1.
Potassium Binders for Hyperkalemia in Chronic Kidney Disease-Diet, Renin-Angiotensin-Aldosterone System Inhibitor Therapy, and Hemodialysis.
Palmer, BF
Mayo Clinic proceedings. 2020;(2):339-354
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Abstract
Hyperkalemia is a potentially life-threatening complication of chronic kidney disease (CKD). The management of CKD requires balancing the benefits of specific treatments, which may exacerbate the potential for hyperkalemia, with the risks of hyperkalemia itself. Renin-angiotensin-aldosterone system (RAAS) inhibitors, which slow CKD progression and improve cardiovascular outcomes, are often discontinued if hyperkalemia develops. Patients with hyperkalemia are frequently advised to restrict dietary potassium (K+), depriving these patients of many heart-healthy foods. Patients receiving hemodialysis are particularly susceptible to hyperkalemia during long interdialytic intervals, and managing this risk without causing hypokalemia can be challenging. Recently, 2 K+-binding agents were approved for the treatment of hyperkalemia: sodium zirconium cyclosilicate and patiromer. These agents offer alternatives to sodium polystyrene sulfonate, which is associated with serious gastrointestinal adverse effects. For this review, PubMed was searched for English-language articles published in 2014-2018 using the terms patiromer, sodium zirconium cyclosilicate, sodium polystyrene sulfonate, hyperkalemia, renin-angiotensin-aldosterone, diet, and dialysis. In randomized controlled studies of patients with hyperkalemia, sodium zirconium cyclosilicate and patiromer effectively reduced serum K+ and were generally well tolerated. Furthermore, patients in these studies could maintain RAAS inhibitor therapy and, in some studies, were not required to limit dietary K+. There may also be a role for these agents in preventing hyperkalemia in patients receiving hemodialysis. Thus, K+-binding agents may allow patients with CKD at risk for hyperkalemia to optimize RAAS inhibitor therapy, receive benefits of a K+-rich diet, and experience improved hemodialysis outcomes. Additional long-term studies are necessary to confirm these effects.
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[Hyperkalemia in heart failure: new solutions for an old problem].
Romani, S, Porcari, A, Fabris, E, Sinagra, G
Giornale italiano di cardiologia (2006). 2019;(10):543-551
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Abstract
Potassium is the main intracellular ion and its homeostasis is finely regulated by the renal and gastrointestinal tract. Renal failure and hyperkalemia are conditions commonly found in patients with heart failure, the result of a complex interaction between heart and kidney (e.g. cardio-renal syndrome) and the side effects of drugs commonly used for treating heart disease (e.g. renin-angiotensin-aldosterone system inhibitors). Although hyperkalemia increases the risk of heart conduction disorders and life-threatening arrhythmias, its prognostic significance in heart failure is uncertain. Hyperkalemia and progression of renal damage are the main limitations to the introduction and titration of heart failure therapies. New drugs for the prevention and chronic treatment of hyperkalemia allow the introduction and modulation of anti-neurohormonal therapies in patients with heart failure otherwise excluded from these treatments due to excessively high serum potassium levels.This review illustrates the pathophysiological, epidemiological and prognostic aspects of hyperkalemia and analyses the possible treatments for this condition in heart failure patients.
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A review of the bioactivity of hydraulic calcium silicate cements.
Niu, LN, Jiao, K, Wang, TD, Zhang, W, Camilleri, J, Bergeron, BE, Feng, HL, Mao, J, Chen, JH, Pashley, DH, et al
Journal of dentistry. 2014;(5):517-33
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Abstract
OBJECTIVES In tissue regeneration research, the term "bioactivity" was initially used to describe the resistance to removal of a biomaterial from host tissues after intraosseous implantation. Hydraulic calcium silicate cements (HCSCs) are putatively accepted as bioactive materials, as exemplified by the increasing number of publications reporting that these cements produce an apatite-rich surface layer after they contact simulated body fluids. METHODS In this review, the same definitions employed for establishing in vitro and in vivo bioactivity in glass-ceramics, and the proposed mechanisms involved in these phenomena are used as blueprints for investigating whether HCSCs are bioactive. RESULTS The literature abounds with evidence that HCSCs exhibit in vitro bioactivity; however, there is a general lack of stringent methodologies for characterizing the calcium phosphate phases precipitated on HCSCs. Although in vivo bioactivity has been demonstrated for some HCSCs, a fibrous connective tissue layer is frequently identified along the bone-cement interface that is reminiscent of the responses observed in bioinert materials, without accompanying clarifications to account for such observations. CONCLUSIONS As bone-bonding is not predictably achieved, there is insufficient scientific evidence to substantiate that HCSCs are indeed bioactive. Objective appraisal criteria should be developed for more accurately defining the bioactivity profiles of HCSCs designed for clinical use.