medigraphic.com
SPANISH

Revista de Nefrología, Diálisis y Trasplante

ISSN 0326-3428 (Print)
Órgano de difusión científica de la Asociación Nefrológica de Buenos Aires
  • Contents
  • View Archive
  • Information
    • General Information        
    • Directory
  • Publish
    • Instructions for authors        
  • medigraphic.com
    • Home
    • Journals index            
    • Register / Login
  • Mi perfil

2022, Number 1

<< Back Next >>

Rev Nefrol Dial Traspl 2022; 42 (1)

Evaluation of Ki-67, CD68 and Bcl-2 staining, dialysis and mortality in crescentic glomerulonephritis

Akda H, Zeybek M, Meteoglu I, Yeniçerioglu Y
Full text How to cite this article

Language: English
References: 32
Page: 56-64
PDF size: 779.71 Kb.


Key words:

crescentic glomerulonephritis, hemodialysis, dialysis, mortality, Ki-67.

ABSTRACT

Introduction: Immunohistochemical staining of Ki-67, CD68 and Bcl-2 have been studied in glomerulonephritis. We aimed to assess these immunohistochemical staining features, hemodialysis initiation and 60 month mortality rates in crescentic glomerulonephritis.Methods: In this retrospective study, patients, with a previous diagnosis of crescentic glomerulonephritis were divided into two groups: Hemodialysis Initiated and Not Initiated groups. Kidney biopsy specimens’Ki-67, CD68 and Bcl-2 staining scores were defined as below 5% “0”, 5-10% “+1”, 11- 20% “+2”, over 20% “+3”. Patients demographic, laboratory data, status of hemodialysis initiation, and mortality were obtained from medical records and immunohistochemical staining scores were compared between groups. Estimated glomerular filtration rates (eGFR) were assessed at 0, 6, and 12 months, except patients’ ongoing hemodialysis. Results: A total of 56 patients were diagnosed as crescentic glomerulonephritis. Pauci-immune crescentic glomerulonephritis (58.9%) was the most common etiology. Hemodialysis was initiated in 36 patients. Mean age, baseline creatinine, urea, C-reactive protein levels were significantly higher and, hemoglobin and proteinuria levels were significantly lower in the Hemodialysis Initiated group. Immunohistochemical staining scores were not significantly different between groups. In Hemodialysis Initiated group, 8.33% of patients were recovered from hemodialysis. Mortality rates were 44,4% and 10% in patients in the group of hemodialysis initiated and not initiated group respectively. When we combine the hemodialysis not initiated patients and patients recovered from hemodialysis; median eGFR at baseline, 6th and 12th month were 32.9, 43.9, and 58.0 mL/ min/1.73m2, respectively (p=0.016). Conclusion: Hemodialysis initiation was associated with high mortality. Degree of immunohistochemical staining was similar in both groups. Increment in eGFR was documented in first year in patients, other than the ones on still on hemodialysis.


REFERENCES

  1. Moroni G, Ponticelli C. Rapidly progressive crescenticglomerulonephritis: early treatment is a must.Autoimmun Rev. 2014;13(7):723-9. doi: 10.1016/j.autrev.2014.02.007.

  2. Jennette JC. Rapidly progressive crescenticglomerulonephritis. Kidney Int. 2003;63(3):1164-77.doi: 10.1046/j.1523-1755.2003.00843.x.

  3. Couser WG. Rapidly progressive glomerulonephritis:classification, pathogenetic mechanisms, and therapy.Am J Kidney Dis. 1988;11(6):449-64. doi: 10.1016/s0272-6386(88)80079-9.

  4. Bullwinkel J, Baron-Lühr B, Lüdemann A, WohlenbergC, Gerdes J, Scholzen T. Ki-67 protein is associatedwith ribosomal RNA transcription in quiescent andproliferating cells. J Cell Physiol. 2006;206(3):624-35.doi: 10.1002/jcp.20494.

  5. Scholzen T, Gerdes J. The Ki-67 protein: fromthe known and the unknown. J Cell Physiol.2000;182(3):311-22. doi: 10.1002/(SICI)1097-4652(200003)182:3<311::AID-JCP1>3.0.CO;2-9.

