Incident ESRD and treatment-resistant hypertension: the reasons for geographic and racial differences in stroke (REGARDS) study.

BACKGROUND: Studies suggest that treatment-resistant hypertension is common and increasing in prevalence among US adults. Although hypertension is a risk factor for end-stage renal disease (ESRD), few data are available for the association between treatment-resistant hypertension and ESRD risk. STUDY DESIGN: Prospective cohort study. SETTING & PARTICIPANTS: We analyzed data from 9,974 REGARDS (Reasons for Geographic and Racial Differences in Stroke) Study participants treated for hypertension without ESRD at baseline. PREDICTOR: Treatment-resistant hypertension was defined as uncontrolled blood pressure (BP) with concurrent use of 3 antihypertensive medication classes including a diuretic or use of 4 or more antihypertensive medication classes including a diuretic regardless of BP. OUTCOME: Incident ESRD was identified by linkage of REGARDS Study participants with the US Renal Data System. MEASUREMENTS: During a baseline in-home study visit, BP was measured twice and classes of antihypertensive medication being taken were determined by pill bottle inspection. RESULTS: During a median follow-up of 6.4 years, there were 152 incident cases of ESRD (110 ESRD cases among 2,147 with treatment-resistant hypertension and 42 ESRD cases among 7,827 without treatment-resistant hypertension). The incidence of ESRD per 1,000 person-years for hypertensive participants with and without treatment-resistant hypertension was 8.86 (95% CI, 7.35-10.68) and 0.88 (95% CI, 0.65-1.19), respectively. After multivariable adjustment, the HR for ESRD comparing hypertensive participants with versus without treatment-resistant hypertension was 6.32 (95% CI, 4.30-9.30). Of participants who developed incident ESRD during follow-up, 72% had treatment-resistant hypertension at baseline. LIMITATIONS: BP, estimated glomerular filtration rate, and albuminuria assessed at a single time. CONCLUSIONS: Individuals with treatment-resistant hypertension are at increased risk for ESRD. Appropriate clinical management strategies are needed to treat treatment-resistant hypertension in order to preserve kidney function in this high-risk group.

Contribution of food additives to sodium and phosphorus content of diets rich in processed foods.

OBJECTIVE: Phosphorus-based food additives increase the total phosphorus content of processed foods. However, the extent to which these additives augment total phosphorus intake per day is unclear. DESIGN AND METHODS: To examine the contribution of phosphorus-based food additives to the total phosphorus content of processed foods, separate 4-day menus for a low-additive and additive-enhanced diet were developed using Nutrition Data System for Research (NDSR) software. The low-additive diet was designed to conform to U.S. Department of Agriculture guidelines for energy and phosphorus intake (∼2,000 kcal/day and 900 mg of phosphorus per day), and it contained minimally processed foods. The additive-enhanced diet contained the same food items as the low-additive diet except that highly processed foods were substituted for minimally processed foods. Food items from both diets were collected, blended, and sent for measurement of energy and nutrient intake. RESULTS: The low-additive and additive-enhanced diet provided approximately 2,200 kcal, 700 mg of calcium, and 3,000 mg of potassium per day on average. Measured sodium and phosphorus content standardized per 100 mg of food was higher each day of the additive-enhanced diet as compared with the low-additive diet. When averaged over the 4 menu days, the measured phosphorus and sodium contents of the additive-enhanced diet were 606 ± 125 and 1,329 ± 642 mg higher than the low-additive diet, respectively, representing a 60% increase in total phosphorus and sodium content on average. When comparing the measured values of the additive-enhanced diet to NDSR-estimated values, there were no statistically significant differences in measured versus estimated phosphorus contents. CONCLUSION: Phosphorus and sodium additives in processed foods can substantially augment phosphorus and sodium intake, even in relatively healthy diets. Current dietary software may provide reasonable estimates of the phosphorus content in processed foods.

Updated Pathway to Micro-elimination of Hepatitis C Virus in the Hemodialysis Population.

Chronic hepatitis C virus (HCV) infection continues to be transmitted to hemodialysis (HD) patients within HD facilities globally. The goal of the World Health Organization to micro-eliminate HCV infection from the HD population by the year 2030 is not on target to be achieved. Obstacles to eliminate HCV in HD settings remain daunting due to a complex system created by a confluence of guidelines, legislation, regulation, and economics. HCV prevalence remains high and seroconversion continues among the HD patient population globally as a result of the HD procedure. Preventive strategies that effectively prevent HCV transmission, treatment-as-prevention, and rapid referral to treatment balanced with kidney transplant candidacy should be added to the current universal precautions approach. A safer system must be designed before HCV transmission can be halted and eliminated from the HD population.

A case of infection-associated antiproteinase-3-negative cytoplasmic antineutrophil cytoplasmic antibody pauci-immune focal necrotizing glomerulonephritis.

