Pal'tsev M A, Varshavskii V A, Maksimov N A, Balkarov I M
Arkh Patol. 1988;50(6):8-15.
The study of a hyperuricemic variant of chronic latent glomerulonephritis in asymptomatic hyperuricemia and gout suggested that relevant pathologic lesion can be morphologically represented by immune-complex glomerulonephritis and reactive mesangial changes as well as secondary tubulointerstitial nephritis. The underlying pathogenetic mechanism in the development of immune-complex glomerulonephritis and secondary tubulointerstitial nephritis is formation of antibodies to antigens of basal glomerular membrane and to alkaline edge of the proximal nephron, respectively. Reactive mesangial changes of the glomeruli reflect mesangiocyte sensitization to the antigens.
对无症状高尿酸血症和痛风患者慢性潜伏性肾小球肾炎的高尿酸血症变体的研究表明，相关病理病变在形态学上可表现为免疫复合物性肾小球肾炎、反应性系膜改变以及继发性肾小管间质性肾炎。免疫复合物性肾小球肾炎和继发性肾小管间质性肾炎发生发展的潜在发病机制分别是针对肾小球基底膜抗原和近端肾小管碱性边缘抗原形成抗体。肾小球的反应性系膜改变反映了系膜细胞对抗原的致敏。
