LBL 组和SLBL组的肾小球硬化率参数和肾小管周围毛细血管数目不同。
The parameters of glomerulus sclerosis rate and the number of peritubular capillary were different between LBL and SLBL groups.
减轻肾小球硬化细胞外基质的积聚。
Cordycepssinensis can alleviate the accumulation of extracellular matrix.
可见部分肾小球硬化。
肾小球脂质沉着指数的计算公式同肾小球硬化指数。
The calculation formula of index of renal corpuscle lipid deposition was the same to glomerulosclerosis index.
结论老年人肾小球已具有肾小球硬化的早期病理基础。
Conclusions There is already early pathological feature of glomerulosclerosis in the glomeruli of normal aging kidneys.
局灶性节段性肾小球硬化，三色染色显示蓝色的胶原沉积。
This trichrome stain of a glomerulus in a patient with focal segmental glomerulosclerosis (FSGS) demonstrates blue collagen deposition.
局灶性节段性肾小球硬化，肾小球中央有一片胶原硬化区。
This is focal segmental glomerulosclerosis (FSGS). An area of collagenous sclerosis runs across the middle of this glomerulus.
因此，抑制肾小球系膜细胞增殖是防治肾小球硬化的重要措施。
It is concluded that it is a key to treat the glomerular sclerosis by inhibiting the proliferation of mesangial cells.
肾脏病理为微小病变肾病、膜性肾病及局灶节段性肾小球硬化症。
Minimal change disease, membranous nephropathy and focal segmental glomerular sclerosis are found pathologically.
它表现为皮质纤维化、肾小球硬化、慢性炎细胞弥散侵润、动脉壁增厚；
The cortex is fibrotic, the glomeruli are sclerotic, there are scattered chronic inflammatory cell infiltrates, and the arteries are thickened.
残余肾功能是存在的，但很少，在有局灶节段性肾小球硬化的病人是更低。
Renal survival was numerically, but not significantly, lower in patients with FSGS.
免疫复合物型肾炎是一种经典的肾炎模型，其病理改变最终将导致肾小球硬化。
Immune complexes nephritis is a typical nephritis model, its pathological change finally lead to glomerular sclerosis.
急性模型病理学改变类似人的微小病变性肾病，慢性模型病理学改变类似人的局灶节段性肾小球硬化。
The acute model is similar to human minimal change disease, and the chronic model is similar to human focal segmental glomerulosclerosis.
目的探讨原发性局灶节段性肾小球硬化（FSGS）的临床表现、肾脏病理和治疗反应的特点及关系。
Objective To investigate the relationship between the clinical character and pathological variants as well as response to treatment of focal segmental glomerulosclerosis(FSGS) in children.
富硒枸杞组与宁夏枸杞组在肾小球硬化率，管周毛细血管数，基底膜厚度等指标有显著性差异（P <0 .0 5 ）。
The parameters of glomerulus sclerosis rate, the number of peritubular capillary, basement membrane thickness were different between LBL and SLBL groups(P<0.05).
GMC增殖可引起细胞外基质（ECM）过量生成和聚集，并最终导致肾小球硬化（GS）、肾脏纤维化及终末期肾功能衰竭。
The proliferation of GMC can induce extracellular matrix(ECM) expansion, which can lead to glomerulosclerosis(GS), renal fibrosis and even end stage renal failure in the final.
肾小球系膜细胞(GMC)的增殖通过影响细胞外基质(ecm)的分泌和对肾小球毛细血管的机械损伤而在肾小球硬化过程中发挥着重要作用。
BackgroundThe GMC proliferation plays an important role in glomerular sclerosis by influencing the ECMs secretion and mechanical injury on the glomerular capillaries.
在任何慢性肾脏疾病，如肾小球肾炎、肾硬化或肾盂肾炎等，淋巴细胞都很常见。
It is not uncommon to see lymphocytes accompany just about any chronic renal disease: glomerulonephritis, nephrosclerosis, pyelonephritis.
计算患者病理切片硬化肾小球数、新月体数和间质纤维化面积百分比。
The ratios of sclerosing glomeruli, crescents and area of interstitial fibrosis were calculated.
计算患者病理切片硬化肾小球数、新月体数和间质纤维化面积百分比。
The ratios of sclerosing glomeruli, crescents and area of interstitial fibrosis were calculated.
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