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肥胖是慢性肾病的主要病因吗?

Is obesity a major cause of chronic kidney disease?

作者信息

Hall John E, Henegar Jeffrey R, Dwyer Terry M, Liu Jiankang, Da Silva Alexandre A, Kuo Jay J, Tallam Lakshmi

机构信息

Department of Physiology and Biophysics and Center of Excellence in Cardiovascular-Renal Research, The University of Mississippi Medical Center, Jackson, MS, USA.

出版信息

Adv Ren Replace Ther. 2004 Jan;11(1):41-54. doi: 10.1053/j.arrt.2003.10.007.

DOI:10.1053/j.arrt.2003.10.007
PMID:14730537
Abstract

Excess weight gain is a major risk factor for essential hypertension and for end-stage renal disease (ESRD). Obesity raises blood pressure by increasing renal tubular sodium reabsorption, impairing pressure natriuresis, and causing volume expansion because of activation of the sympathetic nervous system and renin-angiotensin system and by physical compression of the kidneys, especially when visceral obesity is present. Obesity also causes renal vasodilation and glomerular hyperfiltration that initially serve as compensatory mechanisms to maintain sodium balance in the face of increased tubular reabsorption. In the long-term, however, these changes, along with the increased systemic arterial pressure, create a hemodynamic burden on the kidneys that causes glomerular injury. With prolonged obesity, there is increasing urinary protein excretion and gradual loss of nephron function that worsens with time and exacerbates hypertension. With the worsening of metabolic disturbances and the development of type II diabetes in some obese patients, kidney disease progresses much more rapidly. Weight reduction is an essential first step in the management of obesity, hypertension, and kidney disease. Special considerations for the obese patient, in addition to adequately controlling the blood pressure, include correction of the metabolic abnormalities and protection of the kidneys from further injury.

摘要

体重过度增加是原发性高血压和终末期肾病(ESRD)的主要危险因素。肥胖通过增加肾小管钠重吸收、损害压力性利钠作用以及由于交感神经系统和肾素 - 血管紧张素系统的激活以及肾脏的物理压迫(尤其是存在内脏肥胖时)导致血容量扩张,从而升高血压。肥胖还会导致肾血管舒张和肾小球高滤过,这些最初是作为面对增加的肾小管重吸收时维持钠平衡的代偿机制。然而,从长期来看,这些变化以及全身动脉压升高会给肾脏造成血流动力学负担,进而导致肾小球损伤。随着肥胖时间延长,尿蛋白排泄增加,肾单位功能逐渐丧失,且随时间恶化并加重高血压。在一些肥胖患者中,随着代谢紊乱的恶化和II型糖尿病的发展,肾脏疾病进展得更快。减轻体重是肥胖、高血压和肾脏疾病管理中至关重要的第一步。对于肥胖患者,除了充分控制血压外,特殊考虑还包括纠正代谢异常以及保护肾脏免受进一步损伤。

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