Largest Experience of Safety and Efficacy of Patiromer in Solid Organ Transplant

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Supplemental Digital Content is available in the text.

Related collections

Most cited references 5

Record: found
Abstract: found
Article: not found

Drug-induced hyperkalemia.

Chaker Ben Salem, Atef Badreddine, Neila Fathallah … (2014)

Hyperkalemia is a common clinical condition that can be defined as a serum potassium concentration exceeding 5.0 mmol/L. Drug-induced hyperkalemia is the most important cause of increased potassium levels in everyday clinical practice. Drug-induced hyperkalemia may be asymptomatic. However, it may be dramatic and life threatening, posing diagnostic and management problems. A wide range of drugs can cause hyperkalemia by a variety of mechanisms. Drugs can interfere with potassium homoeostasis either by promoting transcellular potassium shift or by impairing renal potassium excretion. Drugs may also increase potassium supply. The reduction in renal potassium excretion due to inhibition of the renin-angiotensin-aldosterone system represents the most important mechanism by which drugs are known to cause hyperkalemia. Medications that alter transmembrane potassium movement include amino acids, beta-blockers, calcium channel blockers, suxamethonium, and mannitol. Drugs that impair renal potassium excretion are mainly represented by angiotensin-converting enzyme inhibitors, angiotensin-II receptor blockers, direct renin inhibitors, nonsteroidal anti-inflammatory drugs, calcineurin inhibitors, heparin and derivatives, aldosterone antagonists, potassium-sparing diuretics, trimethoprim, and pentamidine. Potassium-containing agents represent another group of medications causing hyperkalemia. Increased awareness of drugs that can induce hyperkalemia, and monitoring and prevention are key elements for reducing the number of hospital admissions, morbidity, and mortality related to drug-induced hyperkalemia.

0 comments Cited 52 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: found

Is Open Access

Patiromer induces rapid and sustained potassium lowering in patients with chronic kidney disease and hyperkalemia

David A Bushinsky, Gordon Williams, Bertram Pitt … (2015)

Patients with chronic kidney disease (CKD) have a high risk of hyperkalemia, which increases mortality and can lead to renin–angiotensin–aldosterone system inhibitor (RAASi) dose reduction or discontinuation. Patiromer, a nonabsorbed potassium binder, has been shown to normalize serum potassium in patients with CKD and hyperkalemia on RAASi. Here, patiromer's onset of action was determined in patients with CKD and hyperkalemia taking at least one RAASi. After a 3-day potassium- and sodium-restricted diet in an inpatient research unit, those with sustained hyperkalemia (serum potassium 5.5 – under 6.5 mEq/l) received patiromer 8.4 g/dose with morning and evening meals for a total of four doses. Serum potassium was assessed at baseline (0 h), 4 h postdose, then every 2–4 h to 48 h, at 58 h, and during outpatient follow-up. Mean baseline serum potassium was 5.93 mEq/l and was significantly reduced by 7 h after the first dose and at all subsequent times through 48 h. Significantly, mean serum potassium under 5.5 mEq/l was achieved within 20 h. At 48 h (14 h after last dose), there was a significant mean reduction of 0.75 mEq/l. Serum potassium did not increase before the next dose or for 24 h after the last dose. Patiromer was well tolerated, without serious adverse events and no withdrawals. The most common gastrointestinal adverse event was mild constipation in two patients. No hypokalemia (serum potassium under 3.5 mEq/l) was observed. Thus, patiromer induced an early and sustained reduction in serum potassium and was well tolerated in patients with CKD and sustained hyperkalemia on RAASis.

0 comments Cited 29 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: found

Is Open Access

Electrolyte and Acid-Base Disorders in the Renal Transplant Recipient

Vaishnavi Pochineni, Helbert Rondon-Berrios (2018)

Kidney transplantation is the current treatment of choice for patients with end-stage renal disease. Innovations in transplantation and immunosuppression regimens have greatly improved the renal allograft survival. Based on recently published data from the Scientific Registry of Transplant recipients, prevalence of kidney transplants is steadily rising in the United States. Over 210,000 kidney transplant recipients were alive with a functioning graft in mid-2016, which is nearly twice as many as in 2005. While successful renal transplantation corrects most of the electrolyte and mineral abnormalities seen in advanced renal failure, the abnormalities seen in the post-transplant period are surprisingly different from those seen in chronic kidney disease. Multiple factors contribute to the high prevalence of these abnormalities that include level of allograft function, use of immunosuppressive medications and metabolic changes in the post-transplant period. Electrolyte disturbances are common in patients after renal transplantation, and several studies have tried to determine the clinical significance of these disturbances. In this manuscript we review the key aspects of the most commonly found post-transplant electrolyte abnormalities. We focus on their epidemiology, pathophysiology, clinical manifestations, and available treatment approaches.

0 comments Cited 15 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): Transplant Direct

Journal ID (iso-abbrev): Transplant Direct

Journal ID (publisher-id): TXD

Title: Transplantation Direct

Publisher: Lippincott Williams & Wilkins (Hagerstown, MD )

ISSN (Electronic): 2373-8731

Publication date Collection: September 2020

Publication date (Electronic): 12 August 2020

Volume: 6

Issue: 9

Electronic Location Identifier: e595

Affiliations

[1 ]Department of Pharmacy, Ohio State University Wexner Medical Center, Columbus, OH.

[2 ]Department of Internal Medicine, Comprehensive Transplant Center, Ohio State University, Columbus, OH.

Author notes

Correspondence: Kendra Schnelle, Department of Pharmacy, Ohio State University Wexner Medical Center, 410 W, 10th Ave, Doan 368, Columbus, OH 43210. ( Kendra.schnelle@ 123456osumc.edu ).

Article

Accession ID: 00005

DOI: 10.1097/TXD.0000000000001037

PMC ID: 7423918

SO-VID: 8bf3dacd-f1ed-4cbf-b662-8d6bc09dca81

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

History

Date received : 30 April 2020

Date revision received : 12 June 2020

Date accepted : 13 June 2020

Custom metadata

SDC T

OPEN-ACCESS TRUE

Data availability:

Largest Experience of Safety and Efficacy of Patiromer in Solid Organ Transplant

Read this article at

Abstract

Related collections

Efficacy of Communicating Science

Most cited references 5

Drug-induced hyperkalemia.

Patiromer induces rapid and sustained potassium lowering in patients with chronic kidney disease and hyperkalemia

Electrolyte and Acid-Base Disorders in the Renal Transplant Recipient

Author and article information

Journal

Affiliations

Author notes

Article

History

Categories

Custom metadata

Comments

Comment on this article

Cited by 3

Most referenced authors 39