de Vinuesa Soledad García, Goicoechea Marian, Kanter Julia, Puerta Marta, Cachofeiro Victoria, Lahera Vicente, Gómez-Campderá Francisco, Luño José
Department of Nephrology, Hospital General Universitario Gregorio Marañón, C/Dr. Esquerdo 47, 28007, Madrid, Spain.
J Am Soc Nephrol. 2006 Dec;17(12 Suppl 3):S206-12. doi: 10.1681/ASN.2006080916.
Patients with chronic kidney disease (CKD) present a high prevalence of insulin resistance (IR). Some studies suggest that angiotensin II may influence some cellular pathways that contribute to the pathogenesis of IR and stimulate the release of proinflammatory cytokines. Fifty-two patients who had stages 3 and 4 CKD and no diabetes were administered an angiotensin receptor blocker (ARB), olmesartan (40 mg), for 16 wk. Before and after ARB treatment, metabolic and inflammatory parameters and adipokines were measured. IR was calculated by Homeostasis Model Assessment (HOMA) index. Baseline data were compared with data that were obtained from 25 healthy control individuals of similar age and normal renal function. Compared with control subjects, patients with CKD presented significantly higher BP and waist circumference, higher triglycerides and lower HDL levels, higher insulin levels, and higher mean HOMA index (6.0 +/- 2.7 versus 2.9 +/- 2.2 muU/ml x mmol/L; P < 0.001). In addition, patients with CKD had increased levels of high-sensitivity C-reactive protein, TNF-alpha, and IL-6. In patients with CKD, leptin was positively correlated to abdominal obesity, insulin levels, and IL-6, and adiponectin was inversely correlated to abdominal obesity and insulin levels. Olmesartan treatment resulted in a significant decrease of BP, urinary protein excretion, plasma glucose (99 +/- 16 versus 92 +/- 14 mg/dl; P < 0.05), insulin (23.1 +/- 8.8 versus 19.9 +/- 9; P < 0.05), HOMA index (6.0 +/- 2.7 versus 4.7 +/- 2.8; P < 0.05), and glycated hemoglobin (5.33 +/- 0.58 versus 4.85 +/- 0.81%; P < 0.01). At the same time, there was a significant reduction of high-sensitivity C-reactive protein levels, from 4.45 mg/L (2.45 to 9.00) to 3.55 mg/L (1.80 to 5.40; P < 0.05) and fibrinogen (412 +/- 100 versus 370 +/- 105 mg/dl; P < 0.05). There were no significant differences in adipokine levels after olmesartan treatment. These data demonstrate that patients with CKD have a high prevalence of IR, metabolic syndrome, and chronic inflammation and that the administration of the ARB olmesartan improves IR and inflammation markers in these patients. Plasma adipokine levels that are related to several metabolic risk factors in patients with CKD were not modified by ARB therapy.
慢性肾脏病（CKD）患者中胰岛素抵抗（IR）的患病率很高。一些研究表明，血管紧张素II可能影响某些导致IR发病机制的细胞途径，并刺激促炎细胞因子的释放。对52例3期和4期CKD且无糖尿病的患者给予血管紧张素受体阻滞剂（ARB）奥美沙坦（40mg），治疗16周。在ARB治疗前后，测量代谢和炎症参数以及脂肪因子。通过稳态模型评估（HOMA）指数计算IR。将基线数据与从25名年龄相似且肾功能正常的健康对照个体获得的数据进行比较。与对照组相比，CKD患者的血压和腰围显著更高，甘油三酯水平更高，高密度脂蛋白水平更低，胰岛素水平更高，平均HOMA指数更高（6.0±2.7对2.9±2.2μU/ml×mmol/L；P<0.001）。此外，CKD患者的高敏C反应蛋白、肿瘤坏死因子-α和白细胞介素-6水平升高。在CKD患者中，瘦素与腹部肥胖、胰岛素水平和白细胞介素-6呈正相关，脂联素与腹部肥胖和胰岛素水平呈负相关。奥美沙坦治疗导致血压、尿蛋白排泄、血糖（99±16对92±
