237: Factors Associated With Quality of Life in African Americans With CKD

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237 FACTORS ASSOCIATED WITH QUALITY OF LIFE IN AFRICAN AMERICANS WITH CKD Anna Porter , 1 Michael Fischer, 1 Deborah Brooks, Marino Bruce, Jeanne Charleston, William Cleveland, Tonya Corbin, Donna Dowie, Marquetta Faulkner, Jennifer Gassman, Tom Greene, Leena Hiremath, Cindy Kendrick, John Kusek, Denyse Thornley-Brown, Xulei Wang, Keith Norris, Mark Unruh, James Lash 1 for the AASK Study Group. 1 Medicine, U. Illinois, Chicago, IL. USA Health-related quality of life (HRQOL) has been evaluated in patients with ESRD but much less is known about HRQOL in patients with CKD, particularly among African Americans. We examined the relationship between HRQOL and demographic, clinical, and psychosocial factors in African Americans with hypertensive CKD with a cross sectional analysis of data drawn from the African American Study of Kidney Disease and Hypertension (AASK) Cohort Study. Quality of life was assessed using the Medical Outcomes Study Short Form (SF-36). Psychosocial factors were assessed utilizing Coping Strategies Inventory Short Form, Interpersonal Support Evaluation List-16, Satisfaction with Life Scale, and Beck Depression Inventory-II. GFR was estimated using the AASK Study equation. Among 691 cohort participants, lower income and unemployment were associated with lower HRQOL scores (p<0.01, p<0.05, respectively). Medical co-morbidities were associated with lower physical component summary (PCS) scores (p<0.01) but not mental component (MCS) scores. While SF-36 MCS scores were similar across the spectrum of eGFR (p=0.23), SF-36 PCS scores were significantly lower in participants with an eGFR < 30 ml/min/1.73m 2 (p<0.01). Subjects with higher HRQOL scores, particularly MCS scores, reported higher social support, coping strategies, and satisfaction with life and lower depressive symptoms (p <0.005). In conclusion, in African Americans with hypertensive CKD, lower income and unemployment were associated with lower HRQOL. Comorbidities and eGFR<30 ml/min/1.73m 2 were associated with lower PCS scores. Higher HRQOL was associated with higher social support, coping strategies, and satisfaction with life and lower depressive symptoms. 238 REDUCTION OF DIETARY PHOSPHORUS ABSORPTION WITH LANTHANUM CARBONATE OR SEVELAMER CARBONATE: A BALANCE STUDY Raymond Pratt 1 , Patrick Martin 1 , Lynne Poole 2 , Jeffrey Dragone 1 . 1 Shire Pharmaceuticals, Wayne, PA; 2 Shire Pharmaceuticals, Basingstoke, UK. Lanthanum carbonate (LC) and sevelamer carbonate (SC) are two noncalcium phosphate binders used for the treatment of hyperphosphatemia in patients with chronic kidney disease. This randomized, open-label, crossover study compared the absorption of dietary phosphorus (P) following single doses of LC or SC. Healthy volunteers underwent 4 treatment periods, separated by 7–14 day washouts. Following admission to the study center volunteers were fasted overnight. The gastrointestinal (GI) tract was cleaned by flushing with 3–4 L of mannitol solution (via nasogastric tube) starting 4 hours prior to ingestion of a meal, standardized for P and calcium content, which was consumed within a 30 minute period. Approximately 10 hours later a second 4-hour GI wash was started and rectal effluent collected. Volunteers completed periods with meal alone, meal plus LC (1000 mg of lanthanum) and meal plus SC (2400 mg); the treatment sequence was randomly assigned. All subjects were fasted in the fourth period. The P content of the duplicate meals and rectal effluent were analyzed by inductively coupled plasma-optical emission spectroscopy. Safety and tolerability were assessed. Net P absorption was analyzed using a standard mixed effect linear model in the pharmacodynamic population (n = 18). The least squares (LS) mean ± SE absorption of P after receiving the meal without a phosphate binder was 281.7 ± 14.1 mg. P absorption after administration of 1000 mg LC was 156.0 ± 14.2 mg and after 2400 mg of SC was 221.8 ± 14.1 mg. There was significantly less absorption of P with LC than with SC (p < 0.001): the difference in LS means (95% CI) was 65.8 (96.0, 35.5) mg. A 1000 mg dose of LC bound 135.1 ± 12.3 mg of P while a 2400 mg dose of SC bound only 63.2 ± 12.3 mg, a difference in LS means (95% CI) of 71.9 (40.0, 103.8) mg (p < 0.001). LC and SC had similar safety and tolerability profiles. A 1000 mg dose of LC bound more than twice as much P as a single 2400 mg dose of SC. These data suggest that LC may be a more effective phosphate binder than SC in clinical practice. 