Preview

Архивъ внутренней медицины

Расширенный поиск

КАНАЛЬЦЕВЫЙ АППАРАТ ПОЧЕК — НАУЧНОЕ И ПРИКЛАДНОЕ ЗНАЧЕНИЕ

https://doi.org/10.20514/2226-6704-2022-12-6-405-421

Аннотация

 

В настоящее время существует высокий научный интерес к изучению особенностей структуры и функций канальцев почек. Актуальность темы обусловлена потенциальной возможностью выявления разнообразных маркеров нарушения функции канальцев и использования их для ранней диагностики не только тубулопатий, но и гломерулярных нарушений. В клинической практике маркеры канальцевой дисфункции используются недостаточно. В статье представлены сведения об анатомо-функциональных особенностях проксимального и дистального отделов канальцевого аппарата, изложены высокоорганизованные механизмы межмолекулярного взаимодействия, представлены основные биологически активные вещества, изменение концентрации которых является следствием повреждения канальцев. Представленная рукопись является продуктом глубокого анализа и систематизации имеющихся данных в российских и зарубежных информационно-аналитических порталах.

Об авторах

Е. С. Левицкая
Федеральное государственное бюджетное образовательное учреждение высшего образования «Ростовский государственный медицинский университет» Министерства здравоохранения Российской Федерации, кафедра внутренних болезней № 2
Россия

Екатерина Сергеевна Левицкая

Ростов-на-Дону



М. М. Батюшин
Федеральное государственное бюджетное образовательное учреждение высшего образования «Ростовский государственный медицинский университет» Министерства здравоохранения Российской Федерации, кафедра внутренних болезней № 2
Россия

Ростов-на-Дону



Список литературы

1. Curthoys NP, Moe OW. Proximal Tubule Function and Response to Acidosis. Clin J Am Soc Nephrol. 2014; 9(9): 1627-1638. doi: 10.2215/CJN.10391012.

2. Andrianova NV, Buyan MI, Zorova LD et al. Kidney Cells Regeneration: Dedifferentiation of Tubular Epithelium, Resident Stem Cells and Possible Niches for Renal Progenitors. Int J Mol Sci. 2019; 20(24): 6326. doi: 10.3390/ijms20246326.

3. Little MH, Kairath P. Does Renal Repair Recapitulate Kidney Development? JASN. 2017; 28 (1): 34-46. doi: 10.1681/ASN.2016070748.

4. Castrop H. The Role of Renal Interstitial Cells in Proximal Tubular Regeneration. Nephron 2019; 141: 265-272. doi: 10.1159/000496278.

5. Yoon YM, Go G, Yun CW et al. Knockdown of CK2α reduces P-cresol-induced fibrosis in human renal proximal tubule epithelial cells via the downregulation of profilin-1. Int J Med Sci. 2020; 17(17): 2850-2860. doi:10.7150/ijms.48429.

6. Chawla LS., Bellomo R, Bihorac A, on behalf of the Acute Disease Quality Initiative Workgroup 16. Acute kidney disease and renal recovery: consensus report of the Acute Disease Quality Initiative (ADQI) 16 Workgroup. Nature Reviews Nephrology. 2017; 13: 241-257. doi:10.1038/nrneph.2017.2.

7. Chevalier RL. The proximal tubule is the primary target of injury and progression of kidney disease: role of the glomerulotubular junction. Am J Physiol Renal Physiol. 2016; 311(1): F145-F161. doi: 10.1152/ajprenal.00164.2016.

8. Fortrie G, de Geus HRH., Betjes MGH. The aftermath of acute kidney injury: a narrative review of long-term mortality and renal function. Crit Care. 2019; 23: 24. doi: 10.1186/s13054-019-2314-z.

9. Pereira BJ, Barreto S, Gentil T et al. Risk factors for the progression of chronic kidney disease after acute kidney injury. J. Bras. Nefrol. 2017; 39: 239-245. d doi: 10.5935/0101-2800.20170041.

