Renovascular hypertension does not influence repair of glomerular lesions induced by anti-thymocyte glomerulonephritis.

Renovascular hypertension does not influence repair of glomerular lesions induced by anti-thymocyte glomerulonephritis.
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肾血管性高血压不影响抗胸腺细胞肾炎引起的肾小球病变的修复。

DOI:
10.1046/j.1523-1755.2000.00270.x
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发表时间:
2000
影响因子:
19.6
通讯作者:
R. Stahl
R. Stahl
中科院分区:
医学1区
文献类型:
--
作者:
U. Wenzel;G. Wolf;F. Thaiss;U. Helmchen;R. Stahl

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背景 全身性高血压是肾脏疾病进展的危险因素。然而,尚不清楚高血压是否对免疫介导的肾小球损伤的愈合或消退有影响。为了评价这种作用,我们应用两肾一夹高血压大鼠肾小球肾炎模型,研究高血压对这种肾炎愈合过程的影响。 方法 在两肾一夹高血压开始后6周,当血压已经升高时,在大鼠中诱导抗胸腺细胞血清(ATS)肾小球肾炎。6周后检查肾脏结构和功能。通过蛋白质印迹法评估α平滑肌肌动蛋白、细胞周期抑制剂p27 Kip 1和转化生长因子-β(TGF-β)的肾小球表达。免疫组化检测肾小球增生、单核细胞浸润和纤维连接蛋白。 结果 与正常血压大鼠相比,高血压大鼠存活率降低,蛋白尿增加,肾小球和肾小管间质损伤增加。在未夹闭的肾脏中,纤连蛋白、α-平滑肌肌动蛋白、TGF-β和p27 Kip 1的表达增加。与肾炎相关的肾小球变化的完全愈合发生在血压正常的肾炎大鼠。令人惊讶的是,在肾血管性高血压大鼠的夹闭和非夹闭肾脏中也发现肾炎完全愈合。高血压伴和不伴肾炎大鼠的生存率、蛋白尿、肾小球大小、增殖、单核细胞/巨噬细胞浸润、硬化、肾小管间质损伤以及α-平滑肌肌动蛋白、TGF-β、纤连蛋白和p27 Kip 1的表达无显著差异。 结论 这些数据表明,肾血管性高血压不影响抗胸腺细胞血清肾炎肾小球病变的愈合。这是一个相当令人惊讶的观察结果,并留下了一个问题,即实际上,血压可能对急性肾小球肾炎的修复阶段有什么作用,或者它的作用是否取决于肾小球肾炎的类型。
BACKGROUND Systemic hypertension is a risk factor for progression of renal disease. However, it is not clear whether hypertension has an effect on healing or regression of immune-mediated glomerular damage. To evaluate this effect, we applied a model of glomerulonephritis in rats with two-kidney, one-clip hypertension and studied the effect of hypertension on the healing process of this nephritis. METHODS The anti-thymocyte serum (ATS) glomerulonephritis was induced in rats six weeks after initiation of two-kidney, one-clip hypertension, when blood pressure was already increased. Renal structure and function were examined six weeks later. Glomerular expression of alpha smooth muscle actin, the cell cycle inhibitor p27Kip1, and transforming growth factor-beta (TGF-beta) was evaluated by Western blotting. Glomerular proliferation, monocyte infiltration, and fibronectin were examined by immunohistochemistry. RESULTS Decreased survival, an increase of proteinuria, as well as increased glomerular and tubulointerstitial damage, were found in hypertensive rats compared with normotensive rats. Expression of fibronectin, alpha-smooth muscle actin, TGF-beta, and p27Kip1 was increased in the nonclipped kidney. Complete healing of the glomerular changes associated with the nephritis occurred in normotensive nephritic rats. Surprisingly, complete healing of the nephritis was also found in the clipped as well as nonclipped kidneys of renovascular hypertensive rats. No significant differences could be found for survival, proteinuria, glomerular size, proliferation, monocyte/macrophage infiltration, sclerosis, tubulointerstitial damage, as well as expression of alpha-smooth muscle actin, TGF-beta, fibronectin, and p27Kip1 between hypertensive rats with and without nephritis. CONCLUSION These data demonstrate that renovascular hypertension does not influence healing of the glomerular lesions in the anti-thymocyte serum nephritis. This is a rather surprising observation and leaves the question open of which role, in fact, blood pressure may have on the reparative phase of an acute glomerulonephritis, or whether its role depends on the type of glomerulonephritis.
DOI: 10.1172/jci115089
发表时间: 1991-03-01
影响因子: 15.9
作者:
JOHNSON, RJ;IIDA, H;GOWN, AM
通讯作者: GOWN, AM
实验性肾小球硬化中的肾小球血流动力学变化与肥大。
DOI: 10.1038/ki.1989.35
发表时间: 1989
影响因子: 19.6
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DOI: 10.1038/ki.1987.257
发表时间: 1987
影响因子: 19.6
作者:
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DOI: --
发表时间: 1994
期刊: The American journal of pathology
影响因子: --
作者:
Barnes,JL;Hastings,RR;DelaGarza,MA
通讯作者: DelaGarza,MA
DOI: 10.1038/ki.1996.432
发表时间: 1996-10-01
影响因子: 19.6
作者:
Shankland, SJ;Hugo, C;Johnson, RJ
通讯作者: Johnson, RJ