Uticaj gustine infiltrata u intersticijumu na prognozu primarnog glomerulonefritisa
Sažetak
Apstrakt
Uvod/Cilj. Razvoj inflamatornih promena i ožiljavanja i gubitak morfoloških struktura intersticijuma zauzimaju značajno mesto u patogenezi primarnih glomerulonefritisa, što utiče na nastanak, tok i prognozu ove bolesti. Cilj istraživanja bio je da se ispita uticaj promena u intersticijumu na prognozu primarnih glomerulonefitisa. Metode. Ispitivanjem je bilo obuhvaćeno 216 bolesnika sa različitim tipovima primarnih glomerulonefritisa lečenih na Klinici za nefrologiju i kliničku imunologiju Kliničkog centra Vojvodine koji su praćeni prosečno 77,5 meseci. Nakon utvrđivanja patohistološke dijagnoze tipa glomerulonefritisa, kvantifikovane su promene u intersticijumu bubrega. Određivana je numerička gustina u jedinici zapremine tkiva i struktura infiltrata korišćenjem Weibel-ovog sistema (M42) inkorporisanog u svetlosni mikroskop. Rutinske analize rađene su standardnom laboratorijskom procedurom. Rezultati: Tokom ispitivanog perioda najveća numerička gustina infiltrata verifikovana je kod esktrakapilarnog glomerulonefritisa (147 869 × mm-3), nešto manja kod membranoproliferativnog glomerulonefritisa (116 800 × mm-3) i fokalnosegmentne glomeruloskleroze (96 147 × mm-3), a najmanja kod glomerulonefritisa sa minimalnim promenama (11 416 × mm-3). Kod svih tipova glomerulonefritisa, osim glomerulonefritisa sa minimalnim promenama, ustanovljena je značajno (p < 0,0005) veća numerička gustina i zastupljenost ćelija infiltrata u odnosu na kontrolnu grupu. Upoređujući numeričku gustinu infiltrata svih ćelija sa parametrima bubrežne funkcije, utvrđena je značajna (p < 0,01) povezanost ovih pojava. Radi boljeg uvida u brzinu progresije bubrežne insuficijencije postavljenjem numeričke granice gustine infiltrata < 100 000 / > 100 000 ćelija/mm3 nezavisno od tipa glomerulonefritisa, ustanovljen je prognostički prediktor na osnovu kojeg su bolesnici sa manjom infiltracijom intersticijuma imali značajno (p < 0,005) sporiju progresiju bubrežne insuficijencije. Zaključak. Gustina infiltrata u intersticijumu kod primarnih glomerulonefritisa je važan, rani prognostički prediktor progresije bubrežne insuficijencije.
Reference
REFERENCES
Platt JL, Grant BW, Eddy AA, Michael AF. Immune cell popu-lations in cutaneous delayed-type hypersensitivity. J Exp Med 1983; 158(4): 1227–42.
Hancock WW, Becker GJ, Atkins RC. A comparison of fixatives and immunohistochemical technics for use with monoclonal antibodies to cell surface antigens. Am J Clin Pathol 1982; 78(6): 825–31.
Hooke DH, Gee DC, Atkins RC. Leukocyte analysis using mo-noclonal antibodies in human glomerulonephritis. Kidney Int 1987; 31(4): 964–72.
Stachura I, Si L, Madan E, Whiteside T. Mononuclear cell subsets in human renal disease. Enumeration in tissue sections with monoclonal antibodies. Clin Immunol Immunopathol 1984; 30(3): 362–73.
Lan HY, Paterson DJ, Atkins RC. Initiation and evolution of interstitial leukocytic infiltration in experimental glomerulonephritis. Kidney Int 1991; 40(3): 425–33.
Hu SY, Jia XY, Li JN, Zheng X, Ao J, Liu G, Cui Z, Zhao MH. T cell infiltration is associated with kidney injury in patients with anti-glomerular basement membrane disease. Sci China Life Sci 2016; 59(12): 1282–9.
Burton CJ, Walls J. Harris KP. Characterisation of the serum factor that stimulates human cortical epithelial cells to produce fibronectin (FN) and PDGF (abstract). J Am Soc Nephrol 1995: 6: 1010.
