Diastolic Dysfunction and Inflammatory Biomarkers in Lupus Nephritis

Lupus nephritis is a frequent and severe manifestation of systemic lupus erythematosus (SLE) and often develops early in the disease course. Its pathophysiology is heterogeneous, driven by genetic, environmental, and immune-mediated mechanisms that produce inflammatory kidney injury. Despite therapeutic advances, lupus nephritis remains a major cause of chronic kidney disease, end-stage kidney disease, death, and reduced quality of life. Lupus nephritis can promote heart failure through intertwined inflammatory, renal, vascular, and hemodynamic pathways. Patients with SLE have increased heart failure risk, and cardiovascular risk is higher when nephritis is present. Renal impairment and proteinuria in lupus nephritis are linked to hypertension, dyslipidemia, endothelial dysfunction, and prothrombotic tendency, which can accelerate myocardial remodeling and dysfunction. Lupus nephritis directly causes diastolic heart failure through systemic inflammation and immune-complex deposition that produce interstitial myocardial fibrosis, edema, and diastolic dysfunction. This study addresses an important gap in patients with lupus nephritis, where subclinical myocardial dysfunction is increasingly recognized but poorly characterized in critically ill patients. Echocardiographic and tissue Doppler abnormalities correlate with inflammatory biomarkers such as CXCL10 and sST2 in SLE. Lupus nephritis is also associated with more severe myocardial involvement and higher inflammatory burden than extra-renal disease. However, adult intensive-care data linking left ventricular diastolic dysfunction parameters with systemic inflammatory biomarkers in lupus nephritis remain limited. This cross-sectional observational study will enroll 90 participants divided into three groups: control group without SLE or lupus nephritis (n=30), SLE without lupus nephritis (n=30), and SLE with lupus nephritis (n=30). Participants will undergo comprehensive clinical assessment, transthoracic echocardiography to assess left ventricular diastolic function (E/A ratio, e', E/e' ratio, LAVI, and LVEF), and blood sampling for inflammatory biomarkers (CRP, ESR, NLR, PLR, and SII). Disease activity will be assessed using the SLEDAI-2K score, and renal function will be assessed by eGFR and CKD stage. The correlation between echocardiographic diastolic parameters and inflammatory biomarkers will be determined, and independent predictors of diastolic dysfunction will be identified.