NKF 2014 Spring Clinical Meetings Abstracts

A102

ORAL FERRIC CITRATE (FC) ELIMINATES THE NEED FOR INTRAVENOUS (IV) IRON IN DIALYSIS PATIENTS: M Sika1, S Kabani1, M Chen2, J Dwyer1, J Lewis1, R Niecestro3, M Koury1, for The Collaborative Study Group, 1Vanderbilt University, Nashville, TN, USA, 2TCM Groups Inc., Berkeley Heights, NJ, USA, 3Independent Consultant, Pocono Pines, PA,USA The majority of dialysis patients receive IV iron because oral ferrous iron salts are insufficient to maintain adequate iron stores for erythro-poiesis. Oral iron absorption is regulated by physiologic mechanisms, whereas acquisition of IV iron is not physiologically regulated. A randomized clinical trial comparing FC, an oral phosphate binder, to active controls (AC) (calcium acetate and/or sevelamer carbonate) in dialysis patients over 52 weeks showed that FC effectively bound phosphate, raised iron stores, and decreased the use of IV iron and erythropoiesis stimulating agents. IV iron was permitted if serum ferritin was < 1,000 ng/mL and transferrin saturation (TSAT) was < 30%. In the last six months of the study, 58% FC subjects and 24% AC subjects received no IV iron; 74 FC subjects and 13 AC subjects (results not reported here) did not receive any iron over 52 weeks. The table compares FC subjects who received IV iron with FC subjects who did not. In the 74 “No IV iron” subjects, iron absorbed from FC increased iron stores and sustained Hgb. Similar serum ferritin, iron and TSAT of the two groups indicate that iron absorption from oral FC was highly regulated. We conclude that oral FC used as a phosphate binder can eliminate the need for IV iron in dialysis patients. Group N Ferritin

(ng/ml) Iron (μg/dL)

TSAT (%)

Hgb (g/dL)

No IV Iron

74 Baseline 588±274 82±31 36 ± 11 11.8±1.4 Week 52 863±494 97±46 43 ± 18 11.7±1.6 P-value* <0.001 <0.001 <0.001 0.885

IV Iron

207 Baseline 595±300 69±28 30 ± 11 11.6±1.2 Week 52 911±486 85 ±41 38±16 11.3±1.4 P-value* <0.001 <0.001 <0.001 0.011

Fe vs$ no FE

P-value$ (week 52)

0.491 0.156 0.219 0.238

*Within group: Baseline versus week 52 $Between groups: “No IV Iron ” versus “IV Iron ” at week 52

DISEASE BURDEN OF DIABETIC FOOT ULCERS IN END-STAGE RENAL DISEASE PATIENTS Scott Sibbel, Mahesh Krishnan, Ami Claxton, Steven Brunelli DaVita Clinical Research, Minneapolis, MN, USA Diabetes is a leading cause of end-stage renal disease (ESRD). Diabetic patients with ESRD are at increased risk of complications related to diabetes, including diabetic foot ulcers (DFU) and lower extremity amputations. This retrospective analysis compared erythropoiesis-stimulating agent (ESA) utilization and inpatient and outpatient (Medicare Parts A and B, respectively) health care expenditures between diabetic dialysis patients with and without DFU. This analysis assessed 2009-2010 Medicare claims using the United States Renal Data System database. Case patients (25,273) with diabetes and DFU (identified via ICD-9 codes) were propensity-score matched (PSM) 1:1 to eligible controls with diabetes but without DFU (total pool of 121,207 potential controls). After PSM, controls and case population were similar with regard to age, sex, race, weight, comorbidity burden, modality/access, alcohol and drug dependence, and inability to ambulate or to transfer. Overall ESRD patients with DFU used more ESA (51,416 to 56,977 units/month), had higher inpatient costs (range $4,668 to $6,209 USD/month), and higher outpatient costs ($1,046 to $1,384 USD/month). Stratified analysis of incident and prevalent patients compared with controls showed similar trends; incident patients with DFU had the highest ESA usage (52,282 to 61,286 units/month), the highest inpatient costs ($4,572 to $6,661 USD/month), and the highest outpatient costs ($1,138 to $1,601 USD/month). Consistent differences were seen between patients with and those without DFU. For diabetic ESRD patients, DFU is potently and independently associated with greater ESA utilization and inpatient and outpatient health care costs. Trials are warranted to assess whether targeted therapies may reduce health economic burden.

