Ikee Ryota, Hamasaki Yoshifumi, Oka Machiko, Maesato Kyoko, Mano Tsutomu, Moriya Hidekazu, Ohtake Takayasu, Kobayashi Shuzo
Department of Nephrology and Kidney and Dialysis Center, Shonan Kamakura General Hospital, Kamakura, Japan.
Nephron Clin Pract. 2008;108(2):c163-8. doi: 10.1159/000115329. Epub 2008 Feb 6.
The relation between insulin resistance and atherosclerosis is widely recognized, but it remains unknown whether glucose metabolism/insulin resistance is related to renal pathology in humans.
We quantitatively evaluated pathological changes in the glomeruli, tubulointerstitium, and vessels in renal biopsy specimens from 23 patients with non-diabetic chronic kidney disease (CKD), all of whom took a 75-gram oral glucose tolerance test. We correlated the renal pathological changes with fasting plasma glucose (FPG), fasting plasma insulin, 2-hour plasma glucose (2-h PG), 2-hour plasma insulin (2-h PI), homeostasis model assessment of insulin resistance (HOMA-IR), and body mass index.
HOMA-IR exceeded 1.73 in 11 patients (47.8%), and 2-h PI exceeded 64.0 microU/ml in 14 (60.9%). FPG significantly correlated with interstitial fibrosis (r = 0.532, p = 0.009). The significance was marginal in the correlation between FPG and tubular atrophy and arterio-arteriolosclerosis. Statistically significant correlation was also found between 2-h PG and arterio-arteriolosclerosis (r = 0.422, p = 0.04) and between HOMA-IR and interstitial fibrosis (r = 0.416, p = 0.04).
Although precise mechanisms remain unknown, glucose metabolism/insulin resistance seem to play pathogenic roles in formation and progression of renal pathological changes, especially tubulointerstitial and vascular lesions, in non-diabetic CKD.
胰岛素抵抗与动脉粥样硬化之间的关系已得到广泛认可，但葡萄糖代谢/胰岛素抵抗是否与人类肾脏病理相关仍不清楚。
我们对23例非糖尿病慢性肾脏病（CKD）患者肾活检标本中的肾小球、肾小管间质和血管的病理变化进行了定量评估，所有患者均进行了75克口服葡萄糖耐量试验。我们将肾脏病理变化与空腹血糖（FPG）、空腹血浆胰岛素、2小时血浆葡萄糖（2-h PG）、2小时血浆胰岛素（2-h PI）、胰岛素抵抗稳态模型评估（HOMA-IR）和体重指数进行了相关性分析。
11例患者（47.8%）的HOMA-IR超过1.73，14例患者（60.9%）的2-h PI超过64.0微单位/毫升。FPG与间质纤维化显著相关（r = 0.532，p = 0.009）。FPG与肾小管萎缩和小动脉-细动脉硬化之间的相关性边缘显著。2-h PG与小动脉-细动脉硬化之间（r = 0.422，p = 0.04）以及HOMA-IR与间质纤维化之间（r = 0.416，p = 0.04）也发现有统计学显著相关性。
虽然确切机制尚不清楚，但在非糖尿病CKD中，葡萄糖代谢/胰岛素抵抗似乎在肾脏病理变化尤其是肾小管间质和血管病变的形成和进展中起致病作用。
