Bertani Tullio, Mazzucco Gianna, Monga Guido
Divisione di Nefrologia, Ospedali Riuniti di Bergamo, Italia.
Nephron. 2002 May;91(1):74-8. doi: 10.1159/000057607.
Although there has been extensive research into the mechanisms involved in glomerular crescent formation, it is not yet fully understood how this change may cause renal function impairment. The aim of this study is to identify morphologic changes which may be responsible for this phenomenon. Thirty-eight renal biopsies showing glomerulonephritis with extracapillary proliferation (20 vasculitis-related, 6 idiopathic, 9 due to immune-complex deposition and 3 superimposed on diabetic nephropathy) were considered, and 146 glomeruli in which both crescents and the urinary pole were found at the same time, were studied. The involvement of the urinary pole by cellular crescents was observed in 93.1 and 100% of the glomeruli with segmental or circumferential crescents, respectively. A tridimensional study, for the evaluation of the glomeruli as a whole, was performed on 8 biopsies by means of the step-section technique and disclosed the involvement of the urinary space and a close contact between crescent and tubular cells in all 54 investigated glomeruli. The reported features do not seem to be related to the type of cells which formed the crescent. Indeed, as shown by immunohistochemical study on 10 cases with anti-cytokeratin and anti-CD68 antisera, the crescent localization at the urinary pole had no correlation with the prevalence of epithelial or macrophagic cells. These findings suggest that crescents, due to epithelial proliferation or macrophage clustering, tend to localize at the urinary pole and thus come into close contact with cells of the proximal convoluted tubule: the formation of a sort of plug or a 'glomerular stone' could well explain the block in the urine flow and the consequent impairment of renal function in the acute phase of the disease, even in those cases where crescents are segmental.
尽管对肾小球新月体形成所涉及的机制已进行了广泛研究，但这种变化如何导致肾功能损害仍未完全清楚。本研究的目的是确定可能导致这一现象的形态学变化。研究纳入了38例显示有毛细血管外增生的肾小球肾炎肾活检病例（20例与血管炎相关，6例特发性，9例因免疫复合物沉积，3例叠加于糖尿病肾病），并对146个同时发现新月体和尿极的肾小球进行了研究。在分别有节段性或环形新月体的肾小球中，细胞性新月体累及尿极的比例分别为93.1%和100%。通过阶梯切片技术对8例活检标本进行了三维研究以评估整个肾小球，结果显示在所有54个研究的肾小球中尿腔均受累，且新月体与肾小管细胞紧密接触。所报道的这些特征似乎与形成新月体的细胞类型无关。实际上，对10例使用抗细胞角蛋白和抗CD68抗血清进行免疫组化研究显示，新月体在尿极的定位与上皮细胞或巨噬细胞的比例无关。这些发现表明，由于上皮细胞增殖或巨噬细胞聚集形成的新月体倾向于定位于尿极，从而与近端曲管细胞紧密接触：形成一种栓子或“肾小球结石”很可能解释了疾病急性期尿流受阻以及随之而来的肾功能损害，即使在那些新月体为节段性的病例中也是如此。
