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PATIROMER REDUCED RECURRENT HYPERKALEMIA IN ADVANCED CKD PATIENTS ON RAASI
NKF 2015 Spring Clinical Meetings Abstracts
301
303
PATIROMER REDUCED RECURRENT HYPERKALEMIA IN ADVANCED CKD PATIENTS ON RAASI: M. Weir1, D. Bushinsky2, M. Mayo3, D. Garza3, Y. Stasiv3, S. Arthur3, L. Berman3, G. Bakris4. 1 Univ. of Maryland, Baltimore, MD; 2Univ. of Rochester, Rochester, NY; 3Relypsa, Redwood City, CA; 4Univ. of Chicago, Chicago, IL Patiromer, the active moiety of which is a nonabsorbed potassium (K+)-binder, reduced serum K+ (s-K+) and hyperkalemia (HK) recurrence in CKD patients (pts) with HK on RAAS inhibitors (RAASi). We present results in the subgroup with CKD Stage 4-5. Pts with baseline (BL) s-K+ 5.1 to <6.5 mEq/L received patiromer (4.2 or 8.4 g BID to start) in a 4-wk Treatment Phase; pts with moderate/severe BL s-K+ (5.5 to <6.5 mEq/L) were eligible for an 8-wk placebo (PBO)-controlled randomized Withdrawal Phase. Endpoints included change in s-K+ from BL to Wk 4 (Treatment Phase); betweengroup difference in s-K+ change over 1st 4 wk of the phase, % of pts with recurrent HK (s-K+ ≥5.5 mEq/L) and time to recurrent HK (≥5.5 mEq/L before Wk 4; ≥5.1 mEq/L from Wk 4-8) (Withdrawal Phase). In 106 Stage 4-5 CKD pts, BL mean (±SE) s-K+ was 5.6±0.04 mEq/L and fell by 0.94±0.05 mEq/L (p<0.001). In the randomized Withdrawal Phase, median s-K+ increase was greater for PBO (0.91 mEq/L, n=23) than patiromer (0.20 mEq/L, n=21; p=0.001). HK recurred in 69% of PBO vs 20% of patiromer pts (p<0.001). Time to HK recurrence increased with patiromer (Fig.). Constipation, the most common adverse event, occurred in 11% (1st phase) and 5% (2nd phase) of patiromer pts (none severe). Proportion with Recurrent Hyperkalemia
1.0 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0.0 Study Week
Time to Recurrent HK (s-K+ ≥5.5 mEq/L before Wk 4; ≥5.1 mEq/L from Wk 4-8)
Placebo Patiromer
Baseline
Wk 1
Wk 2
Wk 3
Wk 4
Wk 5
Wk 6
Wk 7
Wk 8
10 16
7 12
4 11
3 11
1 10
Pts without recurrent HK and still on placebo or patiromer
Placebo Patiromer
23 21
17 19
15 18
12 17
+
AORTIC DISSECTION: A RARE CAUSE OF ACUTE KIDNEY INJURY Sandar Win, Gaurang Mavani , Jordan L Rosenstock, Maria V DeVita, Michael F Michelis, Division of Nephrology, Lenox Hill Hospital/NSLIJ, New York, NY, USA We report a very rare case of acute kidney injury in type B aortic dissection without renal artery involvement. A 34 year old male presented with leg edema that had worsened over one month. His only other complaint on admission was worsening dyspnea on exertion. He had a history of uncontrolled hypertension, but was noncompliant with medications, chronic kidney disease with last creatinine of 3 mg/dL, 6months before admission and hyperlipidemia. His medications included hydralazine, labetalol, nifedipine and furosemide. On exam, his BP was 225/116 mmHg; he had a systolic cardiac murmur and bilateral 3+ lower extremity edema. His creatinine was 14.75 mg/dL on admission. Dialysis was initiated. For further evaluation of his cardiac murmur an echocardiogram was performed which revealed aortic regurgitation, moderate aortic root dilatation and moderately dilated ascending aorta. Subsequently, a CT angiogram showed an aortic dissection extending to both external iliac arteries, left internal iliac artery and left common femoral artery. He required ascending aortic aneurysm repair. He has not regained kidney function and remains on dialysis. Aortic dissection typically occurs in the elderly and is associated with significant back pain or chest pain. This case involves a young man with complaints of shortness of breath and leg swelling. Acute kidney injury is an uncommon presentation in aortic dissection, even with renal artery involvement. As such, it is not always considered as a cause of acute kidney injury (AKI) in the absence of typical findings. This patient did not dissect into his renal arteries but was clearly hypoperfusing his kidneys. Aortic dissection can be considered as an etiology of AKI in the setting of uncontrolled hypertension, even if the patient does not have classic symptoms.