10. Gilbert RE. Proximal Tubulopathy: Prime Mover and Key Therapeutic Target in Diabetic Kidney Disease. Diabetes. 2017; 66: 791-800. doi: 10.2337/db16-0796.

11. Chagnaca A, Zingermana B, Rozen-Zvia B et al. Consequences of Glomerular Hyperfiltration: The Role of Physical Forces in the Pathogenesis of Chronic Kidney Disease in Diabetes and Obesity. Nephron. 2019; 143: 38-42. doi: 10.1159/000499486.

12. Vallon, V., Thomson, S.C. The tubular hypothesis of nephron filtration and diabetic kidney disease. Nat Rev Nephrol. 2020; 16: 317-336. doi: 10.1038/s41581-020-0256-y.

13. Habib SL. Kidney atrophy vs hypertrophy in diabetes: which cells are involved? Cell Cycle. 2018; 17(14): 1683-1687. doi: 10.1080/15384101.2018.1496744.

14. Rosenberg AZ, Kopp JB. Focal Segmental Glomerulosclerosis. Clin J Am Soc Nephrol. 2017; 12: 502-517. doi: 10.2215/CJN.05960616.

15. Denic A, Glassock RJ, Rule AD. Structural and functional changes with the aging kidney. Adv Chronic Kidney Dis. 2016; 23(1): 19-28. doi: 10.1053/j.ackd.2015.08.004.

16. Amini S., Abbaspour H., Morovatdar N. et al. Risk Factors and Outcome of Acute Kidney Injury after Congenital Heart Surgery: A Prospective Observational Study. Indian J Crit Care Med. 2017; 21(12): 847-851. doi: 10.4103/ijccm.IJCCM_459_16.

17. Sales GTM, Foresto RD. Drug-induced nephrotoxicity. Rev. Assoc. Med. Bras. 2020; 66 (1): 82-90 doi: 10.1590/1806-9282.66.S1.82.

18. Gómez BCJ, Na G-PH, Álvarez FO et al. Evolución De tubulopatías renales primarias diagnosticadas en edad pediátrica. Nefrologia. 2021; 41: 182-190. doi:10.1016/j.nefroe.2020.07.001.

19. Silver SA, Harel Z, McArthur E et al. Causes of Death after a Hospitalization with AKI. JASN. 2018; 29 (3): 1001-1010. doi: 10.1681/ASN.2017080882.

20. Wiersema, R., Eck, R.J., Haapio, M. et al. Burden of acute kidney injury and 90-day mortality in critically ill patients. BMC Nephrol. 2020; 21: 1-8. doi: 10.1186/s12882-019-1645-y.

21. Mihevc M., Petreski T., Maver U. et al. Renal proximal tubular epithelial cells: review of isolation, characterization, and culturing techniques. Mol Biol Rep. 2020; 47: 9865-9882. doi: 10.1007/s11033-020-05977-4.

22. Madrazo-Ibarra A, Vaitla P. Histology. Nephron. 2020. [Electronic resource]. URL: https://www.ncbi.nlm.nih.gov/books/NBK554411. (дата обращения: 01.06.2022г).

23. Park HJ, Fan Z, Bai Y et al. Transcriptional Programs Driving Shear Stress-Induced Differentiation of Kidney Proximal Tubule Cells in Culture. Front. Physiol. 2020; 11: 587358. doi: 10.3389/fphys.2020.587358.

24. Lin NYC, Homan KA, Robinson SS. et al. Renal reabsorption in 3D vascularized proximal tubule models. PNAS. 2019; 116 (12): 5399-5404. doi: 10.1073/pnas.1815208116.

25. Chen L, Clark JZ, Nelson JW et al. Renal-Tubule Epithelial Cell Nomenclature for Single-Cell RNA-Sequencing Studies. J Am Soc Nephrol. 2019; 30(8): 1358-1364. doi: 10.1681/ASN.2019040415.

