Rutkowski Przemyslaw, Klassen André, Sebekova Katarina, Bahner Udo, Heidland August
Department of Nephrology, Transplantology, and Internal Diseases, Medical University of Gdansk, Poland.
J Ren Nutr. 2006 Jul;16(3):216-23. doi: 10.1053/j.jrn.2006.04.017.
Excess body weight may be associated with various functional/structural lesions of the kidney. The spectrum ranges from glomerulomegaly with or without focal or segmental glomerulosclerosis, to diabetic nephropathy, to carcinoma of the kidney and nephrolithiasis. The first sign of renal injury is microalbuminuria or frank proteinuria, in particular in the presence of hypertension. The occurrence of microalbuminuria and/or chronic kidney insufficiency (glomerular filtration rate < 60 mL/min/1.73 m2) is related to the increasing number of components of the metabolic syndrome, ie, central obesity, elevated fasting blood glucose level, hypertriglycerides, low high-density lipoprotein cholesterol, and hypertension. In the long run, end-stage renal failure may develop. An increased body mass index is particularly harmful in patients with reduced renal functional mass (unilateral renal agenesis or nephrectomy) and other renal diseases (immunoglobulin A nephritis and chronic graft dysfunction after kidney transplantation). In the pathogenesis of obesity-associated glomerulopathy, hyperfiltration is of fundamental importance. The factors involved are energy intake (high protein and salt), hyperinsulinemia, and enhanced tubuloglomerular feedback because of increased sodium reabsorption. The adrenergic and renin-angiotensin-aldosterone systems as well as glucocorticoids are stimulated. In addition, several active proteins generated in the central adipose tissue, such as leptin, proinflammatory cytokines, plasminogen activator inhibitor-1, angiotensinogen, and growth factors (transforming growth factor-beta1), as well as low levels of the protective adiponectin, may contribute to renal injury. Of greatest importance is the development of hypertension and of diabetes, which are directly related to the severity of central obesity. Obesity-associated renal disease should be prevented or retarded by weight reduction following lifestyle modification (salt restriction, hypocaloric diet, aerobic exercise), or eventually by antiobesity medication or bariatric surgery. In the presence of glomerulopathy and/or hypertension, angiotensin converting enzyme inhibitors or angiotensin II type I receptor blockers are the drugs of choice to improve glomerular hyperfiltration.
体重超标可能与肾脏的各种功能/结构损害相关。其范围从伴有或不伴有局灶性或节段性肾小球硬化的肾小球肿大，到糖尿病肾病，再到肾癌和肾结石。肾损伤的首个迹象是微量白蛋白尿或显性蛋白尿，尤其是在伴有高血压的情况下。微量白蛋白尿和/或慢性肾功能不全（肾小球滤过率<60 mL/min/1.73 m²）的发生与代谢综合征各组分数量的增加有关，即中心性肥胖、空腹血糖水平升高、高甘油三酯、低高密度脂蛋白胆固醇以及高血压。从长远来看，可能会发展为终末期肾衰竭。体重指数增加对肾功能质量降低（单侧肾发育不全或肾切除术）以及其他肾脏疾病（免疫球蛋白A肾病和肾移植后慢性移植物功能障碍）的患者尤其有害。在肥胖相关性肾小球病的发病机制中，高滤过至关重要。涉及的因素包括能量摄入（高蛋白和高盐）、高胰岛素血症以及由于钠重吸收增加导致的肾小管-肾小球反馈增强。肾上腺素能和肾素-血管紧张素-醛固酮系统以及糖皮质激素受到刺激。此外，中央脂肪组织中产生的几种活性蛋白，如瘦素、促炎细胞因子、纤溶酶原激活物抑制剂-1、血管紧张素原和生长因子（转化生长因子-β1），以及保护性脂联素水平降低，可能导致肾损伤。最重要的是高血压和糖尿病的发生，它们与中心性肥胖的严重程度直接相关。肥胖相关性肾病应通过生活方式改变（限盐、低热量饮食、有氧运动）后的体重减轻来预防或延缓，最终可通过抗肥胖药物或减肥手术来实现。在存在肾小球病和/或高血压的情况下，血管紧张素转换酶抑制剂或血管紧张素II 1型受体阻滞剂是改善肾小球高滤过的首选药物。
