin. Invest. 2002;110(3):341-350. doi: 10.1172/JCI15518.
  23. Liu Y. Epithelial to mesenchymal transition in renal fibrogenesis: pathologic significance, molecular mechanism, and therapeutic intervention. J. Am. Soc. Nephrol 2004;15(1):1-12. doi: 10.1097/01.asn.0000106015.29070.e7.
  24. Humphreys B.D., Lin S.L., Kobayashi A., Hudson T.E., Nowlin B. T., Bonventre J. V., Valerius M.T., McMahon A.P., Duffield J.S. Fate tracing reveals the pericyte and not epithelial origin of myofibroblasts in kidney fibrosis. Am. J. Pathol. 2010;176(1):85-97. doi: 10.2353/ajpath.2010.090517.
  25. Rastaldi M.P., Ferrario F., Giardino L., Dell’Antonio G., Grillo C., Grillo P., Strutz F., Mtiller G.A., Colasanti G., D’Amico G. Epithelial-mesenchymal transition of tubular epithelial cells in human renal biopsies. Kidney Int. 2002; 62(1):137-146. doi: 10.1046/j.1523-1755.2002.00430.x.
  26. Tan R.J., Zhou D., Liu Y. Signaling Crosstalk between Tubular Epithelial Cells and Interstitial Fibroblasts after Kidney Injury. Kidney Dis (Basel). 2016;2(3):136-144. doi: 10.1159/000446336
  27. Yang L., Besschetnova T.Y., Brooks C.R., Shah J.V., Bonventre J.V. Epithelial cell cycle arrest in G2/M mediates kidney fibrosis after injury. Nat. Med. 2010;16(5):535-543. doi: 10.1038/nm.2144.
  28. Yang Y. Wnt signaling in develfpment disease. Cell. Biosci. 2012;2:14. doi: 10.1186/2045-3701-2-14.
  29. Tan R.J., Zhou D., Zhou L., Liu Y. Wnt/e-catenin signaling and kidney fibrosis. Kidney Int. Suppl. (2011). 2014;4(1):84-90. doi: 10.1038/kisup.2014.16.
  30. Zhou L., Li Y., Hao S., Zhou D., Tan R.J., Nie J., et al. Multiple genes of the renin-angiotensin system are novel targets of Wnt/e-catenin signaling. J. Am. Soc. Nephrol 2015;26(1):107-120. doi: 10.1681/ASN.2014010085.
  31. Kok H.M., Falke L.L., Goldschmeding R., Nguyen T.Q. Targeting CTGF, EGF and PDGF pathways to prevent progression of kidney disease. Nat. Rev. Nephrol. 2014;10(12):700-711. doi: 10.1038/nrneph.2014.184.
  32. Borges F.T., Melo S.A., Ozdemir B.C., Kato N., Revuelta I., Miller C.A., et al. TGF-e}-containing exosomes from injured epithelial cells activate fibroblasts to initiate tissue regenerative responses and fibrosis. J. Am. Soc. Nephrol. 2013;24(3):385-392. doi: 10.1681/ASN.2012101031.

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