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肥胖相关性局灶节段性肾小球硬化:病变的病理特征及其与心脏肥大和高脂血症的关系。

Obesity-associated focal segmental glomerulosclerosis: pathological features of the lesion and relationship with cardiomegaly and hyperlipidemia.

作者信息

Verani R R

机构信息

Department of Pathology and Laboratory Medicine, University of Texas Medical School, Houston 77030.

出版信息

Am J Kidney Dis. 1992 Dec;20(6):629-34. doi: 10.1016/s0272-6386(12)70230-5.

DOI:10.1016/s0272-6386(12)70230-5
PMID:1462993
Abstract

In a review of the autopsies and medical records of 22 obese patients, focal segmental glomerulosclerosis (FSGS) was present in seven. The FSGS was mild in all but one patient. The FSGS of obese patients has similar features to idiopathic FSGS; however, our findings suggest that it lacks the hyperplasia of glomerular epithelial cells, shows no predilection for the corticomedullary junction, and is probably more often seen in the hilar region of the glomeruli. FSGS or glomerulomegaly was not associated with the degree of obesity. We demonstrated lipid deposition in the kidney of obese patients. Obese patients with FSGS, compared to those without FSGS, had higher blood cholesterol (P < 0.10) and higher triglyceride levels (P < 0.01). The mean heart weight of obese patients with FSGS was greater than that of patients without FSGS (P < 0.01). Also, obese patients with FSGS had larger glomeruli (246 +/- 33 microns) than obese patients without FSGS (218 +/- 16 microns) (P < 0.05). These findings suggest that cardiomegaly with hemodynamic changes and glomerular hyperfiltration may play a significant role in the glomerulomegaly and FSGS of obese patients. The secondary or contributory role of lipids in the development of the FSGS of obese patients remains to be determined.

摘要

在对22例肥胖患者的尸检和病历进行回顾时,发现7例存在局灶节段性肾小球硬化(FSGS)。除1例患者外,其余患者的FSGS均较轻。肥胖患者的FSGS具有与特发性FSGS相似的特征;然而,我们的研究结果表明,它缺乏肾小球上皮细胞增生,对皮髓质交界处无偏好,且可能更常见于肾小球的肾门区域。FSGS或肾小球肿大与肥胖程度无关。我们证实了肥胖患者的肾脏中存在脂质沉积。与无FSGS的肥胖患者相比,患有FSGS的肥胖患者血胆固醇水平更高(P < 0.10),甘油三酯水平更高(P < 0.01)。患有FSGS的肥胖患者的平均心脏重量大于无FSGS的患者(P < 0.01)。此外,患有FSGS的肥胖患者的肾小球(246 +/- 33微米)比无FSGS的肥胖患者的肾小球(218 +/- 16微米)更大(P < 0.05)。这些发现表明,心脏肥大伴血流动力学改变和肾小球高滤过可能在肥胖患者的肾小球肿大和FSGS中起重要作用。脂质在肥胖患者FSGS发生发展中的次要或促成作用仍有待确定。

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