239 HYPERTENSION MANAGEMENT IMPROVED FOR IN- CENTER NOCTURNAL DIALYSIS PATIENTS COMPARED TO CONVENTIONAL DIALYSIS PATIENTS Robert Provenzano 1,2 ; Shane Simon 2 , Ronald Levine 2 , Karen Spach 2 , Allen Nissenson 1,2 1 Office of the Chief Medical Officer, DaVita Inc., Lakewood, Co 2 DaVita Inc., Lakewood, CO Longer dialysis sessions have been shown to improve blood pressure (BP) control and decrease the need for anti-hypertension drugs. To confirm this observation in a large dialysis population, we conducted a retrospective study comparing BP management and anti-hypertensive drug use in 418 patients in the 6 months before and after their switch to in-center nocturnal hemodialysis (NHD). NHD consists of 6-8 hr/treatments, 3 times/wk while conventional, in-center hemodialysis (ICHD) is defined as 3-4 hr/treatments, 3 times/wk. The baseline period was defined as the last 6 months on ICHD prior to starting NHD. The NHD period was defined as months 4 through 9 post-conversion allowing for a clinical stabilization period in the first 3 months of NHD. Results are shown in the table below. NHD ICHD p-value Post dialysis systolic BP (mmHg) 150.7 ± 1.1 151.5 ± 1.1 <0.001 Post dialysis diastolic BP (mmHg) 81.8 ± 0.6 82.8 ± 0.6 <0.001 Pre-dialysis wt (kg) 101.6 101.4 NS Post-dialysis wt (kg) 97.7 97.3 NS Anti-hypertensive drug utilization (%) 80.2% (76.3, 83.6 CI) 84.6 % (81.1, 87.5 CI) <0.01 Analysis of this large, longitudinal cohort of NHD patients confirmed that increased dialysis time on NHD lowered post-dialysis BP and reduced the need for anti-hypertensive therapy. These results suggest both clinical and economic benefits may be realized from NHD. 240 BULIMIA AS A CAUSE OF METBOLIC ALKALOSIS IN A PATIENT WITH CHRONIC KIDNEY DISEASE Praneetha Puskuri MD, Zaher Hamadeh MD, Anjali Acharya MD, Jacobi Medical Center, Division of Nephrology, Albert Einstein College of Medicine, Bronx, NY,USA Chronic kidney disease (CKD) is associated with metabolic acidosis and hyperkalemia because of inability of the kidney to excrete hydrogen and potassium ions. We report a case of a 48 year old African American male with history of Human Immunodeficiency Virus (HIV) and Hepatitis C infection and history of hypertension who was sent for evaluation of Chronic Kidney Disease. Upon presentation he had a potassium level of 3.3 meq/L, bicarbonate (HCO3) level of 42.1 meq/L, and creatinine (Cr) of 2 mg/dl (eGFR of 43 ml/min by the modified MDRD formula) The serum pH on arterial blood gas analysis was 7.51. Patient was on hydrochlorothiazide ( HCTZ) initially but euvolemic. HCTZ was stopped and lab values obtained after 4 days, showed a potassium value of 3.9 meq/L and HCO3 38.8 meq/L. More history revealed daily binge eating followed by induced vomiting. Patient was started on Proton Pump Inhibitors (PPI) based on the assumption that preventing hydrogen secretion might ameliorate metabolic alkalosis. Repeat labs 2 weeks later showed resolving alkalosis. Bulimia can cause multiple electrolyte and acid-base abnormalities including hypokalemia and metabolic alkalosis. The focus of treatment is treating the underlying disorder as well as volume and potassium replacement. Therapy with proton pump inhibitors may be useful to improve hypokalemia and metabolic alkalosis by preventing hydrogen ion secretion in gastric fluid. This case illustrates the importance of history taking. It also highlights that bulimia is not always self evident. Visit K meq/L HCO3 meq/L Cr mg/dl Initial 3.3 42.1 2.0 4 d after stopped HCTZ 2.9 37 2.2 Start of PPI 3.9 38 1.6 2 weeks after PPI 4.6 23 1.9 NKF 2010 Spring Clinical Meetings Abstracts A91