Nikolic-Paterson DJ, Wang S, Lan HY. Macrophages promote renal fibrosis through direct and indirect mechanisms. Kidney Int 2014; 4(1): 34–8.
Han Y, Ma FY, Tesch GH, Manthey CL, Nikolic-Paterson DJ. Role of macrophages in the fibrotic phase of rat crescentic glomerulonephritis. Am J Physiol Renal Physiol 2013; 304(8): F1043–53.
Bob RF, Herman D, Gluhovschi G, Petrica L, Bozdog G, Velciov S, et al. Is The histological scoring system useful in assessing pa-tients with glomerulonephritis?. BANTAO J 2011; 9(2): 72–6.
Bohle A, Christ H, Grund KE, Mackensen S. The role of the in-terstitium of the renal cortex in renal disease. Contrib Nephrol 1979; 16: 109–14.
Chatenoud L, Bach MA. Abnormalities of T-cell subsets in glo-merulonephritis and systemic lupus erythematosus. Kidney Int 1981; 20(2): 267–74.
Ihm CG. Hypertension in Chronic Glomerulonephritis. Elec-trolyte Blood Press 2015; 13(2): 41–5.
Abercrombie M. Estimation of nuclear population from micro-tome sections. Anat Rec 1946; 94: 239–47
Weibel ER, Gomez DM. A principle for counting tissue struc-tures on random sections. J Appl Physiol 1962; 17: 343–8.
Habib R. Classification of glomerulonephritis based on mor-phology. Perspect Nephrol Hypertens 1973; 1 Pt 1: 17–41.
Churg J, Duffy JL. Classification of glomerulonephritis based on morphology. Perspect Nephrol Hypertens 1973; 1 Pt 1: 43–61.
Weibel ER. Stereology: A bridge between morphology and physiology. Acta Stereol 1982; 1: 23–31.
Alexopoulos E, Seron D, Hartley RB, Nolasco F, Cameron JS. The role of interstitial infiltrates in IgA nephropathy: a study with monoclonal antibodies. Nephrol Dial Transplant 1989; 4(3): 187–95.
Schena FP, Mastrolitti G, Jirillo E, Munno I, Pellegrino N, Fracasso AR, et al. Increased production of interleukin-2 and IL-2 re-ceptor in primary IgA nephropathy. Kidney Int 1989; 35(3): 875–9.
Serón D, Alexopoulos E, Raftery MJ, Hartley B, Cameron JS. Number of interstitial capillary cross-sections assessed by monoclonal antibodies: Relation to interstitial damage. Nephrol Dial Transplant 1990; 5(10): 889–93.
Li HL, Hancock WW, Hooke DH, Dowling JP, Atkins RC. Mo-nonuclear cell activation and decreased renal function in IgA nephropathy with crescents. Kidney Int 1990; 37(6): 1552–6.
Danilewicz M, Wagrowska-Danilewicz M. Idiopathic membranous glomerulonephritis: a quantitative study of glomerular and in-terstitial lesions. Pol J Pathol 1995; 46(3): 173–7.
Hao W, Rovin BH, Friedman A. Mathematical model of renal interstitial fibrosis. Proc Natl Acad Sci U S A 2014; 111(39): 14193–8.
Lin TJ, Yang SS, Hua KF, Tsai YL, Lin SH, Ka SM. SPAK plays a pathogenic role in IgA nephropathy through the activation of NF-κB/MAPKs signaling pathway. Free Radic Biol Med 2016; 99: 21–24.
Truong LD, Trostel J, McMahan R, Chen JF, Garcia GE. Macro-phage A2A Adenosine Receptors Are Essential to Protect from Progressive Kidney Injury. Am J Pathol 2016; 186(10): 2601–13.
Bob F, Gluhovschi G, Herman D, Petrica L, Bozdog G, Gluhovschi C, et al. Immunohistochemical study of tubular epithelial cells and vascular endothelial cells in glomerulonephritis. Ren Fail 2014; 36(8): 1208–14.