26. Carney EF. Endocytosis in the proximal tubule. Nat Rev Nephrol. 2019: 15; 2. doi:10.1038/s41581-018-0079-2.

27. Subramanya AR., Ellison DH. Distal Convoluted Tubule. CJASN. 2014; 9 (12): 2147-2163. doi: 10.2215/CJN.05920613.

28. Wang S, Dong Z. Primary cilia and kidney injury: current research status and future perspectives. Am J Physiol Renal Physiol. 2013; 305(8): F1085-F1098. doi: 10.1152/ajprenal.00399.2013.

29. Maggiorani D, Dissard R, Belloy M et al. Shear Stress-Induced Alteration of Epithelial Organization in Human Renal Tubular Cells. PLoS ONE. 2015; 10(7): e0131416. doi:10.1371/journal.pone.0131416.

30. Pluznick JL, Caplan MJ. Chemical and Physical Sensors in the Regulation of Renal Function. CJASN. 2015; 10 (9): 1626-1635. doi: /10.2215/CJN.00730114.

31. Han SJ, Kim J-H, Kim JI et al. Inhibition of microtubule dynamics impedes repair of kidney ischemia/reperfusion injury and increases fibrosis. Sci Rep. 2016; 6: 27775. doi: /10.1038/srep27775.

32. Sivakamasundari V, Bolisetty M, Sivajothi S et al. Comprehensive Cell Type Specific Transcriptomics of the Human Kidney. bioRxiv. 2017; 238063. doi: 10.1101/238063.

33. Elias BC, Mathew S, Srichai MB et al. The Integrin β1 Subunit Regulates Paracellular Permeability of Kidney Proximal Tubule Cells. J Biol Chem. 2014; 289(12): 8532-8544. doi: 10.1074/jbc.M113.526509.

34. Zheng G, Zhang J, Zhao H. et al. a3 Integrin of Cell-Cell Contact Mediates Kidney Fibrosis by Integrin-Linked Kinase in Proximal Tubular E-Cadherin Deficient Mice. Am J Pathol. 2016; 186: 1847-1860. doi: 10.1016/j.ajpath.2016.03.015.

35. Yu ASL. Claudins and the Kidney. J Am Soc Nephrol. 2015; 26(1): 11-19. doi: 10.1681/ASN.2014030284.

36. Mitsuhata Y., Abe T., Misaki K. et al. Cyst formation in proximal renal tubules caused by dysfunction of the microtubule minus-end regulator CAMSAP3. Sci Rep. 2021; 11: 5857. doi: 10.1038/s41598-021-85416-x.

37. Tomilin V, Mamenko M, Zaika O, Pochynyuk O. Role of Renal TRP Ion Channels in Physiology and Pathology. Semin Immunopathol. 2016; 38(3): 371-383. doi: 10.1007/s00281-015-0527-z.

38. Wang K, Kestenbaum B. Proximal Tubular Secretory Clearance. Clin J Am Soc Nephrol. 2018; 13(8): 1291-1296. doi: 10.2215/CJN.12001017.

39. Евтеев В.А., Прокофьев А.Б., Бунятян Н.Д. и др. МАТЕ-транспортеры: участие в фармакокинетике лекарственных средств и межлекарственных взаимодействиях. Фармация. 2019; 68 (7): 44-47. doi: 10.29296/25419218-2019-07-08.

40. Simon N., Hertig A. Alteration of Fatty Acid Oxidation in Tubular Epithelial Cells: From Acute Kidney Injury to Renal Fibrogenesis. Front. Med. (Lausanne). 2015; 2: 52. doi: 10.3389/fmed.2015.00052.

41. Gai Z, Wang T, Visentin M, et al. Lipid Accumulation and Chronic Kidney Disease. Nutrients. 2019; 11(4): 722. doi: 10.3390/nu11040722.

42. Gewin LS. Sugar or Fat? Renal Tubular Metabolism Reviewed in Health and Disease. Nutrients. 2021; 13: 1580. doi: 10.3390/ nu13051580.

