Abstract
In the era of antiretroviral therapy (ART), the development of chronic kidney disease in HIV-infected patients is a significant complication not directly related to acquired immunodeficiency syndrome (AIDS), the risk of which is increased with co-infection with hepatitis C virus (HCV). The pathogenetic pathways of the development of kidney tissue damage and the formation of a morphological substrate for each of the viruses are different, but the immune-mediated mechanisms are a common link for the development of immune complex diseases. We studied renal necropsy samples in 20 patients with HIV/HCV co-infection who did not receive ART, and the dependence of the identified morphological substrate on the level of CD4+ in the blood, to assess and predict their morphogenesis. We observed predominantly segmental mesangial proliferation with an expansion of the mesangial matrix and glomerular involvement ≥50 % in 15 (75 %) cases and glomerular involvement <50 % in 3 (15 %) cases. Endocapillary proliferation (E), infiltration of glomeruli with monocytes, neutrophil leukocytes, segmental macrophages were found in 2 (10 %) cases with the involvement of ≥ 50 % of glomeruli, which was regarded as an exudative component of the inflammatory response. In all cases, sclerosis of capillary loops was verified, which was mainly accompanied by their collapse, thickening of the capillary walls, namely the basement membranes of capillaries and segmental sclerosis of capillary loops of the glomeruli of varying severity. Initial interstitial stromal fibrosis was found in 5 (25 %) cases, degenerative changes in the convoluted tubules — in 9 (45 %), mainly with the T0–T1 level. Positive expression of IgA, IgM, IgG, and C3 complement fractions in the form of linear and granular deposits along the capillary endothelium was detected with an intensity of “+” to “++”. We compared the verified morphological pattern and the level of CD4+ in the blood and found that patients with deeper immunosuppression show fewer changes, mainly characterized as sclerotic. Moreover, with an increase in the level of CD4+, the morphological substrate is enriched with a proliferative component. Expression of immunoglobulins and components of the complement system in immonohistochemical assay, in particular in areas of sclerotic changes, verifies the presence of prolonged immune complex associated lesions. To determine the detailed morphogenesis, it is advisable to perform a further correlation analysis of the data obtained with the control.
Highlights
We studied renal necropsy samples in 20 patients with HIV/hepatitis C virus (HCV) co-infection who did not receive antiretroviral therapy (ART), and the dependence of the identified morphological substrate on the level of CD4+ in the blood, to assess and predict their morphogenesis
Costs for investigation, its analysis, and presentation are covered by the authors only
Summary
Клініко-морфологічна характеристика ураження нирок при коінфекції ВІЛ/ВГС у пацієнтів, які не отримували антиретровірусну терапію. В епоху антиретровірусної терапії (АРТ) розвиток хронічної хвороби нирок (ХХН) серед ВІЛінфікованих пацієнтів є значним ускладненням, не пов’язаним безпосередньо з синдромом набутого імунодефіциту, ризик появи якого значно підвищується при коінфекції вірусом гепатиту С (ВГС). Для оцінки та прогнозування їх морфогенезу ми досліджували автопсію нирок 20 пацієнтів з коінфекцією ВІЛ/ВГС, які не отримували АРТ, та залежність виявленого морфологічного субстрату від рівня CD4+ у крові. Що різний розподіл ВГС-пов’язаних білків у функціональних структурах нирок може підтримувати різні патогенетичні шляхи, що відповідає таким при розвитку ВІЛ-ІК [9, 10]. Виявити та описати морфологічний субстрат ураження нирок при коінфекції ВІЛ/ВГС серед пацієнтів, які не приймали АРТ, та дослідити залежність від рівня імуносупресії для оцінки та прогнозування морфогенезу імунокомплексних уражень
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