We present the case of a man with Gram-negative sepsis and exposure to oral silica who developed pauci-immune focal necrotizing glomerulonephritis (PI-FNGN) in the setting of a subacute polymicrobial central venous line (CVL) infection. He developed a cytoplasmic antineutrophil cytoplasmic autoantibody (C-ANCA) that was antiproteinase-3 (PR-3) and antimyeloperoxidase (MPO) antibody negative. We believe this is the first reported case of Gram-negative sepsis-associated PI-FNGN. Chronic silica exposure is a leading environmental risk factor in the development of ANCA vasculitis. Oral silica is a common pharmaceutical additive and its bioavailability is being recognized. Oral silica, therefore, may also be a risk for development of autoreactivity. The PI-FNGN resolved with antibiotic therapy alone. The C-ANCA titer declined as the PI-FNGN resolved. The case supports experimental and observational research that environmental exposures act as adjuvants for an immune response and also provide epigenetic triggers for autoreactivity. The C-ANCA was negative for PR-3, its major antigen. C-ANCA antigen specificity may depend on the pathogenesis of the underlying disease, potentially elicited by a cross-reaction of an antibody to foreign and self target antigen sequence homology or alternatively elicited by antigenic epitope spread.

Prevalence of apparent treatment-resistant hypertension among individuals with CKD.

BACKGROUND AND OBJECTIVES: Apparent treatment-resistant hypertension is defined as systolic/diastolic BP ≥ 140/90 mmHg with concurrent use of three or more antihypertensive medication classes or use of four or more antihypertensive medication classes regardless of BP level. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: The prevalence of apparent treatment-resistant hypertension among Reasons for Geographic and Racial Differences in Stroke study participants treated for hypertension (n=10,700) was determined by level of estimated GFR and albumin-to-creatinine ratio, and correlates of apparent treatment-resistant hypertension among those participants with CKD were evaluated. CKD was defined as an albumin-to-creatinine ratio ≥ 30 mg/g or estimated GFR<60 ml/min per 1.73 m(2). RESULTS: The prevalence of apparent treatment-resistant hypertension was 15.8%, 24.9%, and 33.4% for those participants with estimated GFR ≥ 60, 45-59, and <45 ml/min per 1.73 m(2), respectively, and 12.1%, 20.8%, 27.7%, and 48.3% for albumin-to-creatinine ratio<10, 10-29, 30-299, and ≥ 300 mg/g, respectively. The multivariable-adjusted prevalence ratios (95% confidence intervals) for apparent treatment-resistant hypertension were 1.25 (1.11 to 1.41) and 1.20 (1.04 to 1.37) for estimated GFR levels of 45-59 and <45 ml/min per 1.73 m(2), respectively, versus ≥ 60 ml/min per 1.73 m(2) and 1.54 (1.39 to 1.71), 1.76 (1.57 to 1.97), and 2.44 (2.12 to 2.81) for albumin-to-creatinine ratio levels of 10-29, 30-299, and ≥ 300 mg/g, respectively, versus albumin-to-creatinine ratio<10 mg/g. After multivariable adjustment, men, black race, larger waist circumference, diabetes, history of myocardial infarction or stroke, statin use, and lower estimated GFR and higher albumin-to-creatinine ratio levels were associated with apparent treatment-resistant hypertension among individuals with CKD. CONCLUSIONS: This study highlights the high prevalence of apparent treatment-resistant hypertension among individuals with CKD.

Blood pressure indexes and end-stage renal disease risk in adults with chronic kidney disease.

BACKGROUND: Few studies have compared different blood pressure (BP) indexes for end-stage renal disease (ESRD) risk among individuals with chronic kidney disease. METHODS: We examined the relationship between systolic BP (SBP), diastolic BP (DBP), pulse pressure (PP) and mean arterial pressure (MAP) and ESRD risk among 2,772 participants with an estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m(2) calculated using the Chronic Kidney Disease Epidemiology Collaboration equation in the REasons for the Geographic And Racial Differences in Stroke (REGARDS) study. BP was measured during a baseline study visit between January 2003 and October 2007 with ESRD incidence through August 2009 ascertained via linkage with the United States Renal Data System (n = 138 ESRD cases). RESULTS: The mean age was 72.1(standard deviation: 8.7) years. After multivariable adjustment for socio-demographic and clinical risk factors including antihypertensive medication use, the hazard ratio (HR) for ESRD associated with one standard deviation higher SBP (18 mm Hg) was 1.67, (95% confidence intervals (CI) 1.43-1.96), DBP (11 mm Hg) was 1.38, (95% CI 1.16-1.63), PP (15 mm Hg) was 1.50, (95% CI 1.27-1.78) and MAP (11 mm Hg) was 1.54, (95% CI 1.32-1.79). Higher levels of SBP remained associated with an increased HR for ESRD after additional adjustment for DBP (1.65, 95% CI: 1.35-2.01), PP (1.73, 95% CI: 1.32-2.26), and MAP (1.61, 95% CI: 1.16-2.23). After adjustment for SBP, the other BP indexes were not significantly associated with incident ESRD. CONCLUSIONS: These data suggest that of several blood pressure indexes including DBP, PP and MAP, SBP may have the strongest association with ESRD incidence among individuals with reduced eGFR.