43. Vasko R. Peroxisomes and Kidney Injury. Antioxid. Redox Signal. 2016; 25: 217-231. doi: 10.1089/ars.2016.6666.

44. Schreiber A, Rousselle A, Klocke J. et al. Neutrophil Gelatinase– Associated Lipocalin Protects from ANCA-Induced GN by Inhibiting TH17 Immunity. J Am Soc Nephrol. 2020; 31(7): 1569-1584. doi: 10.1681/ASN.2019090879.

45. Buonafine M, Martinez-Martinez E, Jaisser F. More than a simple biomarker: the role of NGAL in cardiovascular and renal diseases. Clin Sci (Lond). 2018; 132(9): 909-923. doi:10.1042/CS20171592.

46. Solbu MD., Toft I, Lochen ML et al. N-Acetyl-β-d-Glucosaminidase Does Not Enhance Prediction of Cardiovascular or All-Cause Mortality by Albuminuria in a Low-Risk Population. J Am Soc Nephrol. 2016; 27(2): 533-542. doi: 10.1681/ASN.2014100960.

47. Kim SR, Lee Y, Lee SG et al. Urinary N-acetyl-β-d-glucosaminidase, an early marker of diabetic kidney disease, might reflect glucose excursion in patients with type 2 diabetes. Medicine (Baltimore). 2016; 95(27): e4114. doi: 10.1097/MD.0000000000004114.

48. Chachaj A, Matkowski R, Gröbner G et al. Metabolomics of Interstitial Fluid, Plasma and Urine in Patients with Arterial Hypertension: New Insights into the Underlying Mechanisms. Diagnostics (Basel). 2020; 10(11): 936. doi: 10.3390/diagnostics10110936.

49. Gandhi R, Yi J, Ha J et al. Accelerated receptor sheddinginhibits kidney injury molecule-1 (KIM-1)-mediated efferocytosis. Am J Physiol Renal Physiol. 2014; 307(2): F205–F221. doi: 10.1152/ajprenal.00638.2013.

50. Tanase DM, Gosav EM, Radu S et al. The Predictive Role of the Biomarker Kidney Molecule-1 (KIM-1) in Acute Kidney Injury (AKI) Cisplatin-Induced Nephrotoxicity. Int J Mol Sci. 2019; 20(20): 5238. doi: 10.3390/ijms20205238.

51. Yang L, Brooks CR, Xiao S et al. KIM-1–mediated phagocytosis reduces acute injury to the kidney. J Clin Invest. 2015; 125(4): 1620-1636.

52. Schiano G, Glaudemans B, Olinger E. et al. The Urinary Excretion of Uromodulin is Regulated by the Potassium Channel ROMK. Sci Rep. 2019; 9: 19517. doi: 10.1038/s41598-019-55771-x.

53. Micanovic R, LaFavers K, Garimella PS et al. Uromodulin (Tamm–Horsfall protein): guardian of urinary and systemic homeostasis. Nephrol Dial Transplant. 2020; 35(1): 33-43. doi: 10.1093/ndt/gfy394.

54. Kipp A, Olinger E. What Does Uromodulin Do? CJASN. 2021; 16(1): 150-153. doi: 10.2215/CJN.06390420.

55. Eckardt KU, Alper SL, Antignac C. et al. Autosomal dominant tubulointerstitial kidney disease: diagnosis, classification, and management--A KDIGO consensus report. Kidney Int. 2015; 88(4): 676-83. doi: 10.1038/ki.2015.28.

56. Singh V., Singla SK, Jha, V. et al. Hepatocyte nuclear factor-1β: A regulator of kidney development and cystogenesis. Indian J Nephrol. 2015; 25(2): 70-76. doi: 10.4103/0971-4065.139492.

57. Ferrè S, Igarashi P. New insights into the role of HNF-1β in kidney (patho)physiology. Pediatr Nephrol. 2019; 34(8): 1325-1335. doi: 10.1007/s00467-018-3990-7.

