Obesity and diabetic kidney disease.
Obesity and diabetic kidney disease.
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DOI:
10.1016/j.mcna.2012.10.010
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发表时间:
2013-01
期刊:
影响因子:
--
通讯作者:
Maric-Bilkan C
中科院分区:
文献类型:
--
作者:
Maric-Bilkan C
The prevalence of obesity (body mass index, BMI≥ 30 kg/m2) has risen to epidemic proportions and continues to be a major health problem worldwide 1–3. The high prevalence of obesity is closely linked to the increased incidence of a number of chronic diseases, including type 2 diabetes, hypertension and cardiovascular disease 2, 4–8. Obesity, as well as type 2 diabetes, hypertension and cardiovascular disease are all risk factors for chronic kidney disease (CKD) and end-stage renal disease (ESRD) 9–13, inasmuch as the presence of one or more of these risk factors multiplies the overall risk for disease development and progression (Figure 1). In addition, evidence suggests that obesity may also increase the risk of and ESRD independent of type 2 diabetes and hypertension 14–1616. However, the precise mechanisms by which obesity independently, or in concert with type 2 diabetes and hypertension contributes to the development and/or progression of CKD and ESRD are not completely understood.The two leading causes of ESRD are type 2 diabetes and hypertension, which together account for over 70% of patients with ESRD 17–18. Since the growing prevalence of obesity is a major driving force for the continued increase in the prevalence of type 2 diabetes 7, 19, it is often difficult to dissect out the individual contribution of either obesity, type 2 diabetes or hypertension to the development of ESRD. In fact, the pathophysiology of type 2 diabetes-related renal disease (ie diabetic nephropathy) and obesity-related renal disease are almost identical. Indeed, they both evolve in a sequence of stages beginning with initial increases in glomerular filtration rate (GFR) and intraglomerular capillary pressure (PGc), glomerular hypertrophy and microalbuminuria 20–21. Elevated systolic blood pressure further exacerbates the disease progression to proteinuria, nodular glomerulosclerosis and tubulointerstitial injury and a decline in GFR leading to ESRD 22–23. Diabetes-and obesityrelated renal disease also have common initiating events which include interactions among multiple metabolic and hemodynamic factors which activate common intracellular signaling pathways that in turn trigger the production of cytokines and growth factors, leading to renal
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