  6. Aman NA, Doukoure B, Koffi KD, Koui BS, TraoreZC, Kouyate M, et al. immunohistochemicalevaluation of Ki-67 and comparison withclinicopathologic factors in breast carcinomas. AsianPac J Cancer Prev. 2019;20(1):73-79. doi: 10.31557/APJCP.2019.20.1.73.

  7. Zaha DC. Significance of immunohistochemistry inbreast cancer. World J Clin Oncol. 2014;5(3):382-92.doi: 10.5306/wjco.v5.i3.382.

  8. Tian Y, Ma Z, Chen Z, Li M, Wu Z, Hong M, et al.Clinicopathological and prognostic value of Ki-67expression in bladder cancer: a systematic review andmeta-analysis. PLoS One. 2016;11(7):e0158891. doi:10.1371/journal.pone.0158891.

  9. Chistiakov DA, Killingsworth MC, Myasoedova VA,Orekhov AN, Bobryshev YV. CD68/macrosialin: notjust a histochemical marker. Lab Invest. 2017;97(1):4-13. doi: 10.1038/labinvest.2016.116.

  10. Dias CB, Malafronte P, Lee J, Resende A, Jorge L,Pinheiro CC, et al. Role of renal expression of CD68 inthe long-term prognosis of proliferative lupus nephritis.J Nephrol. 2017;30(1):87-94. doi: 10.1007/s40620-015-0252-7.

  11. Zhao L, David MZ, Hyjek E, Chang A, MeehanSM. M2 macrophage infiltrates in the early stages ofANCA-associated pauci-immune necrotizing GN. ClinJ Am Soc Nephrol. 2015;10(1):54-62. doi: 10.2215/CJN.03230314.

  12. Yang B, Johnson TS, Thomas GL, Watson PF,Wagner B, Furness PN, et al. A shift in the Bax/Bcl-2balance may activate caspase-3 and modulate apoptosisin experimental glomerulonephritis. Kidney Int.2002;62(4):1301-13. doi: 10.1111/j.1523-1755.2002.kid587.x.

  13. Goumenos DS, Tsamandas AC, Kalliakmani P, TsakasS, Sotsiou F, Bonikos DS, et al. Expression of apoptosisrelatedproteins bcl-2 and bax along with transforminggrowth factor (TGF-beta1) in the kidney of patientswith glomerulonephritides. Ren Fail. 2004;26(4):361-7. doi: 10.1081/jdi-120039818.

  14. Levey AS, Stevens LA, Schmid CH, Zhang YL, CastroAF 3rd, Feldman HI, et al.; CKD-EPI (Chronic KidneyDisease Epidemiology Collaboration). A new equationto estimate glomerular filtration rate. Ann InternMed.2009;150(9):604-12. doi: 10.7326/0003-4819-

  15. 150-9-200905050-00006.15) López-Gómez JM, Rivera F; Spanish Registry ofGlomerulonephritis. Renal biopsy findings in acuterenal failure in the cohort of patients in the SpanishRegistry of Glomerulonephritis. Clin J Am Soc Nephrol.2008;3(3):674-81. doi: 10.2215/CJN.04441007.

  16. Koyama A, Yamagata K, Makino H, ArimuraY, Wada T, Nitta K, et al. Japan RPGN RegistryGroup. A nationwide survey of rapidly progressiveglomerulonephritis in Japan: etiology, prognosis andtreatment diversity. Clin Exp Nephrol. 2009;13:633-50.doi: 10.1007/s10157-009-0201-7.

  17. Jennette JC. Rapidly progressive crescenticglomerulonephritis. Kidney Int. 2003;63(3):1164-77.doi: 10.1046/j.1523-1755.2003.00843.x.

  18. Chen S, Tang Z, Xiang H, Li X, Chen H, ZhangH, et al. Etiology and outcome of crescenticglomerulonephritis from a single center in China: a 10-year review. Am J Kidney Dis. 2016;67(3):376-83. doi:10.1053/j.ajkd.2015.07.034.

  19. Rampelli SK, Rajesh NG, Srinivas BH, HarichandraKumar KT, Swaminathan RP, Priyamvada PS.Clinical spectrum and outcomes of crescenticglomerulonephritis: A single center experience. IndianJ Nephrol. 2016;26(4):252-6. doi: 10.4103/0971-4065.158574.