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Am J Kidney Dis. 2014;63(5):A1-A121

REDUCTION IN SERUM K+ WITH ZS-9 IN CKD PATIENTS WITH HYPERKALEMIA ON RAAS INHIBITORS (RAASi): Bhupinder Singh1, Stephen R. Ash2, Philip Lavin3, Alex Yang4, Henrik S. Rasmussen5. 1Southwest Clin. Research Inst., Tempe, AZ; 2IU Health Arnett, Lafayette, IN; 3Boston Biostats. Research Fdn., Framingham, MA; 4Xelay Acumen, Belmont, CA; 5ZS Pharma, Coppell, TX, USA. Hyperkalemia (HK) is associated with significant mortality and limits use of life-saving RAASi, yet prevalent treatments are poorly tolerated and not always effective. ZS-9 is a nonsystemic, selective cation exchanger designed to entrap excess potassium (K+). In a Phase 2 trial in 90 patients with CKD and HK, ZS-9 produced a rapid and sustained decrease in serum K+ vs placebo, with a favorable safety profile (Ash et al. ASN 2013). Here we present 1° efficacy data in the RAASi subsets. Patients (eGFR: 30-60 mL/min/1.73 m2; serum K+: 5-6 mEq/L) received ZS-9 10g (N=24) or placebo (N=30) orally TID for 2-4 days with regular meals (8am, 12pm, 6pm), depending on serum K+ (only 2 days needed for ZS-9 10g). The 1° efficacy endpoint was the difference in the serum K+ rate of decrease over the first 48 hr between groups, using longitudinal modeling. RAASi were continued during the study. Mean baseline serum K+ (mEq/L) in the RAASi subsets was 5.1 for ZS-9 10g (n=20) and 5.2 for placebo (n=18). Compared with placebo, ZS-9 10g decreased serum K+ in patients on RAASi (1° efficacy endpoint p<0.0001; Fig), with maximal -1.1 mEq/L mean change from baseline at 38 hr (p<0.0001) and -0.8 mEq/L reduction at 48 hr (p=0.001).

ZS-9 may provide a rapid and robust treatment of hyperkalemia in CKD patients on RAASi therapy

HIGHER SERUM PHOSPHORUS AND RISK OF ANEMIA IN A NON CKD POPULATION John J. Sim, Amy I. Liu, Connie Rhee, Kamyar Kalantar-Zadeh.

Kaiser Permanente Los Angeles Medical Center, Los Angeles, CA, USA Elevations in serum phosphorus have been associated with

anemia in the ESRD population but this association is not well studied in earlier CKD stages or those without CKD. We sought to evaluate whether non-CKD individuals with higher phosphorus levels were at greater risk of anemia among a large ethnically diverse population. Cross sectional study in the period 1/1/1998 through 12/31/2009 was performed within the Kaiser Permanente Southern California health system. Individuals age>18 with 1) documented serum phosphorus, 2) hemoglobin value, and 3) eGFR>60ml/min were evaluated. Anemia was defined as hemoglobin<11g/dl. Serum phosphorus levels were categorized into population based quartiles. Multivariable logistic regression analyses were used to calculate odds ratios (ORs) for anemia based on phosphorus quartiles and phosphorus in increments of 0.5mg/dl. Total of 32,907 individuals (mean age 52 yrs, 62% women,

15% blacks, 26% Hispanics and 7% Asians) were identified. Serum phosphorus ranged from 1.9 to 5.7mg/dl. 13% met criteria for anemia. Multivariable ORs for anemia per every 0.5mg/dl increase in phosphorus was 1.07 (1.04-1.10). ORs for phosphorus quartiles 3.1-3.5, 3.5-3.9, and 3.9-5.7 (ref: phosphorus 1.9-3.1mg/dl) were 0.85, 0.90, and 1.05 respectively. These ORs were more pronounced in men. Hence, there is an incremental and strictly linear trend for

higher risk of anemia in individuals with higher serum phosphorus levels who do not have obvious CKD.

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