After controlling s-K , patiromer reduced HK recurrence compared to PBO in CKD Stage 4-5 pts on RAASi, with good tolerability.
302 APPLICATION OF THE MEES/OK MODEL OF SODIUM RESTRICTION AND FLUID REMOVAL TO CONTROL BLOOD PRESSURE IN HEMODIALYSIS PATIENTS: Caroline Williams1, Stefanie Abbate1, Mikhail Artemyev 1, Surendra Gupta2, Tahir Hafeez2, Paul Parker2, Elisabeth Tillotson2, Alice Wei2, Nathan Levin1,1Renal Research Institute, 2Fresenius Medical Care, US Volume control in hemodialysis (HD) in the USA is notoriously inefficient with consequent hypertension and cardiac dysfunction. Short dialysis times, vague post dialysis weight targets and high UFRs perpetuate the problem. Following the quality improvement methods of Mees and Ok who have established normotension in 90% of HD patients over 2 decades, interdialytic and intradialytic sodium loading have been reduced by facility and patient education AND by 200300g/treatment reduction in post dialysis weight in hypertensive and hypotensive patients at 3 dialysis units in New York and Portland ME. Mean IDWG, weight and pre-dialysis systolic BP are compared over 2-3 months in BP groups (see Table). In “untouched” patients mean changes in BP groups were -4.1, +2.7 and +12.8 mmHg respectively over time. Decreases in target weight over 2-3months were associated with BP reduction especially in the >160mmHg group. Increase in BP in the<120mmHg group suggests improved cardiac efficiency. These simple but demanding approaches to care confirm the value of earlier work. Broader application could be useful in reducing hospitalization and mortality.
A90
304 VARIABILITY OF ARGININE VASOPRESSIN (AVP) LEVELS IN HOSPITALIZED PATIENTS WITH HYPONATREMIA Sandar Win, Gaurang Mavani, Maria V. DeVita, Michael F. Michelis, Division of Nephrology, Lenox Hill Hospital/NSLIJ, New York, NY, USA. Hyponatremia is the most common electrolyte disorder seen in hospitalized patients. Many of these patients are believed to exhibit excess AVP activity with stimulation of renal V2 receptors as the cause of their low serum sodium. We decided to obtain vasopressin levels in consecutive patients with hyponatremia. The primary diagnosis and types of medications used by the patients were also tabulated. Diagnoses included CNS disorders, edematous states and drug effect. Vasopressin levels varied from 0.5 to 4.6 pg/mL with a mean value of 1.8 ±1.3. Serum sodium levels varied from 123 to 132 mEq/L with a mean value of 127.1 ± 3.0 and urine osmolality varied from 241 to 551 mOsm/kg of water with a mean value of 288.0 ± 101.7. The vasopressin levels did not seem to be related to the level of serum sodium (r = .04, p = 0.89) or the level of urine osmolality (r = .10, p = 0.75). The data suggests that vasopressin levels are neither consistently elevated nor bear any relation to the serum sodium or urine osmolality observed. It should be considered that V2 receptor dysfunction or hypersensitivity may be responsible for some of the findings demonstrated in this study.
