Projects / Programmes
Renin-angiotensin-aldosterone system inhibitor associated renal dysfunction and hyperkalaemia in heart failure: epidemiology, prognosis and potassium binders
| Code |
Science |
Field |
Subfield |
| 3.06.00 |
Medical sciences |
Cardiovascular system |
|
| Code |
Science |
Field |
| 3.02 |
Medical and Health Sciences |
Clinical medicine |
Heart failure; Hyperkalaemia; Renal function; Potassium binders
Data for the last 5 years (citations for the last 10 years) on
April 25, 2024;
A3 for period
2018-2022
Data for ARIS tenders (
04.04.2019 – Programme tender,
archive
)
| Database |
Linked records |
Citations |
Pure citations |
Average pure citations |
| WoS |
969 |
80,875 |
76,770 |
79.23 |
| Scopus |
948 |
89,590 |
85,384 |
90.07 |
Researchers (9)
Organisations (3)
Abstract
Heart failure remains a life-threatening syndrome with substantial morbidity and mortality and still represents an unmet need of modern medicine. Inhibitors of the renin-angiotensin-aldosterone system (RAASi) are the cornerstones of heart failure therapy. Hyperkalaemia and chronic kidney disease are among most frequently cited reasons for under-dosing, underuse and discontinuation of RAAS inhibitors. Hyperkalaemia management focuses primarily on acute episodes, where immediate therapy is needed to prevent potentially fatal complications. What remains largely neglected is management of chronic hyperkalaemia or prevention of therapy induced hyperkalaemia. In last decade, new potassium bunders (patiromer, ZS9) have been have shown potential to be considered for these purposes. Based on available evidence, several gaps in knowledge exist thus we have conceived comprehensive investigator initiated research project proposal which aims to address epidemiological aspects of RAASi associated renal dysfunction and hyperkalaemia in heart failure. We will also investigate the post discharge prognostic implications in terms of hospitalisations and mortality. Finally, we will conduct a randomized trial to investigate the effects of potassium binder for RAASi optimization in patients hospitalized with acute heart failure. In first phase, we will conduct retrospective review of medical documentation from General Hospital Murska Sobota. All patients discharged with heart failure related ICD code in years 2015-2020 will be reviewed for presence of hyperkalaemia (K >5.0 mmol/L) and worsening renal function (KDIGO/AKIN criteria) anytime during the hospital stay. We will also record admission and discharge medication to analyze any modifications. Patient data will be cross-linked with national hospitalization database and central population registry to study associations with hospitalisations and mortality. Primary endpoints will be presence of hyperkalaemia (K >5.0 mmol/L) and worsening renal function (KDIGO/AKIN stage 1-3) at any time during hospitalization; secondary endpoints will be RAASi modification from admission to discharge, ICD codes for hyperkalaemia and worsening renal function and 12-month all-cause hospitalization or death. In the second phase, we will conduct two randomized, double blind, placebo controlled trials to test the effects of patiromer on RAASi therapy in patients with acute heart failure and hyperkalaemia/worsening renal function. All consecutive admissions for acute heart failure in our hospital will be screened for hyperkalaemia and worsening renal function as defined for our retrospective study. They will be eligible for randomization if on prior RAASi therapy diagnosed with hyperkaalemia or worsening renal function and we will form two patient strata: - Stratum 1: K 5.0-6.0 mmol/L or stage 1 worsening renal function - Stratum 2: K >6.0 mmol/L or stage 2/3 worsening renal function Stratum 1 patients will be invited for first randomized trial. In these patients, RAASi therapy will be either maintained or adjusted and we will start patiromer therapy in-hospital and continue 7 days post discharge. In stratum 2 patients, RAASi therapy will be stopped and then reinitiated after resolution of laboratory changes. At discharge, patients will be randomized to patiromer or placebo until day 30 post discharge. Primary endpoint will be RAASi therapy at day 30. Secondary endpoints will be RAASi therapy days 180 and 360; RAASi dose at days 30, 180 and 360; all-cause hospitalization and all cause death at days 180 and 360; potassium level at days 7 and 30; renal function at days 7 and 30. Based on literature and clinical trial database search, there are no competing trials. Our project proposal therefore has sufficient novelty and pending results can be considered as original and relevant for scientific and clinical community.