Transcript of 237: Factors Associated With Quality of Life in African Americans With CKD

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FACTORS ASSOCIATED WITH QUALITY OF LIFE IN AFRICAN AMERICANS WITH CKD Anna Porter,1 Michael Fischer,1Deborah Brooks, Marino Bruce, Jeanne Charleston, William Cleveland, Tonya Corbin, Donna Dowie, Marquetta Faulkner, Jennifer Gassman, Tom Greene, Leena Hiremath, Cindy Kendrick, John Kusek, Denyse Thornley-Brown, Xulei Wang, Keith Norris, Mark Unruh, James Lash1 for the AASK Study Group. 1Medicine, U. Illinois, Chicago, IL. USA Health-related quality of life (HRQOL) has been evaluated in patients with ESRD but much less is known about HRQOL in patients with CKD, particularly among African Americans. We examined the relationship between HRQOL and demographic, clinical, and psychosocial factors in African Americans with hypertensive CKD with a cross sectional analysis of data drawn from the African American Study of Kidney Disease and Hypertension (AASK) Cohort Study. Quality of life was assessed using the Medical Outcomes Study Short Form (SF-36). Psychosocial factors were assessed utilizing Coping Strategies Inventory Short Form, Interpersonal Support Evaluation List-16, Satisfaction with Life Scale, and Beck Depression Inventory-II. GFR was estimated using the AASK Study equation. Among 691 cohort participants, lower income and unemployment were associated with lower HRQOL scores (p<0.01, p<0.05, respectively). Medical co-morbidities were associated with lower physical component summary (PCS) scores (p<0.01) but not mental component (MCS) scores. While SF-36 MCS scores were similar across the spectrum of eGFR (p=0.23), SF-36 PCS scores were significantly lower in participants with an eGFR < 30 ml/min/1.73m2

(p<0.01). Subjects with higher HRQOL scores, particularly MCS scores, reported higher social support, coping strategies, and satisfaction with life and lower depressive symptoms (p <0.005). In conclusion, in African Americans with hypertensive CKD, lower income and unemployment were associated with lower HRQOL. Comorbidities and eGFR<30 ml/min/1.73m2 were associated with lower PCS scores. Higher HRQOL was associated with higher social support, coping strategies, and satisfaction with life and lower depressive symptoms.

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REDUCTION OF DIETARY PHOSPHORUS ABSORPTION WITH LANTHANUM CARBONATE OR SEVELAMER CARBONATE: A BALANCE STUDY Raymond Pratt1, Patrick Martin1, Lynne Poole2, Jeffrey Dragone1. 1Shire Pharmaceuticals, Wayne, PA; 2Shire Pharmaceuticals, Basingstoke, UK. Lanthanum carbonate (LC) and sevelamer carbonate (SC) are two noncalcium phosphate binders used for the treatment of hyperphosphatemia in patients with chronic kidney disease. This randomized, open-label, crossover study compared the absorption of dietary phosphorus (P) following single doses of LC or SC. Healthy volunteers underwent 4 treatment periods, separated by 7–14 day washouts. Following admission to the study center volunteers were fasted overnight. The gastrointestinal (GI) tract was cleaned by flushing with 3–4 L of mannitol solution (via nasogastric tube) starting 4 hours prior to ingestion of a meal, standardized for P and calcium content, which was consumed within a 30 minute period. Approximately 10 hours later a second 4-hour GI wash was started and rectal effluent collected. Volunteers completed periods with meal alone, meal plus LC (1000 mg of lanthanum) and meal plus SC (2400 mg); the treatment sequence was randomly assigned. All subjects were fasted in the fourth period. The P content of the duplicate meals and rectal effluent were analyzed by inductively coupled plasma-optical emission spectroscopy. Safety and tolerability were assessed. Net P absorption was analyzed using a standard mixed effect linear model in the pharmacodynamic population (n = 18). The least squares (LS) mean ± SE absorption of P after receiving the meal without a phosphate binder was 281.7 ± 14.1 mg. P absorption after administration of 1000 mg LC was 156.0 ± 14.2 mg and after 2400 mg of SC was 221.8 ± 14.1 mg. There was significantly less absorption of P with LC than with SC (p < 0.001): the difference in LS means (95% CI) was −65.8 (−96.0, −35.5) mg. A 1000 mg dose of LC bound 135.1 ± 12.3 mg of P while a 2400 mg dose of SC bound only 63.2 ± 12.3 mg, a difference in LS means (95% CI) of 71.9 (40.0, 103.8) mg (p < 0.001). LC and SC had similar safety and tolerability profiles. A 1000 mg dose of LC bound more than twice as much P as a single 2400 mg dose of SC. These data suggest that LC may be a more effective phosphate binder than SC in clinical practice.

