The current study aimed to investigate if clinical markers such as the BUN/Cr ratio, BUN, or creatinine can stratify the AKI mortality risk in ADHF patients and whether these markers are associated with the outcome, length of hospital stay, and death.

This study observed a significant increase in NYHA class 4 on day 1 in group IV compared to group I and on days 2 and 3 in group IV compared to groups I and III. There was a substantial decrease in SBP and DBP in group IV compared to groups I and III. In line, Takaya et al. [2] reported that compared to the other groups, blood pressure (systolic and diastolic) is lower in group 4, and it is usually treated with IV dopamine and dobutamine therapy.

Our study demonstrated a significant increase in creatinine at the first and third readings in groups III and IV compared to group I. Similar findings were observed in the second reading, with a significant elevation in group III compared to group I.

First readings of urea and BUN showed a significant rise in groups III and IV compared to group I, and in group IV compared to groups I and III. Comparable results were reported in the second and third readings.

The BUN/Cr ratio readings demonstrated a significant rise in group IV compared to groups I, II, and III. There was a substantial decline in GFR in groups III and IV compared to group I in the three GFR readings. These results are compatible with Takaya et al. [2], who reported that AKI patients with high BUN/Cr have lower GFR but higher BUN, creatinine, and BUN/Cr levels than the other groups.

Higher creatinine levels may be due to either permanent renal damage or congestion relief. On the other hand, urea excretion is decreased by renal vasoconstriction and decreased GFR caused by neurohormonal components, such as the sympathetic nervous system and renin–angiotensin–aldosterone system [8, 9].

Additionally, flow- and concentration-dependent urea absorption is increased by neurohormonal activity [10]. Low cardiac output causes arterial underfilling that induces arginine vasopressin production, encouraging urea reabsorption [10]. While urea is disproportionately reabsorbed during neurohormonal activation, causing an increased BUN/Cr ratio, the glomerulus freely filters creatinine, which is not reabsorbed. [11]. Therefore, a higher BUN/Cr more accurately represents neurohormonal activity than a higher creatinine or a lower estimated GFR [2].

In regression analysis for predicting AKI, only HTN, creatinine, and BUN were independent predictors of AKI. Takaya et al. [2] observed that BUN, creatinine, and intravenous dobutamine are independent risk factors for AKI. Additionally, Tung et al. [12] stated that age, GFR, WBCS, Hb, BUN, creatinine, B-type natriuretic peptide, Cystatin C, and neutrophil gelatinase-associated lipocalin are associated with AKI in the univariate analysis. However, no variable remained significant after multivariate analysis.

The current study has some limitations: the first is the observational nature of the study. Second, the non-neurohormonal factors affecting the BUN/Cr ratio include a high-protein diet, cachexia, and muscular atrophy; however, these elements were not examined in this investigation. Third, the time interval for serum creatinine tests was not just 48 h since the timing of laboratory measurements was allowed at the treating physicians' discretion, thereby underestimating the incidence of AKI. Finally, the AKI network criteria use urine output and serum creatinine to define AKI; however, we only used serum creatinine. Therefore, these results need to be supported by data from sizable, well-planned trials to advance our understanding of the BUN/Cr in AHF patients.