Background To reduce the cardiovascular disease burden, Healthy People 2020 established U.S. hypertension goals for adults to: (1) decrease prevalence to 26.9%. (2) raise treatment to 69.5% and control to 61.2%, which requires controlling 88.1% on treatment. Methods and Results To assess current status and progress toward these Healthy People 2020 goals, time trends in National Health and Nutrition Examination Surveys 1999–2012 data in twoyear blocks were assessed in adults ≥18 years old age-adjusted to U.S. 2010. From 1999–2000 to 2011–2012, prevalent hypertension was unchanged (30.1% vs. 30.8%, p=0.32). Hypertension treatment (59.8% vs. 74.7%, p<0.001) and proportion of treated adults controlled (53.3% to 68.9%, p=0.0015) increased. Hypertension control to <140/<90 mmHg rose every two years from 1999–2000 to 2009–2010 (32.2% vs. 53.8%, p<0.001) before declining to 51.2% in 2011–2012. Modifiable factor(s) significant in multivariable logistic regression modeling include: (a) increasing body mass index with prevalent hypertension (odds ratio [OR] 1.44). (b) lack of health insurance (OR 1.68) and <2 healthcare visits/year (OR 4.24) with untreated hypertension. (c) healthcare insurance (OR 1.69), ≥2 healthcare visits/year (OR 3.23) and cholesterol treatment (OR 1.90) with controlled hypertension. Conclusions The NHANES 1999–2012 analysis suggests that Healthy People 2020 goals for hypertension: (1) prevalence show no progress (2) treatment was exceeded (3) control has flattened below target. Findings are consistent with evidence that: (a) obesity prevention and treatment could reduce prevalent hypertension (b) healthcare insurance, ≥2 healthcare visits/year, and guideline-based cholesterol treatment could improve hypertension control.

Animals with experimental renal disease maintained on diets restricted in protein develop less severe renal lesions and less proteinuria than do animals maintained on a normal or high protein diet. To determine whether restriction of dietary protein will reduce urinary albumin excretion in patients with established nephrosis and whether such dietary restriction will result in decreased albumin pools, we performed paired studies on nine nephrotic patients. They were fed sequential diets with a protein content of 1.6 and then 0.8 g/kg body wt, each for 2 weeks. Caloric intake remained constant at 35 Kcal/kg. In six patients the high protein diet was fed first; in three the order of dietary administration was reversed. Urinary albumin excretion was reduced on the low protein diet in all patients regardless of dietary order. Both the renal clearance of albumin and the fractional renal albumin clearance were reduced significantly on the low protein diet. The rate of albumin synthesis was greater on the high protein diet, but so was the rate of albuminuria. Despite the higher rate of albumin synthesis during the period of high protein intake, serum albumin concentration and plasma albumin mass were both less than during the period of low protein intake. Thus, dietary protein restriction in patients with established nephrosis results in decreased urinary albumin excretion in excess of any reduction in creatinine clearance. Total albumin mass is preserved and plasma albumin mass is actually increased during the period of dietary protein restriction. Protein restriction may be feasible in nephrotic patients.(ABSTRACT TRUNCATED AT 250 WORDS)

It has been established previously that nephrotic hyperlipidemia is characterized by both an increase in lipid synthesis and a defect in removal of lipoproteins. The relationship between these defects and altered albumin metabolism is uncertain. One hypothesis is that hepatic lipogenesis increases in parallel with albumin synthesis. To test this hypothesis, albumin synthesis was increased in nephrotic rats fed an 8.5% protein diet (LPN) by increasing dietary protein to 40% (HPN). Proteinuria was modulated in half of the rats fed 40% protein by enalapril (HPE). Albumin synthesis was the same in both HPN and HPE, but proteinuria was reduced in HPE compared to HPN, and so were serum cholesterol and triglycerides (TG). To examine the effect of serum albumin on lipid clearance in the absence of proteinuria, plasma clearance of chylomicrons (CM) and VLDL was measured in Nagase analbuminemic rats (NAR) and found to be no different than in normal SD rats. When proteinuria was induced in NAR and in SD rats, a severe and identical defect in both CM and VLDLL clearance was acquired in both groups and blood lipid levels were increased to a similar degree in both groups. Neither hyperlipidemia nor defective removal of lipoproteins from the circulation are linked to albumin synthesis or serum albumin concentration but result, at least in part, from proteinuria. Postheparin lipoprotein lipase (LPL) activity was reduced slightly in nephrotic animals compared to nonnephrotic controls, but the most striking finding was a highly significant decrease in postheparin LPL activity in normal NAR compared to SD rats (P < 0.001), suggesting that reduced LPL activity is not responsible for reduced clearance of CM and VLDL in nephrotic rats. (J. Clin. Invest. 1990. 86:500-505.)

These results indicate that specific inhibition of iNOS blocks the development of pathologic renal disease in MRL/lpr mice.