肥胖相关性肾病

超重与多种功能例及器质性肾脏疾病有关，如肾小球肥大伴或不伴局灶节段性肾小球硬化、糖尿病肾病、肾癌、肾结石等。早期肾脏损伤的标志为微量白蛋白尿，高血压时尤为显著。微量白蛋白尿和／或慢性肾功能不全的发生与代谢综合征中的各组分有关，如中心性肥胖、糖代谢异常、脂代谢异常和高血压等。在肥胖相关性肾小球病的发病机制中，高滤过的作用十分重要，与其相关的因素包括摄入（高蛋白和高盐）、高胰岛素血症和球管反馈加强；肾上腺素、肾素一血管紧张素一醛固酮系统的激活在肥胖相关性肾小球病的发病机制中也发挥了一定的作用。另外，脂肪组织分泌一些活性蛋白，如瘦素、促炎症因子、纤溶酶原激活物抑制因子-1、血管紧张素原和转化生长因子-β1水平的增加及脂联素水平降低，这些都可以加重肾损害。而通过生活方式的改善、减轻体重及药物治疗可使肥胖相关性肾病得到一定程度预防和改善。     

肥胖相关性肾病

随着肥胖发病率的逐年增高,肥胖相关性肾病越来越受到重视,本文就肥胖相关性肾病的临床特征、可能的发病机制及治疗进展作一综述.     

肥胖相关性肾病

超重与多种功能性及器质性肾脏疾病有关,如肾小球肥大伴或不伴局灶节段性肾小球硬化、糖尿病肾病、肾癌、肾结石等.早期肾脏损伤的标志为微量白蛋白尿,高血压时尤为显著.微量白蛋白尿和/或慢性肾功能不全的发生与代谢综合征中的各组分有关,如中心性肥胖、糖代谢异常、脂代谢异常和高血压等.在肥胖相关性肾小球病的发病机制中,高滤过的作用十分重要,与其相关的因素包括摄入(高蛋白和高盐)、高胰岛素血症和球管反馈加强;肾上腺素、肾素一血管紧张素一醛固酮系统的激活在肥胖相关性肾小球病的发病机制中也发挥了一定的作用.另外,脂肪组织分泌一些活性蛋白.如瘦素、促炎症因子、纤溶酶原激活物抑制因子-1、血管紧张素原和转化生长因子-β1水平的增加及脂联索水平降低,这些都可以加重肾损害.而通过牛活方式的改善,减轻体重及药物治疗可使肥胖相关性肾病得到一定程度预防和改善.     

肥胖相关性肾病

随着肥胖发病率的逐年增高，肥胖相关性肾病越来越受到重视，本文就肥胖相关性肾病的临床特征、可能的发病机制及治疗进展作一综述。     

肥胖相关性肾病

随着肥胖发病率的逐年增高,肥胖相关性肾病越来越受到重视,本文就肥胖相关性肾病的临床特征、可能的发病机制及治疗进展作一综述.     

肥胖相关性肾病

随着肥胖发病率的逐年增高,肥胖相关性肾病越来越受到重视,本文就肥胖相关性肾病的临床特征、可能的发病机制及治疗进展作一综述.     

肥胖相关性肾病

随着肥胖发病率的逐年增高,肥胖相关性肾病越来越受到重视,本文就肥胖相关性肾病的临床特征、可能的发病机制及治疗进展作一综述.     

肥胖相关性肾病

随着肥胖发病率的逐年增高,肥胖相关性肾病越来越受到重视,本文就肥胖相关性肾病的临床特征、可能的发病机制及治疗进展作一综述.     

肥胖相关性肾病

随着肥胖发病率的逐年增高,肥胖相关性肾病越来越受到重视,本文就肥胖相关性肾病的临床特征、可能的发病机制及治疗进展作一综述.     

肥胖相关性肾病

随着肥胖发病率的逐年增高,肥胖相关性肾病越来越受到重视,本文就肥胖相关性肾病的临床特征、可能的发病机制及治疗进展作一综述.     

肥胖相关性肾病

随着肥胖发病率的逐年增高,肥胖相关性肾病越来越受到重视,本文就肥胖相关性肾病的临床特征、可能的发病机制及治疗进展作一综述.     

肥胖相关性肾病

随着肥胖发病率的逐年增高,肥胖相关性肾病越来越受到重视,本文就肥胖相关性肾病的临床特征、可能的发病机制及治疗进展作一综述.     

Obesity-related glomerulopathy: an emerging epidemic

BACKGROUND: We report the first large renal biopsy-based clinicopathologic study on obesity-related glomerulopathy. METHODS: Obesity was defined as body mass index (BMI)> 30 kg/m2. Obesity-related glomerulopathy (ORG) was defined morphologically as focal segmental glomerulosclerosis and glomerulomegaly (O-FSGS; N = 57) or glomerulomegaly alone (O-GM; N = 14). RESULTS: Review of 6818 native renal biopsies received from 1986 to 2000 revealed a progressive increase in biopsy incidence of ORG from 0.2% in 1986-1990 to 2.0% in 1996-2000 (P = 0.0001). Mean BMI in ORG was 41.7 (range 30.9 to 62.7). Indications for renal biopsy included proteinuria (N = 40) or proteinuria and renal insufficiency (N = 31). Seventy-one patients with ORG were compared to 50 patients with idiopathic FSGS (I-FSGS). Patients with ORG were older (mean 42.9 vs. 32.6 years, P < 0.001) and more often Caucasian (75% vs. 52%; P = 0.003). ORG patients had a lower incidence of nephrotic range proteinuria (48% vs. 66%; P = 0.007) and nephrotic syndrome (5.6% vs. 54%; P < 0.001), with higher serum albumin (3.9 vs. 2.9 g/dL; P < 0.001), lower serum cholesterol (229 vs. 335 mg/dL; P < 0.001), and less edema (35% vs. 68%; P = 0.003). On renal biopsy, patients with ORG had fewer lesions of segmental sclerosis (10 vs. 39%; P < 0.001), more glomerulomegaly (100% vs. 10%; P < 0.001), and less extensive foot process effacement (40 vs. 75%; P < 0.001). Glomerular diameter in ORG (mean 226 mu) was significantly larger than age- and sex-matched normal controls (mean 168 mu; P < 0.001). Follow-up was available in 56 ORG patients (mean 27 months) and 50 idiopathic FSGS controls (mean 38 months). A total of 75% of ORG patients received angiotensin-converting enzyme (ACE) inhibition or A2 blockade while 78% of the I-FSGS patients received immunosuppressive therapy. ORG patients had less frequent doubling of serum creatinine (14.3% vs. 50%; P < 0.001) and progression to ESRD (3.6% vs. 42%; P < 0.001). On multivariate analysis, presenting serum creatinine and severity of proteinuria were the only predictors of poor outcome in ORG. CONCLUSION: ORG is distinct from idiopathic FSGS, with a lower incidence of nephrotic syndrome, more indolent course, consistent presence of glomerulomegaly, and milder foot process fusion. The ten-fold increase in incidence over 15 years suggests a newly emerging epidemic. Heightened physician awareness of this entity is needed to ensure accurate diagnosis and appropriate therapy.