肾小球肾炎和钠潴留：嘌呤霉素诱导的肾病综合征大鼠和自发性狼疮样肾小球肾炎小鼠共有集合管中 Na+/K+-ATPase 活性的增强,Nephrology Dialysis Transplantation

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肾小球肾炎和钠潴留：嘌呤霉素诱导的肾病综合征大鼠和自发性狼疮样肾小球肾炎小鼠共有集合管中 Na+/K+-ATPase 活性的增强
Nephrology Dialysis Transplantation ( IF 4.8 ) Pub Date : 1999-09-01 , DOI: 10.1093/ndt/14.9.2192
Einath Zolty , Nabila Ibnou-Zekri , Shozo Izui , Eric Féraille , Hervé Favre

背景在嘌呤霉素氨基葡萄糖苷诱导 (PAN) 肾病综合征大鼠中，显微穿刺研究已将钠潴留部位定位到集合管。我们已经证实了这一发现，证明 Na+/K+-ATPase 活性增加了两倍，特别限于 PAN 大鼠的皮质集合管。为了进一步确定这种现象是依赖于肾病综合征的化学诱导还是在肾小球肾炎中观察到的普遍现象，我们测量了自发性狼疮样肾炎小鼠肾单位节段中的 Na+/K+-ATPase 活性。方法在三个分离的肾单位节段中测量 Na+/K+-ATPase 的水解活性：近曲小管、粗升肢和皮质集合管。Na+/K+-ATPase 活性在 PAN 大鼠、假注射对照组、在 (MRL x BXSB) F1 雄性小鼠中，它们在 4 个月大时发展为自发性狼疮样肾小球肾炎及其对照。对照小鼠具有相同的遗传背景，但缺乏负责自身免疫加速的 Yaa 突变基因，并且在 4 个月大时没有肾小球病变。结果在 (MRL x BXSB) F1 雄性小鼠中，Na+/K+-ATPase 在近曲小管和粗升肢中与对照小鼠相似。相比之下，(MRL x BXSB) F1 小鼠的皮质集合管 Na+/K+-ATPase 活性是对照组的两倍。与分别在腹膜内注射嘌呤霉素或等渗盐水后 7 天研究的假注射对照相比，这些结果与在 PAN 大鼠中观察到的结果相同。结论定位于皮质集合管的 Na+/K+-ATPase 活性的增强是肾小球肾炎的一般特征，与其诱导模式无关，即化学与自身免疫。因此，PAN 的实验模型适用于研究导致 Na+/K+-ATPase 功能障碍的潜在机制。

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Glomerulonephritis and sodium retention: enhancement of Na+/K+-ATPase activity in the collecting duct is shared by rats with puromycin induced nephrotic syndrome and mice with spontaneous lupus-like glomerulonephritis

BACKGROUND In rats with puromycin aminoglucoside-induced (PAN) nephrotic syndrome, micropuncture studies have localized the site of sodium retention to the collecting duct. We have confirmed this finding by demonstrating a two-fold increase in Na+/K+-ATPase activity specifically limited to the cortical collecting duct in PAN rats. To further define whether this phenomenon was dependent on the chemical induction of the nephrotic syndrome or was a general phenomenon observed in glomerulonephritis, we measured Na+/K+-ATPase activity in nephron segments from mice with spontaneous lupus-like nephritis. METHODS Hydrolytic activity of Na+/K+-ATPase was measured in three isolated nephron segments: proximal convoluted tubule, thick ascending limb and cortical collecting duct. The Na+/K+-ATPase activities were measured in PAN rats, sham-injected controls, and in (MRL x BXSB) F1 male mice which develop a well established spontaneous lupus-like glomerulonephritis by 4 months of age and their controls. Control mice have the same genetic background, but lack the Yaa mutant gene responsible for autoimmune acceleration and are free of glomerular lesions at 4 months of age. RESULTS In (MRL x BXSB) F1 male mice, Na+/K+-ATPase was similar to control mice in the proximal convoluted tubule and the thick ascending limb. In contrast, cortical collecting duct Na+/K+-ATPase activity was two times higher in (MRL x BXSB) F1 mice than controls. These results were identical to those observed in PAN rats compared to their sham-injected controls studied 7 days after an intraperitoneal injection of puromycin or isotonic saline, respectively. CONCLUSIONS Enhancement of Na+/K+-ATPase activity localized to the cortical collecting duct is a general characteristic of glomerulonephritis independent of its mode of induction, i.e. chemical versus autoimmune. Therefore, the experimental model of PAN is suitable to study the underlying mechanisms leading to Na+/K+-ATPase dysfunction.

更新日期：1999-09-01

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