Neurohumoral Dysregulation in Acute Myocardial Infarction With Chronic Kidney Disease: Implications for Prognosis and Management

Background Acute myocardial infarction (AMI) and chronic kidney disease (CKD) often coexist, and both are associated with neurohumoral imbalances that may worsen cardiovascular outcomes. Reduced kidney function can contribute to arterial stiffness and activation of the renin-angiotensin-aldosterone system (RAAS), which promotes vasoconstriction, sodium and water retention, myocardial remodeling, and fibrosis, mechanisms that exacerbate both cardiac and renal dysfunction. Endothelial injury is also common in these patients, and von Willebrand factor (vWF) serves as a recognized marker of endothelial dysfunction, contributing to thrombotic risk and microvascular impairment. Objective To explore the cross-sectional associations between renal function and the biomarkers aldosterone, angiotensin-converting enzyme (ACE), atrial natriuretic peptide (ANP), and vWF in patients with AMI and heart failure. Methods In this cross-sectional study, 106 patients hospitalized for AMI and heart failure were stratified by estimated glomerular filtration rate (GFR) into Group 1 (≤90 mL/min) and Group 2 (>90 mL/min). While CKD is conventionally defined as GFR <60 mL/min, the ≤90 mL/min cutoff was chosen to evaluate biomarker variation across a broader renal function range, including early decline. All eligible patients from the study period were included; no formal power calculation was performed. Neurohumoral markers were measured via enzyme-linked immunosorbent assay (ELISA). Heart failure was an inclusion criterion for all participants. Results Baseline characteristics were comparable between groups. Aldosterone and ACE were higher in patients with GFR ≤90 mL/min (p-values 0.01-0.05; below the prespecified α = 0.01). ANP and vWF did not differ between groups, which may reflect limited sensitivity to early renal function differences or other physiological influences. Conclusion The observed association between reduced GFR and elevated aldosterone and ACE suggests RAAS-related neurohumoral activation in AMI patients with heart failure. The lack of difference in ANP and vWF highlights potential marker-specific limitations. Targeting RAAS and other relevant pathways may offer therapeutic benefits for improving outcomes in this population; however, such approaches require confirmation in prospective interventional trials. These findings are exploratory and hypothesis-generating, underscoring the need for larger, longitudinal, and interventional studies to clarify the prognostic and therapeutic implications.