58. Li L, Dong M, Wang XG. The Implication and Significance of Beta 2 Microglobulin: A Conservative Multifunctional Regulator. Chin Med J (Engl). 2016; 129(4): 448-455. doi: 10.4103/0366-6999.176084.

59. Гасанов М.З., Батюшин М.М., Терентьев В.П. и др. Протеомный спектр мочи пациентов с хроническим гломерулонефритом. Клиническая нефрология. 2012; 5-6: 28-32.

60. Гасанов М.З., Батюшин М.М., Терентьев В.П. и др. Особенности протеомного зеркала мочи пациентов с различными гломерулонефропатиями различного генеза. Кубанский научный медицинский вестник. 2012; 4(133): 37-42.

61. Батюшин М.М., Левицкая Е.С., Терентьев В.П. и др. Почечные и коронарные предикторы прогноза у больных ишемической болезнью сердца, перенесших реваскуляризацию миокарда. Российский кардиологический журнал. 2012; 6 (98): 45-50.

62. Zi M, Xu Y. Involvement of cystatin C in immunity and apoptosis. Immunol Lett. 2018; 196: 80-90. doi: 10.1016/j.imlet.2018.01.006.

63. Kim SS, Song SH, Kim IJ et al. Urinary Cystatin C and Tubular Proteinuria Predict Progression of Diabetic Nephropathy. Diabetes Care. 2013; 36(3): 656-661. doi: 10.2337/dc12-0849.

64. Клинические практические рекомендации KDIGO 2012 по диагностике и лечению хронической болезни почек. Нефрология и диализ. 2017; 19(1): 22-206.

65. Zakiyanov O, Kalousová M, Zima T et al. Matrix Metalloproteinases in Renal Diseases: A Critical Appraisal. Kidney Blood Press Res. 2019; 44: 298-330. doi: 10.1159/000499876.

66. Wen X, Zhang J, Wan X. et al. Tissue Inhibitor of Metalloproteinases-2 Mediates Kidney Injury during Sepsis. Nephron. 2020; 144: 644-649. doi: 10.1159/000511165.

67. Jia HM., Huang LF., Zheng Y. et al. Diagnostic value of urinary tissue inhibitor of metalloproteinase-2 and insulin-like growth factor binding protein 7 for acute kidney injury: a metaanalysis. Crit Care. 2017; 21: 77. doi: 10.1186/s13054-017-1660-y.

68. Jin L, Shen F, Weinfeld M et al. Insulin Growth Factor Binding Protein 7 (IGFBP7)-Related Cancer and IGFBP3 and IGFBP7 Crosstalk. Front. Oncol. 2020; 10: 727. doi: 10.3389/fonc.2020.00727.

69. Wang GQ, Bonkovsky HL, Lemos A et al. Recent insights into the biological functions of liver fatty acid binding protein 1. J Lipid Res. 2015; 56(12): 2238-2247. doi: 10.1194/jlr.R056705.

70. Viswanathan V, Sivakumar S, Sekar V et al. Clinical significance of urinary liver-type fatty acid binding protein at various stages of nephropathy. Indian J Nephrol 2015; 25: 269-73. doi: 10.4103/0971-4065.145097.

71. Tsai IT, Wu CC, Hung WC et al. FABP1 and FABP2 as markers of diabetic nephropathy. Int J Med Sci. 2020; 17(15): 2338-2345. doi: 10.7150/ijms.49078.

72. Chen X, Cobbs A, George J et al. Endocytosis of Albumin Induces Matrix Metalloproteinase-9 by Activating the ERK Signaling Pathway in Renal Tubule Epithelial Cells. Int J Mol Sci. 2017; 18(8): 1758. doi: 10.3390/ijms18081758.

73. Bieniaś B, Zajączkowska M, Borzęcka Halina et al. Early Markers of Tubulointerstitial Fibrosis in Children With Idiopathic Nephrotic Syndrome. Medicine. 2015; 94(42): e1746. doi: 10.1097/MD.0000000000001746.

