无症状高尿酸血症和痛风患者肾活检结果的差异与交集

R. Gancheva, Maria Hristova, T. Kundurzhiev, P. Yankova, Milena Nikolova, A. Koundurdjiev
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摘要

本研究旨在确定无症状高尿酸血症和痛风与肾活检的形态学和免疫荧光变化之间的关联。这项回顾性研究共纳入了 64 例患者,其中 46 例为无症状高尿酸血症患者,18 例为痛风患者。研究人员利用医疗文件对肾活检结果、临床和实验室数据进行了分析。我们没有发现两组慢性肾功能衰竭患者的分布有明显差异。在痛风组中,肾结石患者的比例较高(p 50%),痛风组明显高于痛风组(p = 0.032),但肾小管萎缩> 50%的分布没有发现差异(p = 0.183)。在未接受降尿酸治疗的受试者中,不同阶段的肾小管萎缩和间质纤维化的血清尿酸水平相当。我们发现,在无症状高尿酸血症和痛风中,上皮下、内皮下、间质和血管壁都有免疫沉积物沉积。在痛风中,肾脏受到的影响更大。我们认为,不仅血清尿酸升高很重要,沉积在肾间质的尿酸单钠结晶也会引起慢性炎症过程,继而导致纤维化。我们认为,可溶性尿酸和结晶激活了先天性免疫系统,随后在体内形成一种促炎状态,导致补体激活,免疫沉积物沉积在肾脏中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Differences and Intersections in Renal Biopsy Findings in Patients with Asymptomatic Hyperuricemia and Gout
The aim of this study is to establish the association between asymptomatic hyperuricemia and gout with morphological and immunofluorescent changes in the renal biopsy. A total of 64 patients, 46 with asymptomatic hyperuricemia and 18 with gout were included in this retrospective study. Renal biopsy findings, clinical and laboratory data were analyzed by using medical documentation. We did not find a significant difference in the distribution of chronic renal failure between the two groups. In the gout group, the proportion of patients with nephrolithiasis was higher (p <0.001), and the presence of erythrocyturia was more common (p = 0.047). The percentage of damaged glomeruli (p = 0.249) and the distribution of mesangial proliferation (p = 0.536) was similar in the groups. The proportion of patients with interstitial fibrosis > 50$% was significantly higher in the gout group (p = 0.032), but no difference was observed in the distribution of tubular atrophy > 50% (p = 0.183). In subjects not receiving urate-lowering therapy, serum uric acid levels were comparable in the different stages of tubular atrophy and interstitial fibrosis. We found that in both asymptomatic hyperuricemia and gout, there is a deposition of immune deposits subepithelially, subendothelially, in the mesangium and in the vessel walls. In gout, the kidneys are affected to a much greater extent. We consider that not only the increased serum uric acid is important, but also monosodium urate crystals deposited in the renal interstitium causing a chronic inflammatory process followed by fibrosis. We suggest that the activation of the innate immune system by soluble uric acid and crystals with the subsequent development of a proinflammatory state in the body has led to the activation of complement and deposition of immune deposits in the kidneys.
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