Am J Kidney Dis. 2015;65(4):A1-A93
301
303
PATIROMER REDUCED RECURRENT HYPERKALEMIA IN ADVANCED CKD PATIENTS ON RAASI: M. Weir1, D. Bushinsky2, M. Mayo3, D. Garza3, Y. Stasiv3, S. Arthur3, L. Berman3, G. Bakris4. 1 Univ. of Maryland, Baltimore, MD; 2Univ. of Rochester, Rochester, NY; 3Relypsa, Redwood City, CA; 4Univ. of Chicago, Chicago, IL Patiromer, the active moiety of which is a nonabsorbed potassium (K+)-binder, reduced serum K+ (s-K+) and hyperkalemia (HK) recurrence in CKD patients (pts) with HK on RAAS inhibitors (RAASi). We present results in the subgroup with CKD Stage 4-5. Pts with baseline (BL) s-K+ 5.1 to <6.5 mEq/L received patiromer (4.2 or 8.4 g BID to start) in a 4-wk Treatment Phase; pts with moderate/severe BL s-K+ (5.5 to <6.5 mEq/L) were eligible for an 8-wk placebo (PBO)-controlled randomized Withdrawal Phase. Endpoints included change in s-K+ from BL to Wk 4 (Treatment Phase); betweengroup difference in s-K+ change over 1st 4 wk of the phase, % of pts with recurrent HK (s-K+ ≥5.5 mEq/L) and time to recurrent HK (≥5.5 mEq/L before Wk 4; ≥5.1 mEq/L from Wk 4-8) (Withdrawal Phase). In 106 Stage 4-5 CKD pts, BL mean (±SE) s-K+ was 5.6±0.04 mEq/L and fell by 0.94±0.05 mEq/L (p<0.001). In the randomized Withdrawal Phase, median s-K+ increase was greater for PBO (0.91 mEq/L, n=23) than patiromer (0.20 mEq/L, n=21; p=0.001). HK recurred in 69% of PBO vs 20% of patiromer pts (p<0.001). Time to HK recurrence increased with patiromer (Fig.). Constipation, the most common adverse event, occurred in 11% (1st phase) and 5% (2nd phase) of patiromer pts (none severe). Proportion with Recurrent Hyperkalemia
1.0 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0.0 Study Week
Time to Recurrent HK (s-K+ ≥5.5 mEq/L before Wk 4; ≥5.1 mEq/L from Wk 4-8)
Placebo Patiromer
Baseline
Wk 1
Wk 2
Wk 3
Wk 4
Wk 5
Wk 6
Wk 7
Wk 8
10 16
7 12
4 11
3 11
1 10
Pts without recurrent HK and still on placebo or patiromer
Placebo Patiromer
23 21
17 19
15 18
12 17
+
AORTIC DISSECTION: A RARE CAUSE OF ACUTE KIDNEY INJURY Sandar Win, Gaurang Mavani , Jordan L Rosenstock, Maria V DeVita, Michael F Michelis, Division of Nephrology, Lenox Hill Hospital/NSLIJ, New York, NY, USA We report a very rare case of acute kidney injury in type B aortic dissection without renal artery involvement. A 34 year old male presented with leg edema that had worsened over one month. His only other complaint on admission was worsening dyspnea on exertion. He had a history of uncontrolled hypertension, but was noncompliant with medications, chronic kidney disease with last creatinine of 3 mg/dL, 6months before admission and hyperlipidemia. His medications included hydralazine, labetalol, nifedipine and furosemide. On exam, his BP was 225/116 mmHg; he had a systolic cardiac murmur and bilateral 3+ lower extremity edema. His creatinine was 14.75 mg/dL on admission. Dialysis was initiated. For further evaluation of his cardiac murmur an echocardiogram was performed which revealed aortic regurgitation, moderate aortic root dilatation and moderately dilated ascending aorta. Subsequently, a CT angiogram showed an aortic dissection extending to both external iliac arteries, left internal iliac artery and left common femoral artery. He required ascending aortic aneurysm repair. He has not regained kidney function and remains on dialysis. Aortic dissection typically occurs in the elderly and is associated with significant back pain or chest pain. This case involves a young man with complaints of shortness of breath and leg swelling. Acute kidney injury is an uncommon presentation in aortic dissection, even with renal artery involvement. As such, it is not always considered as a cause of acute kidney injury (AKI) in the absence of typical findings. This patient did not dissect into his renal arteries but was clearly hypoperfusing his kidneys. Aortic dissection can be considered as an etiology of AKI in the setting of uncontrolled hypertension, even if the patient does not have classic symptoms.