74. Shu KH, Wang CH, Wu CH et al. Urinary π-glutathione S-transferase Predicts Advanced Acute Kidney Injury Following Cardiovascular Surgery. Sci Rep. 2016; 6: 26335. doi: 10.1038/srep26335.

75. Hirooka Y, Nozaki Y. Interleukin-18 in Inflammatory Kidney Disease. Front. Med. 2021; 8: 639103. doi: 10.3389/fmed.2021.639103.

76. Yang Y, Zhang ZX, Lian D et al. IL-37 inhibits IL-18-induced tubular epithelial cell expression of pro-inflammatory cytokines and renal ischemia-reperfusion injury. Kidney International. 2015; 87: 396-408. doi:10.1038/ki.2014.295.

77. Su H, Lei CT, Zhang С et al. Interleukin-6 Signaling Pathway and Its Role in Kidney Disease: An Update. Front Immunol. 2017; 8: 405. doi: 10.3389/fimmu.2017.00405.

78. Norlander AE, Madhur MS. Inflammatory cytokines regulate renal sodium transporters: how, where, and why? Am J Physiol Renal Physiol. 2017; 313(2): F141-F144. doi: 10.1152/ajprenal.00465.2016.

79. Stiegel M.A., Pleil J.D., Sobus J.R. et al. Kidney injury biomarkers and urinary creatinine variability in nominally healthy adults. [Electronic resource]. URL: file:///C:/Users/%D0%95%D0%BA%D0%B0%D1%82%D0%B5%D1%80%D0%B8%D0%BD%D0%B0/Downloads/KIP2%2012242014PRESUB2 %20(1).PDF. (дата обращения: 01.06.2022г).

80. Katou S, Globke B, Morgul M.H et al. Urinary Biomarkers α-GST and π-GST for Evaluation and Monitoring in Living and Deceased Donor Kidney Grafts. J Clin Med. 2019; 8(11): 1899. doi: 10.3390/jcm8111899.

81. Schinstock CA, Semret MH, Wagner SJ et al. Urinalysis is more specific and urinary neutrophil gelatinase-associated lipocalin is more sensitive for early detection of acute kidney injury. Nephrology Dialysis Transplantation. 2013; 28(5): 1175-1185. doi: 10.1093/ndt/gfs127.

82. Clerico A, Galli C, Fortunato A et al. Neutrophil gelatinaseassociated lipocalin (NGAL) as biomarker of acute kidney injury: a review of the laboratory characteristics and clinical evidences. Clin Chem Lab Med. 2012; 50(9): 1505-1517. doi 10.1515/cclm-2011-0814.

83. Hong N, Lee M, Park S et al. Elevated urinary N-acetyl-β-Dglucosaminidase is associated with high glycoalbumin-tohemoglobin A1c ratio in type 1 diabetes patients with early diabetic kidney disease. Sci Rep. 2018; 8: 6710. doi: 10.1038/s41598-018-25023-5.

84. Liu Q, Zong R, Li H et al. Distribution of urinary N-acetylbeta- D-glucosaminidase and the establishment of reference intervals in healthy adults. J Clin Lab Anal. 2021; 35(5): e23748. doi: 10.1002/jcla.23748.

85. Loko F, Robic D, Bondiou MT et al. Concentrations of N-Acetyl- β-D-glucosaminidase and its Intermediate Isoenzymes in Serum of Patients with Renal Transplants. CLINICAL CHEMISTRY. 1991; 37(4):583-584.

86. Bank J, Ruhaak R, Soonawala D et al. Urinary TIMP-2 Predicts the Presence and Duration of Delayed Graft Function in Donation After Circulatory Death Kidney Transplant Recipients. Transplantation. 2019; 103 (5): 1014-1023. doi: 10.1097/TP.0000000000002472.