  20. Nagaraju SP, Laxminarayana SLK, Kosuru S,Parthasarathy R, Attur RP, Rangaswamy D, et al.Clinicopathological characteristics and outcomesof diffuse crescentic glomerulonephritis: a singlecenter experience from Southern India. J ClinDiagn Res. 2017;11(9):OC21-OC24. doi: 10.7860/JCDR/2017/28307.

  21. Alexander S, Yusuf S, Rajan G, Elias John E, Roy S,Annamalai VC, et al. Crescentic glomerulonephritis:what’s different in South Asia? A single centerobservational cohort study. Wellcome Open Res.2020;5:164. doi:10.12688/wellcomeopenres.16071.1.

  22. Nabokov A, Waldherr R, Ritz E. Demonstration of theproliferation marker Ki-67 in renal biopsies: correlationto clinical findings. Am J Kidney Dis. 1997;30(1):87-97. doi: 10.1016/s0272-6386(97)90569-2.

  23. Nitta K, Horita S, Honda K, Uchida K, WatanabeT, Nihei H, et al. Glomerular expression of cellcycle-regulatory proteins in human crescenticglomerulonephritis. Virchows Arch. 1999;435(4):422-7. doi: 10.1007/s004280050420.

  24. Kim O. Immunohistochemical study of the expressionof alpha-smooth muscle actin and the proliferationmarker Ki-67 of glomerulonephritis. J Korean Med Sci.2001;16(4):455-61. doi: 10.3346/jkms.2001.16.4.455.

  25. Dalkilic E, Filiz G, Yavuz M, Dilek K, Ersoy A,Yurtkuran M, et al. Ki-67 proliferation index inrenal biopsy samples of patients with systemic lupuserythematosus and its correlation with clinical findings.Iran J Kidney Dis. 2013;7(3):198-203.

  26. Rahbar MH, Rahbar MR, Mardanpour N, MardanpourS. The potential diagnostic utility of coexpression ofKi-67 and P53 in the renal biopsy in pediatric lupusnephritis. Int J Nephrol Renovasc Dis. 2018;11:343-50.doi: 10.2147/IJNRD.S175481.

  27. Maekawa K, Shibano T, Sawaki J, Mae H, Hattori M,Tanizawa T. [Clinical usefulness of CD68 staining inchildren with various glomerular diseases]. Nihon JinzoGakkai Shi. 2014;56(4):532-7.

  28. Liu ZH, Chen SF, Zhou H, Chen HP, Li LS.Glomerular expression of C-C chemokines in differenttypes of human crescentic glomerulonephritis. NephrolDial Transplant. 2003;18(8):1526-34. doi: 10.1093/ndt/gfg172.

  29. Nakopoulou L, Stefananki K, Papadakis J, BoletisJ, Zeis PM, Kostakis A, et al. Expression of bcl-2oncoprotein in various types of glomerulonephritisand renal allografts. Nephrol Dial Transplant.1996;11(6):997-1002.

  30. Ko K, Wang J, Perper S, Jiang Y, Yanez D, KaverinaN, et al. Bcl-2 as a therapeutic target in humantubulointerstitial inflammation. Arthritis Rheumatol.2016;68(11):2740-51. doi: 10.1002/art.39744.

  31. Qiu LQ, Sinniah R, I-Hong Hsu S. Downregulationof Bcl-2 by podocytes is associated with progressiveglomerular injury and clinical indices of poorrenal prognosis in human IgA nephropathy. J AmSoc Nephrol. 2004;15(1):79-90. doi: 10.1097/01.asn.0000104573.54132.2e.

  32. Li J, Li H, Li Q, Xue Y. Repaglinide inhibitscyclosporine A-induced renal tubular toxicity by affectingapoptosis and Bax and Bcl-2 expression. Turk J Med Sci.2018;48(4):880-5. doi: 10.3906/sag-1707-44




2020     |     www.medigraphic.com

Mi perfil

C?MO CITAR (Vancouver)

Rev Nefrol Dial Traspl. 2022;42