After controlling s-K , patiromer reduced HK recurrence compared to PBO in CKD Stage 4-5 pts on RAASi, with good tolerability.
302 APPLICATION OF THE MEES/OK MODEL OF SODIUM RESTRICTION AND FLUID REMOVAL TO CONTROL BLOOD PRESSURE IN HEMODIALYSIS PATIENTS: Caroline Williams1, Stefanie Abbate1, Mikhail Artemyev 1, Surendra Gupta2, Tahir Hafeez2, Paul Parker2, Elisabeth Tillotson2, Alice Wei2, Nathan Levin1,1Renal Research Institute, 2Fresenius Medical Care, US Volume control in hemodialysis (HD) in the USA is notoriously inefficient with consequent hypertension and cardiac dysfunction. Short dialysis times, vague post dialysis weight targets and high UFRs perpetuate the problem. Following the quality improvement methods of Mees and Ok who have established normotension in 90% of HD patients over 2 decades, interdialytic and intradialytic sodium loading have been reduced by facility and patient education AND by 200300g/treatment reduction in post dialysis weight in hypertensive and hypotensive patients at 3 dialysis units in New York and Portland ME. Mean IDWG, weight and pre-dialysis systolic BP are compared over 2-3 months in BP groups (see Table). In “untouched” patients mean changes in BP groups were -4.1, +2.7 and +12.8 mmHg respectively over time. Decreases in target weight over 2-3months were associated with BP reduction especially in the >160mmHg group. Increase in BP in the<120mmHg group suggests improved cardiac efficiency. These simple but demanding approaches to care confirm the value of earlier work. Broader application could be useful in reducing hospitalization and mortality.
A90
304 VARIABILITY OF ARGININE VASOPRESSIN (AVP) LEVELS IN HOSPITALIZED PATIENTS WITH HYPONATREMIA Sandar Win, Gaurang Mavani, Maria V. DeVita, Michael F. Michelis, Division of Nephrology, Lenox Hill Hospital/NSLIJ, New York, NY, USA. Hyponatremia is the most common electrolyte disorder seen in hospitalized patients. Many of these patients are believed to exhibit excess AVP activity with stimulation of renal V2 receptors as the cause of their low serum sodium. We decided to obtain vasopressin levels in consecutive patients with hyponatremia. The primary diagnosis and types of medications used by the patients were also tabulated. Diagnoses included CNS disorders, edematous states and drug effect. Vasopressin levels varied from 0.5 to 4.6 pg/mL with a mean value of 1.8 ±1.3. Serum sodium levels varied from 123 to 132 mEq/L with a mean value of 127.1 ± 3.0 and urine osmolality varied from 241 to 551 mOsm/kg of water with a mean value of 288.0 ± 101.7. The vasopressin levels did not seem to be related to the level of serum sodium (r = .04, p = 0.89) or the level of urine osmolality (r = .10, p = 0.75). The data suggests that vasopressin levels are neither consistently elevated nor bear any relation to the serum sodium or urine osmolality observed. It should be considered that V2 receptor dysfunction or hypersensitivity may be responsible for some of the findings demonstrated in this study.
Am J Kidney Dis. 2015;65(4):A1-A93