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SODIUM (NA) INTAKE VARIES ACROSS THE AFRICAN DIASPORA AND IS ASSOCIATED WITH BMI Alexander R Chang, Holly Kramer, Amy Luke, Guichan Gao, Ramon Durazo-Arvizu, Richard Cooper Loyola University Medical Center Differences in Na intake may explain the wide range of hypertension (HTN) prevalence across the African Diaspora. Methods: The Sodium Study is a cross-sectional survey of adults of African ancestry from 3 different countries [Maywood, IL, U.S. (n=949), Kingston, Jamaica (n=1033), and Igbo-ora, Nigeria (n=964)] conducted from Dec 19, 2000 to May 30, 2003 and aims to explore the interaction between Na intake and genetic factors on blood pressure across the African Diaspora. We present the findings on Na intake and its association with BMI. Participants were adults >25 years old not receiving treatment for HTN and without diabetes. Blood pressure was measured using standardized methods and the average of 3 measurements was used. Na intake was defined as the mean Na excretion in three 24-hour urine collections on a usual diet. Participants were grouped by World Health Organization BMI categories and average Na intake and blood pressure were compared across BMI categories within each country using analysis of covariance. Mean age (years) was 42 in U.S., 39.5 in Jamaica and 37.7 in Nigeria. Average SBP (mmHg) and daily Na intake were highest in U.S. (122.3 mmHg and 172 meq) and lowest in Nigeria (119.2 mmHg and 120.0 meq). Across BMI groups, average Na intake was consistently highest in the U.S. (figure 1). Among adults with BMI ≥ 30 kg/m2, Na intake was 60 meq higher in U.S. adults compared to adults from Nigeria or Jamaica after adjustment for age and sex. Conclusion: Across the African Diaspora, Na intake is substantially higher in the U.S. compared to Nigeria or Jamaica, especially among the obese.

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CHRONIC BRONCHIECTASIS AND PERINUCLEAR-ANCA (pANCA) CRESCENTIC GLOMERULONEPHRITIS William Chen, Andrew Chin. UC Davis Medical Center, Sacramento, CA, USA. 61 year old black female with a history of asthma, mitral stenosis, and hypertension was initially evaluated eight years ago for a chronic cough. She underwent a transbronchial biopsy revealing chronic inflammation and fibrosis. Infectious etiologies were ruled out, including mycobacterium and fungus. Upon our evaluation, the patient presented with nausea and malaise. On physical exam, she had dry oral and ocular mucus membranes, and crackles at her lower lung bases. On admission, she presented with a creatinine of 13.2 mg/dL. Further work up revealed positive rheumatoid factor (472 IU/mL), ANA (1:640), pANCA (1:320),and mpo Ab (537 AU/mL). Her anti-GBM Ab, anti-dsDNA Ab, complements, hepatitis B and C, and HIV were either normal or negative. Renal biopsy revealed a cellular crescentic GN involving 90% of the glomeruli without significant tubulointerstitial involvement. Immunofluorescence revealed mesangial staining with IgG (1+), IgA (1+), IgM (trace), C1q (trace), C3 (1-2+), lambda/kappa light chains (trace). Electron microscopy revealed mild foot process effacement. She was diagnosed with primary Sjogrens syndrome based on sialadenitis, xerophthalmia, positive anti-ssA/ssB Abs, and CT sinus showing fat replacement of her parotid glands. CT chest revealed chronic bronchiectasis. The patient required renal replacement therapy, but was treated with steroids and cyclophosphamide. There is one prior case series describing chronic bronchiectasis associated with pANCA crescentic GN. In all cases, the lung findings preceded renal involvement. This case highlights the potential relationship between bronchiectasis and ANCA mediated renal disease. Since the renal injury is potentially reversible, this condition should not be overlooked.

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THE ASSOCIATION BETWEEN SODIUM (Na) AND POTASSIUM (K) INTAKE AND SYSTOLIC BLOOD PRESSURE (SBP) ACROSS THE AFRICAN DIASPORA

Frank Y Chen, Holly Kramer, Amy Luke, Guichan Cao, Ramon Durazo, and Richard Cooper. Loyola University Medical Center, Maywood, IL, USA Hypertension prevalence varies substantially across the African Diaspora and dietary factors likely account for some of this divergence. We examined Na and K intake and BP among adults across the African Diaspora using data from the Sodium Study, a cross-sectional survey of adults of African ancestry, conducted from December 19, 2000 to May 30, 2003. Adults > 25 years old without hypertension treatment were enrolled in Maywood, IL (n=949), Kingston, Jamaica (n=1033), and Igbo-ora, Nigeria (n=964) with similar mean age at 42, 40, and 38 years respectively. Na intake was defined as the mean Na excretion in three 24-hour urine collections on a usual diet and BP was an average of 3 measurements. The association between SBP and Na and K intake was determined using linear regression while adjusting for age, sex, BMI and regression dilution bias. Mean Na (meq) and K (meq) intake were 172 and 44 in U.S., 133 and 40 in Jamaica, and 120 and 45 in Nigeria. Mean Na intake was significantly associated with SBP in the U.S. and Jamaica but not Nigeria (Table 1). Na and K intake showed the strongest associations with SBP in the U.S. even after standardizing the coefficients for blood pressure variance across sites. Differences in Na and K intake may explain in part the higher prevalence of hypertension in US Blacks compared to adults in Nigeria or Jamaica. Regression Coefficients for Urinary Na and K excretion after adjustment for age, sex, BMI (sample of data) Site Dependent Independent Coeff 95% CI Maywood SBP (mmHg) Na (meq) 0.046 0.024, 0.067

K (meq) -0.689 -0.783, -0.596 Jamaica SBP Na 0.029 0.010, 0.048

K -0.032 -0.089, 0.025 Nigeria SBP Na 0.019 -0.007, 0.045

K -0.163 -0.227, -0.098

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A NOVEL CENTRAL MECHANISM IN UREMIC BONE DISEASE Wai Cheung, Chaim Vanek, Urszula Iwaniec, Russell Turner, Robert Klein, Robert Mak, Department of Pediatrics, University of California San Diego, La Jolla, CA Patients with chronic kidney disease have elevated leptin levels and bone disease. We tested whether leptin signaling, via the hypothalamic melanocortin system, is an important cause of uremic bone disease. We performed nephrectomy (N) or sham operation (S) in c57BL/6J wild-type (WT), leptin-deficient (ob/ob), and melanocortin receptor 4 null (MC4-RKO) mice. Additional WT-N mice were treated with agouti-related (AgRP), an antagonist of MC4-R, or vehicle (V). WT-N mice were fed ad libitum while other mice were pair-fed with WT-N mice. Whole body composition was assessed by DEXA. Blood chemistry was analyzed. Excised left femoral composition was determined by DEXA and X-ray microtomographic scanning and femoral strength was assessed by 3-point failure test. Architecture of right femoral bone was analyzed by μCT. N mice were uremic. WT-N mice displayed a classic uremic bone phenotype characterized by changes in femoral composition, decreased femoral length, bone mineral content, bone mineral density, and failure load when compared to WT-S mice. Bone architectural parameters such as femoral volume, cortical area and thickness were significantly reduced in WT-N than WT-S mice. Skeletal integrity was maintained despite nephrectomy in mouse strains with impaired leptin or melanocortin signaling (ob/ob-N, MC4-RKO-N and WT-N mice given AgRP). Our results showed that leptin is an important cause of uremic bone disease via signaling through its receptor. These findings may have significant clinical and pharmacotherapeutic implications.

NKF 2010 Spring Clinical Meetings AbstractsA48