Abstract
Various studies describe that interstitial and glomerular renal diseases are characterized by macrophage accumulation and sustained macrophage infiltration resulting in irreversible fibrosis, tissue destruction and progressive chronic kidney disease. Aim of our study is to perform the comparative analysis of CD 68 positivity in renal stroma of various renal diseases in order to understand the basic pathophysiology of macrophage infiltration and clinicopathological role of this marker in prognosis. We evaluated total of 80 consecutive native kidney biopsies performed for diagnostic purposes and were diagnosed as minimal change disease (MCD,10 cases), chronic tubulointerstitial nephritis (CTIN, 10 cases), IgA nephropathy (IgAN, 20 cases), diabetic nephropathy (DN, 20 cases) and lupus nephritis (LN, 20 cases) respectively. A biopsy material remaining after routine light microscopy and immunofluorescence, was stained for CD68 as macrophage infiltration marker. Quantitative evaluation was conducted on consecutive high power fields, avoiding glomeruli, and estimated as number of positive cells/high power field (hpf) for macrophage infiltration in total interstitial area, atrophic area and in most inflamed area. Serum creatinine along with areas of interstitial fibrosis and tubular atrophy (IFTA) were recorded in all cases and chronicity index in lupus nephritis cases were statistically correlated with CD 68 positive cells/hpf in various areas. A total of 80 cases of different etiologies were evaluated with average age of 38.2 years. Median values of CD 68 positive cells/hpf in various renal disorders were as follows: Tabled 1DisorderCD 68/hpf (total interstitial area)CD 68/hpf (atrophic area)CD 68/hpf (most inflamed area)MCD0.950.03.0CTIN13.6517.7523.15IgAN11.719.522.75DN15.519.5527LN14.50.019.5Combined11.112.621.85 Open table in a new tab On an average percentage of IFTA was maximum in diabetic cases (49 %) followed by CTIN (36 %), IgAN (27.7 %), LN (6.5%) and MCD (1.9%). On performing Pearson correlation results were as follows: Tabled 1CorrelationsMCDCTINIgANDNLNCombinedIFTA with CD 68/hpf (total)r- 0.92p- 0.0001r- 0.32p- 0.36r- 0.59p- 0.01r- 0.42p- 0.06r- 0.37p- 0.11r- 0.44p- 4.0IFTA with CD 68/hpf (atrophic area)r- 0.98p- 1.05r- 0.27p- 0.45r- 0.58p- 0.01r-0.16p- 0.5r- 0.74p-0.0002r- 0.55p- 1.4S. creatinine with CD 68/hpf (total)r- 0.04p- 0.92r- 0.02p- 0.9r-0.53p- 0.02r-0.37p- 0.1r- 0.31p- 0.18r- 0.27p- 0.01S. creatinine with CD 68/ hpf (atrophic area)r- 0.1p- 0.8r- 0.11p- 0.76r-0.52p- 0.02r-0.3p- 0.2r- 0.3p- 0.2r- 0.34p- 0.002S. creatinine with CD 68/hpf (most inflamed area)r- 0.12p- 0.7r- 0.001p- 0.99r- 0.56p- 0.01r- 0.37p- 0.1r- 0.31p- 0.2r- 0.3p- 0.01Chronicity index with CD 68/hpf (total)r- 0.18p- 0.5Chronicity index with CD 68/hpf (atrophic area)r- 0.73p- 0.0002 Open table in a new tab p <0.05 is significant This study emphasizes that CD 68 can be considered as a marker of chronicity irrespective of glomerular or tubulointerstitial etiology of renal disorder. Levels of serum creatinine at diagnosis also showed good correlation with this marker establishing its clinicopathological role in prognosis.The limitation of our study was lack of follow-up of these cases in order to establish CD68 as a prognostic marker of chronicity. We recommend follow-up clinicopathological studies to establish the role of this marker for determining chronicity and future outcome of the disease at early stages.
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