Safety
Designed for patient tolerability with minimal GI adverse effects1
Most common (≥1/100 to <1/10) adverse reactions observed in clinical studies were mild-to-moderate and generally resolved spontaneously or with treatment1
- Consipation 6.2%
- Hypomagnesemia* 5.3%
- Diarrhoea 3.0%
- Abdominal pain 2.9%
- Flatulance 1.8%
Uncommon adverse reactions (≥1/1,000 to <1/100) included nausea/vomiting1
Hypokalemia has not been identified as an ADR for Veltassa®1,2†
No dose-related oedema observed in over 52 weeks of treatment3
Veltassa® has few known drug-drug interactions1
- Concomitant administration of Veltassa® showed reduced bioavailability of only 3 drugs:1,4
- Ciprofloxacin
- Levothyroxine
- Metformin§
- No interaction was found with administration of oral drugs at least 3 hours apart from Veltassa®1
- Quinidine showed a potential drug interaction in vitro1
- As a precautionary measure, administration of Veltassa® should therefore be separated by at least 3 hours from other oral medicinal products1
With Veltassa® there is no additional CV or renal risk due to sodium1,5,6
Excess sodium intake is associated with increased CV and renal risks:6–17
Increased blood pressure7–9
Decreased renoprotective benefits of RAASi medication14–16**
CV morbidity and mortality7,10–13
Increased oedema risk17
Increased albuminuria6,9
When RAASi are working to decrease Na+, Veltassa® binds K+ without Na+ release1,18
References & footnotes
Footnotes
*Hypomagnesaemia was mild-to-moderate, with no patient developing a serum magnesium level <1 mg/dL (0.4 mmol/L). Serum magnesium should be monitored for at least 1 month after initiating treatment, and magnesium supplementation considered in patients who develop low serum magnesium levels.1
†Since excessive doses of Veltassa® may result in hypokalemia, serum potassium levels should be monitored when initiated and uptitrated.1
§Effect of concomitant administration of Veltassa® with metformin is similar to taking metformin with food.4
**In a post hoc analysis of the RENAAL and IDNT trials, treatment effects of angiotensin receptor blockers on renal and cardiovascular outcomes were compared in subgroups of 1,177 patients with type 2 diabetes, nephropathy, and protein urea. Patients with available 24-h urinary sodium measurements were assessed over a 30-month follow-up period. The subgroups, based on dietary sodium intake were: low sodium intake: Na:Cr≤121mmol/g; medium sodium intake: Na:Cr121–≤153 mmol/g; high sodium intake: Na:Cr. The renal outcome in this analysis was defined as a composite of a confirmed doubling of serum creatinine from baseline or end-stage renal disease. The latter was defined as the need for chronic dialysis or renal transplantation. An additional definition for end-stage renal disease of a serum creatinine ≥6mg/dl (≥530μmol/l) applied in the IDNT trial. Compared to non-RAASi, the trend in risk for renal events was significantly reduced by 43%, not changed, or increased by 37% for each tertile of increased sodium intake.14
Abbreviations
ADR, adverse drug reaction; CV, cardiovascular; GI, gastrointestinal; K+, potassium; Na+, sodium; RAASi, renin-angiotensin-aldosterone-system inhibitor.
References
- Veltassa SmPC.
- Pina IL, et al. Effect of patiromer on serum potassium in hyperkalemic patients with heart failure: Pooled analysis of 3 randomized trials. Prog Cardiovasc Dis. 2020;20:30163–8.
- Bakris GL, et al. Effect of Patiromer on Serum Potassium Level in Patients With Hyperkalemia and Diabetic Kidney Disease. JAMA 2015;314(2):151–61.
- Lesko LJ, et al. Evaluation of the Potential for Drug Interactions With Patiromer in Healthy Volunteers. J Cardiovasc Pharmacol Ther. 2017;22(5):434-446.
- Montagnani A, et al. Optimization of RAASi Therapy with New Potassium Binders for Patients with Heart Failure and Hyperkalemia: Rapid Review and Meta-Analysis. J Clin Med. 2021;10(23);5483.
- McMahon EJ, et al. A randomized trial of dietary sodium restriction in CKD. J Am Soc Nephrol. 2013;24(12):2096–103.
- INTERSALT. Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Intersalt Cooperative Research Group. BMJ. 1988;297(6644):319–28.
- He FJ, et al. Effect of modest salt reduction on blood pressure: a meta-analysis of randomized trials. Implications for public health. J Hum Hypertens. 2002;16(11):761–70.
- Garofalo C, et al. Dietary Salt Restriction in Chronic Kidney Disease: A Meta-Analysis of Randomized Clinical Trials. Nutrients. 2018;10(6). pii:E732.
- Mills KT, et al. Sodium Excretion and the Risk of Cardiovascular Disease in Patients With Chronic Kidney Disease. JAMA. 2016;315(20):2200–10.
- Cook NR, et al. Sodium Intake and All-Cause Mortality Over 20 Years in the Trials of Hypertension Prevention. J Am Coll Cardiol. 2016;68(15):1609–17.
- O’Donnell MJ, et al. Urinary sodium and potassium excretion and risk of cardiovascular events. JAMA. 2011;306(20):2229–38.
- Philipson H, et al. Salt and fluid restriction is effective in patients with chronic heart failure. Eur J Heart Fail. 2013;15(11):1304–10.
- Heerspink HJ, et al. Moderation of dietary sodium potentiates the renal and cardiovascular protective effects of angiotensin receptor blockers. Kidney Int. 2012;82(3):330–7.
- Vegter S, et al. Sodium Intake, ACE Inhibition, and Progression to ESRD. J Am Soc Nephrol. 2012;23:165–73.
- Jones-Burton C, et al. An in-depth review of the evidence linking dietary salt intake and progression of chronic kidney disease. Am J Nephrol. 2006;26:268–75.
- Slagman MCJ, et al. Moderate dietary sodium restriction added to angiotensin converting enzyme inhibition compared with dual blockade in lowering proteinuria and blood pressure: randomised controlled trial. BMJ. 2011:10.1136/bmj.d4366.
- Fountain JH, Lappin, SL. Physiology, Renin Angiotensin System. StatPearls [Internet], StatPearls Publishing 2019.