87. Larsen MB, Stephens RW, Brunner N et al. Quantification of Tissue Inhibitor of Metalloproteinases 2 in Plasma from Healthy Donors and Cancer Patients. Scandinavian Journal of Immunology. 2004: 61; 449-460. doi: 10.1111/j.1365-3083.2005.01585.x.

88. Woziwodzka K, Małyszko J, Koc-Zórawska E et al. Renal Impairment Detectors: IGFBP-7 and NGAL as Tubular Injury Markers in Multiple Myeloma Patients. Medicina. 2021; 57: 1348. doi.org/ 10.3390/medicina57121348.

89. Kamijo-Ikemori A, Sugaya T, Yasuda T et al. Clinical Significance of Urinary Liver-Type Fatty Acid–Binding Protein in Diabetic Nephropathy of Type 2 Diabetic Patients. Diabetes Care. 2011; 34(3): 691-696. doi: 10.2337/dc10-1392.

90. Di Carlo A. Matrix metalloproteinase-2 and -9 and tissue inhibitor of metalloproteinase-1 and -2 in sera and urine of patients with renal carcinoma. ONCOLOGY LETTERS. 2014; 7: 621-626. doi: 10.3892/ol.2013.1755.

91. Дементьев И.О., Нюшко К.М., Карякин О.Б. и др. Роль биомаркеров острого повреждения почек в прогнозировании функциональных результатов хирургического лечения у больных локализованным раком почки. Исследования и практика в медицине. 2021; 8(3): 97-107. doi: 10.17709/2410- 1893-2021-8-3-9.

92. Зыков М.В., Кашталап В.В., Быкова И.С. и др. Клиническое и прогностическое значение сывороточного интерлейкина-18 у больных инфарктом миокарда с подъёмом сегмента ST. Российский кардиологический журнал. 2015; 11(127): 70-74. doi: 10.15829/1560-4071-2015-11-70-74.

93. Муркамилов И.Т., Айтбаев К.А., Муркамилова Ж.А. и др. Бета-2-микроглобулин как биомаркер при хронической болезни почек. The scientific heritage. 2021; 2 (59): 45-55. doi: 10.24412/9215-0365-2021-59-2-45-55.

94. Главнова О.Б., Ярмолинская М.И., Суслова С.В. и др. Возможности использования цистатина С в диагностике различных заболеваний. Журнал акушерства и женских болезней. 2018; 67(4): 40-47. doi:10.17816/JOWD67440.

95. Song J, Park DW, Moon S et al. Diagnostic and prognostic value of interleukin-6, pentraxin 3, and procalcitonin levels among sepsis and septic shock patients: a prospective controlled study according to the Sepsis-3 definitions. BMC Infect Dis. 2019; 19: 968. doi: 10.1186/s12879-019-4618-7.

96. Муркамилов И.Т., Айтбаев К.А., Фомин В.В. и др. Провоспалительные цитокины у больных с хронической болезнью почек: в фокусе интерлейкин-6. Архивъ внутренней медицины. 2019; 9(6): 428-433. doi: 10.20514/2226-6704-2019-9-6-428-433.


Рецензия

Для цитирования:


Левицкая Е.С., Батюшин М.М. КАНАЛЬЦЕВЫЙ АППАРАТ ПОЧЕК — НАУЧНОЕ И ПРИКЛАДНОЕ ЗНАЧЕНИЕ. Архивъ внутренней медицины. 2022;12(6):405-421. https://doi.org/10.20514/2226-6704-2022-12-6-405-421

For citation:


Levitskaya E.s., Batiushin M.M. Kidney Tubules — Scientific and Applied Value. The Russian Archives of Internal Medicine. 2022;12(6):405-421. https://doi.org/10.20514/2226-6704-2022-12-6-405-421

Просмотров: 829


Creative Commons License
Контент доступен под лицензией Creative Commons Attribution 4.0 License.


ISSN 2226-6704 (Print)
ISSN 2411-6564 (Online)