LVH is present from the earliest stages of progressive renal disease. This, and other forms of uremic cardiomyopathy, is linked to increased QT interval and dispersal, and with minor rhythm abnormalities, providing a link with the high risk of sudden death in this population.

Also in the general population, measurement of urinary albumin excretion may prove to be a valuable tool to detect subjects at risk for later development of renal failure, independent of the presence of other cardiovascular risk factors.

Diabetes is the leading cause of kidney failure, accounting for .45% of new cases of dialysis. Diabetic nephropathy is characterized by inflammation, fibrosis, and oxidant stress, pathologic features that are shared by many other chronic inflammatory diseases. The cytokine IL-17A was initially implicated as a mediator of chronic inflammatory diseases, but recent studies dispute these findings and suggest that IL-17A can favorably modulate inflammation. Here, we examined the role of IL-17A in diabetic nephropathy. We observed that IL-17A levels in plasma and urine were reduced in patients with advanced diabetic nephropathy. Type 1 diabetic mice that are genetically deficient in IL-17A developed more severe nephropathy, whereas administration of low-dose IL-17A prevented diabetic nephropathy in models of type 1 and type 2 diabetes. Moreover, IL-17A administration effectively treated, prevented, and reversed established nephropathy in genetic models of diabetes. Protective effects were also observed after administration of IL-17F but not IL-17C or IL-17E. Notably, tubular epithelial cell-specific overexpression of IL-17A was sufficient to suppress diabetic nephropathy. Mechanistically, IL-17A administration suppressed phosphorylation of signal transducer and activator of transcription 3, a central mediator of fibrosis, upregulated anti-inflammatory microglia/macrophage WAP domain protein in an AMP-activated protein kinasedependent manner and favorably modulated renal oxidative stress and AMP-activated protein kinase activation. Administration of recombinant microglia/macrophage WAP domain protein suppressed diabetes-induced albuminuria and enhanced M2 marker expression. These observations suggest that the beneficial effects of IL-17 are isoform-specific and identify low-dose IL-17A administration as a promising therapeutic approach in diabetic kidney disease. CKDs such as diabetic nephropathy are a serious public health problem. In the United States, .20 million adults have CKD, and 20%-40% of patients with diabetes develop nephropathy. The financial burden of diabetes is estimated to be $245 billion per year in the United States alone, and the cost for diabetic nephropathy is estimated to be .$20 billion per year. While intensive insulin therapy and control of hypertension can delay the onset of diabetic nephropathy, 1-3 these therapies cannot reverse CKD once it has developed. Recently, feeding mice a strictly ketogenic diet (5% carbohydrate, 8% protein, 87% fat) reversed a mild form of nephropathy. 4 Although implementing such an extreme diet

Using data collected from 9,823 participants in the 2007-2008 and 2009-2010 cycles of the National Health and Nutrition Examination Survey, we formally investigated potentially modifiable factors linking low socioeconomic status (SES) to chronic kidney disease (CKD) for their presence and magnitude of mediation. SES was defined using the poverty income ratio. The main outcome was CKD, defined as estimated glomerular filtration rate <60 mL/minute/1.73 m(2) (using the Chronic Kidney Disease Epidemiology Collaboration equation) and/or urinary albumin:creatinine ratio ≥30 mg/g. In mediation analyses, we tested the contributions of health-related behaviors (smoking, alcohol intake, diet, physical activity, and sedentary time), comorbid conditions (diabetes, hypertension, obesity, abdominal obesity, and hypercholesterolemia), and access to health care (health insurance and routine health-care visits) to this association. Except for sedentary time and diet, all examined health-related behaviors, comorbid conditions, and factors related to health-care access mediated the low SES-CKD association and contributed 20%, 32%, and 11%, respectively, to this association. In race/ethnicity-specific analyses, identified mediators tended to explain more of the association between low SES and CKD in non-Hispanic blacks than in other racial/ethnic groups. In conclusion, potentially modifiable factors like health-related behaviors, comorbid conditions, and health-care access contribute substantially to the association between low SES and CKD in the United States, especially among non-Hispanic blacks.