The influence of concomitant experimental hypertension and glomerulonephritis.
The influence of concomitant experimental hypertension and glomerulonephritis.
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伴随实验性高血压和肾小球肾炎的影响。
DOI：
10.1038/ki.1987.257
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发表时间：
1987
影响因子：
19.6
通讯作者：
Wilson,CB
中科院分区：
文献类型：
--
作者：
Blantz,RC;Gabbai,F;Gushwa,LC;Wilson,CB
实验性高血压合并肾小球肾炎的影响。利用两肾一夹Goldblatt模型（CH），我们研究了高血压对抗肾小球基底膜抗体诱导的肾小球肾炎（GN）过程的影响，在CH和GN诱导后的10至14周内，利用清醒大鼠未浸肾的肾脏微穿刺和形态学分析（对照组[C]， GN， CH和GN+CH）进行评估。代谢研究显示，GN和GN+CH大鼠出现蛋白尿、血清肌酐和血压升高（P <0.05）。GN+CH导致两个肾小球滤过率（GFR）显著降低，低于C值，与CH相比，未浸肾的GFR显著降低。GN和CH大鼠肾小球毛细血管静水压力和压力梯度（ΔP）升高约4至5 mm Hg， GN+CH大鼠肾小球静水压力和压力梯度（ΔP）高于GN和CH值6 mm Hg。GN和GN+CH的肾小球超滤系数（LpA）降低至C的约40%，尽管ΔP进一步增加。各组表面肾单位滤过率相似，提示肾小球功能障碍主要发生在GN+CH的表面以下肾单位。形态学评估显示GN+CH分别表现为GN和CH的弥漫性和局灶性硬化病变。经证实，pgg进一步升高并未使肾小球形态恶化，但肾脏GFR确实下降。高血压引起的表面下肾单位肾小球功能的恶化与明显的形态学恶化无关，而是GN和CH特征的结合。
The influence of concomitant experimental hypertension and glomerulonephritis. Utilizing the two kidney–one clip Goldblatt model (CH), we have examined the influence of hypertension upon the course of antiglomerular basement membrane antibody-induced glomerulonephritis (GN) over a period of 10 to 14 weeks after induction of CH and GN, utilizing evaluations in the awake rat by renal micropuncture of the undipped kidney and morphologic analysis (control [C], GN, CH, and GN+CH). Metabolic studies revealed that GN and GN+CH rats developed proteinuria, elevations in serum creatinine and blood pressure (P <0.05). GN+CH resulted in significant reductions in two kidney glomerular filtration rate (GFR) below values in C, and GFR in the undipped kidney was markedly reduced when compared to CH. The glomerular capillary hydrostatic pressure and the pressure gradient (ΔP) were elevated ∼4 to 5 mm Hg in GN and CH rats and 6 mm Hg above GN and CH values in the GN+CH rats. The glomerular ultrafiltration coefficient (LpA) was reduced to ∼40% of C in both GN and GN+CH in spite of further increases in ΔP. Surface nephron filtration rate was similar in all groups, suggesting glomerular dysfunction was primarily in nephrons below the surface in GN+CH. Morphologic evaluation revealed that GN+CH exhibited a combination of diffuse and focally sclerotic lesions characteristic of GN and CH, respectively. Documented further increases in PGdid not worsen glomerular morphology, but kidney GFR did decrease. Hypertension induced deterioration of glomerular function in nephrons below the surface was not associated with marked morphologic deterioration, but a combination of the characteristics of GN and CH.