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[慢性肾小球肾炎患者近端肾单位上皮细胞、肾小管周围毛细血管内皮细胞的细胞化学特征及肾脏功能状态]

[The cytochemical characteristics of the epithelium of the proximal nephron and of the endothelium of the peritubular capillaries and kidney functional status in chronic glomerulonephritis patients].

作者信息

Kaiukov I G, Klechikov V Z, Vyrikov K A, Nikogosian Iu A, Abissova N A

出版信息

Urol Nefrol (Mosk). 1993 Sep-Oct(5):36-9.

PMID:8310583
Abstract

To assess the role of metabolic shifts in pathogenesis of excretory renal dysfunction arising in chronic glomerulonephritis (CGN), two groups of patients were considered. Fourteen patients of group 1 had CGN in a preazotemia stage, thirteen patients of group 2 died of CGN-induced uremia. Cortical nephrobiopsies obtained intravitally (group 1) and renal tissue specimens obtained at autopsies during postmortal hours 0-2 (group 2) were investigated. Apical epithelium of proximal canaliculi in group 1 showed higher levels of acid phosphatase (AP), though much lower of succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH) compared to group 2. In basal proximal nephrothelium of group 1 the activity of LDH and AP was inhibited against these values in group 2. The activity of NADPN2-dehydrogenase, SDH and AP in group 1 surpassed that in group 2 in endothelium of renal cortex peritubular capillaries. These structures LDH and AP proved more active in group 1. The authors observed a series of significant multidirectional correlations between the activity of the enzymes studied and renal excretion. The growing activity of NADN2-dehydrogenase and AP was associated with diminution of electrolyte and water excretion, while enhancing LDH activity exhibited the opposite effect. It is concluded that progression of cortical disorders in the kidneys of CGN patients entails serious metabolic derangement reflected by imbalance in aerobic and anaerobic metabolism. These biochemical shifts result in ambiguous functional sequelae and may contribute both to renal retention of fluid, electrolytes and their excretion. The latter is likely a compensatory mechanism involved in maintenance of water-salt homeostasis in relevant patients.

摘要

为评估代谢变化在慢性肾小球肾炎(CGN)所致排泄性肾功能不全发病机制中的作用,研究了两组患者。第一组14例患者处于CGN的氮质血症前期,第二组13例患者死于CGN所致尿毒症。对第一组患者活体获取的皮质肾活检标本以及第二组患者在死后0 - 2小时尸检获取的肾组织标本进行了研究。与第二组相比,第一组近端小管的顶端上皮显示酸性磷酸酶(AP)水平较高,而琥珀酸脱氢酶(SDH)和乳酸脱氢酶(LDH)水平则低得多。在第一组近端肾小皮的基底部分,LDH和AP的活性与第二组相比受到抑制。第一组肾皮质肾小管周围毛细血管内皮中的NADPN2 - 脱氢酶、SDH和AP的活性超过第二组。这些结构中的LDH和AP在第一组中更活跃。作者观察到所研究的酶活性与肾脏排泄之间存在一系列显著的多向相关性。NADN2 - 脱氢酶和AP活性的增加与电解质和水排泄的减少相关,而LDH活性增强则表现出相反的效果。得出的结论是,CGN患者肾脏皮质病变的进展会导致严重的代谢紊乱,表现为有氧和无氧代谢失衡。这些生化变化导致功能后果不明确,可能既导致肾脏对液体、电解质的潴留,也导致其排泄。后者可能是相关患者维持水盐稳态的一种代偿机制。

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