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HYPERTENSION MANAGEMENT IMPROVED FOR IN-CENTER NOCTURNAL DIALYSIS PATIENTS COMPARED TO CONVENTIONAL DIALYSIS PATIENTSRobert Provenzano1,2; Shane Simon2, Ronald Levine2, Karen Spach2,Allen Nissenson1,2

1Office of the Chief Medical Officer, DaVita Inc., Lakewood, Co 2DaVita Inc., Lakewood, CO

Longer dialysis sessions have been shown to improve blood pressure (BP) control and decrease the need for anti-hypertension drugs. To confirm this observation in a large dialysis population, we conducted a retrospective study comparing BP management and anti-hypertensive drug use in 418 patients in the 6 months before and after their switch to in-center nocturnal hemodialysis (NHD). NHD consists of 6-8 hr/treatments, 3 times/wk while conventional, in-center hemodialysis (ICHD) is defined as 3-4 hr/treatments, 3 times/wk. The baseline period was defined as the last 6 months on ICHD prior to starting NHD. The NHD period was defined as months 4 through 9 post-conversion allowing for a clinical stabilization period in the first 3 months of NHD. Results are shown in the table below.

NHD ICHD p-value Post dialysis systolic BP (mmHg)

150.7 ± 1.1 151.5 ± 1.1 <0.001

Post dialysis diastolic BP (mmHg)

81.8 ± 0.6 82.8 ± 0.6 <0.001

Pre-dialysis wt (kg) 101.6 101.4 NS Post-dialysis wt (kg) 97.7 97.3 NS Anti-hypertensive drug utilization (%)

80.2% (76.3, 83.6 CI)

84.6 % (81.1, 87.5 CI)

<0.01

Analysis of this large, longitudinal cohort of NHD patients confirmed that increased dialysis time on NHD lowered post-dialysis BP and reduced the need for anti-hypertensive therapy. These results suggest both clinical and economic benefits may be realized from NHD.

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BULIMIA AS A CAUSE OF METBOLIC ALKALOSIS IN A PATIENT WITH CHRONIC KIDNEY DISEASEPraneetha Puskuri MD, Zaher Hamadeh MD, Anjali Acharya MD, Jacobi Medical Center, Division of Nephrology, Albert Einstein College of Medicine, Bronx, NY,USA Chronic kidney disease (CKD) is associated with metabolic acidosis and hyperkalemia because of inability of the kidney to excrete hydrogen and potassium ions. We report a case of a 48 year old African American male with history of Human Immunodeficiency Virus (HIV) and Hepatitis C infection and history of hypertension who was sent for evaluation of Chronic Kidney Disease. Upon presentation he had a potassium level of 3.3 meq/L, bicarbonate (HCO3) level of 42.1 meq/L, and creatinine (Cr) of 2 mg/dl (eGFR of 43 ml/min by the modified MDRD formula) The serum pH on arterial blood gas analysis was 7.51. Patient was on hydrochlorothiazide ( HCTZ) initially but euvolemic. HCTZ was stopped and lab values obtained after 4 days, showed a potassium value of 3.9 meq/L and HCO3 38.8 meq/L. More history revealed daily binge eating followed by induced vomiting. Patient was started on Proton Pump Inhibitors (PPI) based on the assumption that preventing hydrogen secretion might ameliorate metabolic alkalosis. Repeat labs 2 weeks later showed resolving alkalosis.

Bulimia can cause multiple electrolyte and acid-base abnormalities including hypokalemia and metabolic alkalosis. The focus of treatment is treating the underlying disorder as well as volume and potassium replacement. Therapy with proton pump inhibitors may be useful to improve hypokalemia and metabolic alkalosis by preventing hydrogen ion secretion in gastric fluid. This case illustrates the importance of history taking. It also highlights that bulimia is not always self evident.

Visit K meq/L HCO3 meq/L Cr mg/dl

Initial 3.3 42.1 2.0 4 d after stopped HCTZ

2.9 37 2.2

Start of PPI 3.9 38 1.6 2 weeks after PPI

4.6 23 1.9

NKF 2010 Spring Clinical Meetings Abstracts A91