Department of Nephrology and Kidney and Dialysis Center, Shonan Kamakura General Hospital, Kamakura, Kanagawa, Japan.
Hypertens Res. 2010 May;33(5):499-504. doi: 10.1038/hr.2010.22. Epub 2010 Feb 26.
Hypertension has an important function in the formation of renal arterio-arteriolosclerosis. However, renal arterio-arteriolosclerosis is sometimes found in biopsy specimens of normotensive patients, which indicates unknown factors may contribute to renal arterio-arteriolosclerosis. In this study, we aimed to evaluate the effects of glucose metabolism/insulin resistance on renal arterio-arteriolosclerosis. Forty-eight patients with biopsy-proven non-diabetic chronic glomerular disease were included. Renal arterio-arteriolosclerosis was evaluated as the percentage of vessels showing hyaline changes or wall thickening. We correlated renal arterio-arteriolosclerosis with clinical parameters including indices obtained by 75 g oral glucose tolerance test. Of the 48 patients, 30 had hypertension. The results of univariate analysis showed significant association of renal arterio-arteriolosclerosis with hypertension, increased serum creatinine (S-Cr), hypertriglyceridemia, increased 2-h plasma glucose (PG) and increased 2-h plasma insulin (PI). In stepwise multiple regression analysis, hypertension (beta=0.344, P=0.009), S-Cr (beta=0.287, P=0.03) and 2-h PG (beta=0.274, P=0.03) were independently associated with renal arterio-arteriolosclerosis. Eleven of the 30 hypertensive patients did not have renal arterio-arteriolosclerosis. The hypertensive patients with renal arterio-arteriolosclerosis showed significantly higher 2-h PG (134+/-25 vs. 106+/-26 mg per 100 ml, P=0.008) and higher 2-h PI (67.7+/-34.9 vs. 48.3+/-30.0 microU ml(-1), P=0.04) compared with those without renal arterio-arteriolosclerosis, but the difference in S-Cr was not significant. Postprandial hyperglycemia and hyperinsulinemia may contribute to the formation of renal arterio-arteriolosclerosis independently of hypertension.
高血压在肾小动脉中层玻璃样变和小动脉硬化的形成中具有重要作用。然而，在血压正常的患者的活检标本中有时也会发现肾小动脉中层玻璃样变和小动脉硬化，这表明可能有未知因素导致肾小动脉中层玻璃样变和小动脉硬化。在这项研究中，我们旨在评估葡萄糖代谢/胰岛素抵抗对肾小动脉中层玻璃样变和小动脉硬化的影响。纳入 48 例经活检证实的非糖尿病性慢性肾小球疾病患者。肾小动脉中层玻璃样变和小动脉硬化的评估方法是计算出现玻璃样变或管壁增厚的血管所占的百分比。我们将肾小动脉中层玻璃样变和小动脉硬化与临床参数相关联，这些参数包括口服 75 g 葡萄糖耐量试验获得的指标。在 48 例患者中，30 例有高血压。单因素分析结果显示，肾小动脉中层玻璃样变和小动脉硬化与高血压、血清肌酐（S-Cr）升高、高三酰甘油血症、2 小时血糖（PG）升高和 2 小时胰岛素（PI）升高显著相关。在逐步多元回归分析中，高血压（β=0.344，P=0.009）、S-Cr（β=0.287，P=0.03）和 2 小时 PG（β=0.274，P=0.03）与肾小动脉中层玻璃样变和小动脉硬化独立相关。在 30 例高血压患者中，有 11 例没有肾小动脉中层玻璃样变和小动脉硬化。有肾小动脉中层玻璃样变和小动脉硬化的高血压患者的 2 小时 PG（134±25 比 106±26 mg/100 ml，P=0.008）和 2 小时 PI（67.7±34.9 比 48.3±30.0 μU/ml，P=0.04）明显高于无肾小动脉中层玻璃样变和小动脉硬化的患者，但 S-Cr 的差异无统计学意义。餐后高血糖和高胰岛素血症可能独立于高血压导致肾小动脉中层玻璃样变和小动脉硬化的形成。
