Clinical and Biochemical Determinants of Acute Kidney Injury in Acute Decompensated Heart Failure: A Prospective Observational Study From a Tertiary Care Centre in North India.

Background Cardiorenal syndrome type 1 (CRS-1), manifesting as acute kidney injury (AKI) during episodes of acute decompensated heart failure (ADHF), constitutes a clinically significant complication with independent adverse effects on both short- and long-term patient outcomes. Delineating the clinical, echocardiographic, and biochemical factors predisposing to this complication is foundational to risk-guided cardiorenal management. Prospective regional data from the Indian subcontinent addressing this clinical question remain insufficient. Materials and methods A prospective observational investigation enrolled 100 sequential adults who met the 2021 European Society of Cardiology (ESC) criteria for ADHF and were admitted to the Intensive Cardiac Care Unit and Medical ICU at Maharishi Markandeshwar University of Medical Sciences and Research (MMIMSR), Ambala, Haryana, India. AKI was ascertained using the Kidney Disease: Improving Global Outcomes (KDIGO) 2012 serum creatinine thresholds after exclusion of competing aetiologies. Comorbid diagnoses, echocardiographic indices (Left Ventricular Ejection Fraction (LVEF), phenotypic classification), and admission biochemistry including serum sodium and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were prospectively documented. Associations between different variables and AKI were evaluated using Chi-square analysis, independent-samples t-test or Mann-Whitney U test, unadjusted odds ratios (OR) with 95% confidence intervals, and ROC curve analysis. A two-tailed p-value below 0.05 denoted statistical significance. Results Half the enrolled cohort (50%) fulfilled criteria for AKI. The Heart Failure with Preserved Ejection Fraction (HFrEF) phenotype (LVEF ≤40%) was present in 80.0% of AKI patients relative to 68.0% of AKI-free patients (OR 1.88; 95% CI 0.73-4.82; χ² = 1.87; p = 0.171). Among comorbid conditions, only diabetes mellitus attained statistical significance (OR 4.37; 95% CI 1.89-10.08; χ² = 11.95; p < 0.001). Biochemically, AKI patients exhibited substantially higher median NT-proBNP (16,832.5 vs 6,599.5 pg/mL; p < 0.001), and lower serum sodium (135.96 ± 4.38 vs 137.98 ± 4.03 mEq/L; p = 0.018). NT-proBNP yielded the greatest discriminatory capacity (AUC 0.74; 95% CI 0.64-0.83), ahead of serum sodium (area under the curve (AUC) 0.64) and LVEF (AUC 0.60). Conclusion AKI is encountered in half of patients hospitalised with ADHF at a North Indian tertiary centre. Diabetes mellitus represents the predominant metabolic risk determinant, while admission NT-proBNP furnishes the strongest single-biomarker discriminatory signal. These routinely obtainable parameters constitute a clinically actionable framework for cardiorenal risk stratification at hospital admission.