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Introduction: This consensus statement of Australian clinicians provides new recommendations for the pharmacological management of heart failure based on studies reported since the publication of the 2018 Australian heart failure guidelines.Main Recommendations: ▪Use of sodium-glucose cotransporter 2 (SGLT2) inhibitors to prevent hospitalisation for heart failure in type 2 diabetes mellitus can be extended to patients with multiple cardiovascular risk factors, albuminuric chronic kidney disease, or atherosclerotic cardiovascular disease. ▪New evidence supports the use of a mineralocorticoid receptor antagonist (finerenone) to prevent heart failure in type 2 diabetes mellitus associated with albuminuric chronic kidney disease. ▪In addition to renin angiotensin system inhibitors (angiotensin receptor neprilysin inhibitor preferred), beta blockers and mineralocorticoid receptor antagonists, an SGLT2 inhibitor (dapagliflozin or empagliflozin) is recommended in all patients with heart failure with reduced left ventricular ejection fraction (LVEF ≤ 40%) (HFrEF). Lower quality evidence supports these therapies in patients with heart failure with mildly reduced LVEF (41-49%) (HFmrEF). ▪A soluble guanylate cyclase stimulator (vericiguat), selective cardiac myosin activator (omecamtiv mecarbil) and, if iron deficient, intravenous iron (ferric carboxymaltose) provide additional benefits in persistent HFrEF. ▪An SGLT2 inhibitor (empagliflozin) should be considered in patients with heart failure with preserved LVEF (≥ 50%) (HFpEF). Key changes in management from this statement: This document broadens the scope of angiotensin receptor neprilysin inhibitor use in patients with HFrEF and HFmrEF. SGLT2 inhibitor use expands to become a cornerstone therapy in HFrEF, with increasing evidence to support its use in HFmrEF and HFpEF. [ABSTRACT FROM AUTHOR]

In Australia, approximately 1.7 million adults have evidence of chronic kidney disease (CKD). This complex disease can result in a multitude of complications, including hyperkalaemia, which is common and well recognised. The advent of new therapeutics aimed at lowering serum potassium has raised the possibility of optimising potassium control to enable greater use of renin–angiotensin–aldosterone system inhibitors in the management of CKD. Recent studies suggest that hyperkalaemia also has implications for peripheral neuropathy in CKD, a complication that substantially contributes to patient morbidity. This review examines evidence of the relationship between potassium and peripheral neuropathy, with a discussion of clinical implications. We searched PubMed for original and review articles using pre‐specified key words, clinical guidelines and population data. The major findings were that contemporary CKD cohorts demonstrate a high prevalence of peripheral neuropathy, even in stage 3–4 CKD, including those without diabetes. The severity of the problem has been emphasised by an ominous rise in foot complications and amputation rates in dialysis patients, highlighting the need for increased awareness of the condition in earlier stages of CKD and targeted treatment strategies. It is likely that the pathophysiology of peripheral neuropathy in CKD is multifaceted, with potential influences from potassium, vascular abnormalities, diabetes, inflammation and unknown middle molecules. Despite these complexities, the relationship between potassium and nerve function in dialysis has been well established, and recent research in stage 3–4 CKD suggests that assertive potassium control may improve neuromuscular outcomes in CKD. These small studies should be confirmed in large, multicentre settings. [ABSTRACT FROM AUTHOR]

Previously, management of hypertension has concentrated on lowering elevated blood pressure. However, the target has shifted to reducing absolute cardiovascular ( CV) risk. It is estimated that two in three Australian adults have three or more CV risk factors at the same time. Moderate reductions in several risk factors can, therefore, be more effective than major reductions in one. When managing hypertension, therapy should be focused on medications with the strongest evidence for CV event reduction, substituting alternatives only when a primary choice is not appropriate. Hypertension management guidelines categorise angiotensin-converting enzyme inhibitors ( ACEI) and angiotensin receptor blockers ( ARB) interchangeably as first-line treatments in uncomplicated hypertension. These medications have different mechanisms of action and quite different evidence bases. They are not interchangeable and their prescription should be based on clinical evidence. Despite this, currently ARB prescriptions are increasing at a higher rate than those for ACEI and other antihypertensive classes. Evidence that ACEI therapy prevents CV events and death, in patients with coronary artery disease or multiple CV risk factors, emerged from the European trial on reduction of cardiac events with perindopril in stable coronary artery disease ( EUROPA) and Heart Outcomes Prevention Evaluation (HOPE) trials respectively. The consistent benefit has been demonstrated in meta-analyses. The clinical trial data for ARB are less consistent, particularly regarding CV outcomes and mortality benefit. The evidence supports the use of ACEI (Class 1a) compared with ARB despite current prescribing trends. [ABSTRACT FROM AUTHOR]

The renin-angiotensin system (RAS) plays a critical role in placentation and nephrogenesis. Failure to thrive during intrauterine life, possibly related to placental dysfunction and impaired expression of the renal RAS, as well as prematurity, results in smaller kidneys at birth and reduced nephron number. The remaining nephrons are therefore hyperfiltering from birth. Hyperfiltration, infections and Type 2 diabetes cause glomerular and tubular fibrosis, leading to further reductions in nephron number. The intrarenal RAS plays a key role in promoting tubulointerstitial fibrosis. Low birth weight and a high incidence of preterm birth program Indigenous children for early onset renal disease in adult life. Indigenous Australians have 404 000 fewer nephrons than non-Indigenous Australians. This, coupled with the high incidence of infectious diseases (particularly acute post-streptococcal glomerulonephritis) and the increasing prevalence of Type 2 diabetes, explains why end-stage renal disease is of epidemic proportions in Indigenous Australians. The existence of RAS gene polymorphisms and inflammatory cytokines may further potentiate susceptibility to renal disease in Indigenous Australians., (© 2013 Wiley Publishing Asia Pty Ltd.)