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Hyperkalemia Treatment Standard Palmer Biff F Clegg Deborah J

  • SKU: BELL-58294656
Hyperkalemia Treatment Standard Palmer Biff F Clegg Deborah J
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Hyperkalemia Treatment Standard Palmer Biff F Clegg Deborah J instant download after payment.

Publisher: Oxford University Press
File Extension: PDF
File size: 1.16 MB
Author: Palmer Biff F., Clegg Deborah J.
Language: English
Year: 2024

Product desciption

Hyperkalemia Treatment Standard Palmer Biff F Clegg Deborah J by Palmer Biff F., Clegg Deborah J. instant download after payment.

DOI: 10.1093/ndt/gfae056 Nephrology Dialysis Transplantation, 39, 7, 29-02-2024. Abstract: Hyperkalemia is a common electrolyte disturbance in both inpatient and outpatient clinical practice. The severity and associated risk depends on the underlying cause and rate of potassium (K+) increase. Acute hyperkalemia requires immediate attention due to potentially life-threatening manifestations resulting from the rapid increase in plasma K+ concentration. Treatment is initially focused on stabilizing the cardiac membrane, followed by maneuvers to shift K+ into the cells, and ultimately initiating strategies to decrease total body K+ content. Chronic hyperkalemia develops over a more extended period of time and manifestations tend to be less severe. Nevertheless, the disorder is not benign since chronic hyperkalemia is associated with increased morbidity and mortality. The approach to patients with chronic hyperkalemia begins with a review of medications potentially responsible for the disorder, ensuring effective diuretic therapy and correcting metabolic acidosis if present. The practice of restricting foods high in K+ to manage hyperkalemia is being reassessed since the evidence supporting the effectiveness of this strategy is lacking. Rather, dietary restriction should be more nuanced, focusing on reducing the intake of nonplant sources of K+. Down-titration and/or discontinuation of renin–angiotensin–aldosterone inhibitors should be discouraged since these drugs improve outcomes in patients with heart failure and proteinuric kidney disease. In addition to other conservative measures, K+ binding drugs and sodium–glucose cotransporter 2 inhibitors can assist in maintaining the use of these drugs.

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