Background Protein-energy wasting is common in chronic kidney disease and is associated with reductions in body muscle and fat stores and poor outcomes. The accuracy and reliability of field methods to measure body composition is unknown in this population. Study Design Cross sectional, observational study. Setting and Participants 118 maintenance hemodialysis patients were seen at the General Clinical Research Center at Harbor-UCLA Medical Center. Index Tests Triceps skinfold, near-infrared interactance, and bioelectrical impedance analysis using the Segal, Kushner and Lukaski equations Reference Test Dual energy X-ray absorptiometry (DEXA) Results Participants (42% women, 52% diabetics, 40% African-Americans and 38% Hispanics were 49.4±11.5 (mean±SD) years old, and had undergone dialysis for 41.1±32.9 months. Their body mass index was 27.0±6.0 kg/m2. Using DEXA as the reference test, the bioelectrical impedance analysis–Kushner equation, and triceps skinfold and near-infrared interactance were most accurate of the index tests in estimating total body fat percentage, whereas bioelectrical impedance analysis–Segal equation and bioelectrical impedance analysis–Lukaski equation overestimated total body fat percentage. Bland-Altman analyses and Difference plots showed that bioelectrical impedance analysis–Kushner and near-infrared interactance were most similar to the reference test. Bioelectrical impedance analysis–Kushner, triceps skinfold and near-infrared interactance had the smallest mean differences from DEXA, especially in women (1.6%, 0.7% and 1.2%, respectively). Similar results were observed in African-American participants (n=47). Limitations Measurements were performed one day after hemodialysis treatment leading to more fluid retention, which may have affected reference and index tests differently. Conclusions Using DEXA as the reference test, both near-infrared interactance and bioelectrical impedance analysis-Kushner method yield more consistent estimates of total body fat percentage in maintenance hemodialysis patients compared to the other index tests. The near-infrared interactance is not affected by skin color. Field methods with portable devices may provide adequate precision.

Background: Chronic consumption of a high-salt diet causes hypertension (HTN) and renal injury in Dahl salt-sensitive (SSR) but not salt-resistant rats (SRR). These events are, in part, mediated by oxidative stress and inflammation in the kidney and vascular tissues. Activation of the angiotensin II type 1 (AT₁) receptor plays an important role in the pathogenesis of oxidative stress and inflammation in many hypertensive disorders. However, the systemic renin-angiotensin system (RAS) is typically suppressed in salt-sensitive HTN. This study was designed to test the hypothesis that differential response to a high-salt diet in SSR versus SRR may be related to upregulation of tissue RAS and pathways involved in inflammation and reactive oxygen species (ROS) production. Methods and Results: SSR and SRR were studied 3 weeks after consumption of high- (8%) or low-salt (0.07%) diets. The SSR consuming a low-salt diet exhibited significant increases in AT₁ receptor, cyclooxygenase (COX) 2, plasminogen activator inhibitor (PAI) and phospho-IĸB in the kidney as compared to those found in SRR. The high-salt diet resulted in severe HTN and proteinuria (in SSR but not SRR) and marked elevations of renal tissue monocyte chemoattractant protein 1, p22^phox, NADPH oxidase subunit 4, angiotensin-II-positive cell count, infiltrating T cells and macrophages and further increases in AT₁ receptor, COX-2, PAI-1 and phospho-IĸB in the SSR group. The high-salt diet significantly lowered plasma renin activity (PRA) in SRR but not in the SSR. COX-1 abundance was similar on the low-salt diet and rose equally with the high-salt diet in both groups. Among subgroups of animals fed the low-salt diet, kidney glutathione peroxidase (GPX) abundance was significantly lower in the SSR than SRR. The high-salt diet raised GPX and mitochondrial superoxide dismutase (SOD) abundance in the SRR kidneys but failed to do so in SSR. Cu/Zn-SOD abundance was similar in the subgroups of SSR and SRR fed the low-salt diet. The high-salt diet resulted in downregulation of Cu/Zn-SOD in SSR but not SRR. Conclusions: Salt sensitivity in the SSR is associated with upregulations of the intrarenal angiotensin system, ROS-generating and proinflammatory/profibrotic proteins and an inability to raise antioxidant enzymes and maximally suppress PRA in response to high salt intake. These events can contribute to renal injury with high salt intake in SSR.

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