Sebeková K, Klassen A, Bahner U, Heidland A
Vedecko-výskumná základna Slovenskej zdravotníckej univerzity, Ustav preventívnej a klinickej medicíny, Bratislava, Slovenská republika.
Vnitr Lek. 2004 Jul;50(7):544-9.
Overweight/obesity represent an underestimated risk factor of renal disease. The incidence of obesity-related glomerulopathy (ORG) tremendously increased within the last decade. The first sign of renal damage in overweight conditions is microalbuminuria or proteinuria, indicating the potential risk of its progression to renal insufficiency and the development of premature cardiovascular events. In the early stage of obesity renal hemodynamics are characterized by a renal hypercirculation and glomerular hyperfiltration, particularly in the presence of hypertension. The hyperfiltration is especially harmful in patients with pre-existing inflammatory and metabolic renal disease, or under the conditions of reduced renal mass. Histopathologically, ORG is characterized by glomerulomegaly with/without signs of focal segmental glomerulosclerosis. Pathogenetically, numerous factors are involved, e.g. enhanced glomerular capillary pressure, adrenergic nerve overactivity, inappropriate activation of the renin-angiotensin-aldosterone system, insulin resistance, hyperinsulinemia and hyperleptinemia, dyslipidemia, enhanced clotting tendency and sodium retention. Diabetic nephropathy is one of the most serious complications of obesity-induced diabetes. In the industrial nations type 2 diabetes is the single most frequent cause of end-stage renal disease. After kidney transplantation, overweight/obesity is associated with a less favourable prognosis for the survival of the graft and the patient. Incidence of renal cell carcinomas is enhanced in overweight/obesity. Obesity-related renal disease may be prevented/postponed by an early weight reduction, by dietary intervention combined with physical exercise. In the advanced stages of renal disease benefits of weight reduction are minimal. Concomitant administration of angiotensin-converting-enzyme inhibitors or angiotensin II receptor 1 blockers exerts antiproteinuric effects and thereby aid in retarding the disease progression. Aimed prevention and treatment of obesity represent a challenge for the healthcare system. The concerted action of physicians, patients and the public health authorities is needed.
超重/肥胖是一种被低估的肾脏疾病风险因素。在过去十年中,肥胖相关性肾小球病(ORG)的发病率大幅上升。超重情况下肾脏损害的首个迹象是微量白蛋白尿或蛋白尿,这表明其进展为肾功能不全以及发生过早心血管事件的潜在风险。在肥胖早期,肾脏血流动力学的特征是肾血流增加和肾小球高滤过,尤其是在存在高血压的情况下。这种高滤过对已有炎症性和代谢性肾脏疾病的患者或肾实质减少的情况下尤其有害。组织病理学上,ORG的特征是肾小球肿大,伴有或不伴有局灶节段性肾小球硬化的迹象。在发病机制上,涉及多种因素,例如肾小球毛细血管压力升高、肾上腺素能神经活动过度、肾素-血管紧张素-醛固酮系统的不适当激活、胰岛素抵抗、高胰岛素血症和高瘦素血症、血脂异常、凝血倾向增强和钠潴留。糖尿病肾病是肥胖诱发糖尿病最严重的并发症之一。在工业化国家,2型糖尿病是终末期肾病最常见的单一病因。肾移植后,超重/肥胖与移植物和患者存活的预后较差有关。超重/肥胖会增加肾细胞癌的发病率。通过早期减重、饮食干预结合体育锻炼,可以预防/延缓肥胖相关性肾脏疾病。在肾脏疾病的晚期,减重的益处微乎其微。联合使用血管紧张素转换酶抑制剂或血管紧张素II受体1阻滞剂可发挥抗蛋白尿作用,从而有助于延缓疾病进展。旨在预防和治疗肥胖对医疗保健系统构成了挑战。需要医生、患者和公共卫生当局的协同行动。