Hyponatremia in Acute Decompensated Heart Failure as a Predictor of Acute Cardiorenal Syndrome Type-1

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INTRODUCTION

Acute cardiorenal syndrome (CRS type-1) is the development of acute kidney injury (AKI) and renal dysfunction in a patient with an acute cardiac disease, typically acute decompensated heart failure (ADHF).^[1] Acute kidney damage (AKI) that develops in this situation has repeatedly been linked to higher all-cause death rates over the short- and long-term, as well as cardiovascular mortality, and to a quicker progression of more advanced renal disease.^[2]

AKI’s pathogenesis in the context of ADHF is complex and multifaceted. Hemodynamic variables, neurohormonal activation, and congestion are three major contributory mechanisms. Quantification of hemodynamic disturbance is possible; however, the level of fluid overload and the exposure of the kidney to numerous activated neurohormonal systems is difficult to quantify clinically.

The most common electrolyte disorder that is frequently seen in ADHF patients as well as in a variety of therapeutic settings is hyponatremia.^[3] Low sodium levels have been linked to mortality and recurrent hospitalizations for decompensation, according to numerous investigations on patients with heart failure (HF).

Compared to outpatients with stable disease, hospitalized patients with deteriorating HF have a much higher prevalence of hyponatremia^[4] and volume overload. AKI may also be more likely to occur in the kidneys due to neurohormonal activation, renal vasoconstriction, and decreased renal blood flow, in addition to the impact of hyponatremia on survival, severe volume overload, and related venous congestion.^[5] Therefore, the purpose of this study is to investigate the hypothesis that hyponatremia may portend the onset of AKI in the setting of ADHF.

MATERIALS AND METHODS

After receiving properly informed consent, patients meeting the inclusion and exclusion criteria will be enrolled in this study. Before the trial, a medication history including diuretics and nephrotoxic medications will be obtained.

We looked at the relationship between hyponatremia and AKI in two distinct cohorts: (1) Patients with AKI in ADHF and (2) patients without AKI in ADHF.

AKI is defined as an increase of >0.3 mg/dL in creatinine from baseline. Sodium levels below 136 mmoL/L are considered hyponatremia. Between June and August 2022, adults (>18 years of age) with ADHF were enrolled. Electronic medical records were used to obtain clinical data. The permitted error was ±2%, and α = 0.05 bilateral when estimating the sample size using the formula for calculating the sample size of cross-sectional studies. The estimated sample size was 100.

RESULTS

The study included 100 patients in total, of whom 75 (75%) were men and 25 (25%) were women. The participants’ average age was 51.60 years. It was noted that 26 (26%) participants were between the ages of 21 and 40, 42 (42%) were between the ages of 41 and 60, and 32 (32%) were over the age of 60 [Table 1]. Depending on whether AKI was present or not, we split the study population into two groups [Table 2].

The mean N-terminal pro-brain natriuretic peptide (NT ProBNP) levels were 3284 pg/mL and the mean left ventricular ejection fraction (LVEF) was 30% [Table 3]. In our study, 17 diabetic patients (32.7%), 21 hypertensive patients (40.4%), and eight chromic smokers (15.4%) all suffered from AKI; however, none of these percentages were statistically significant [Table 4].

One finding was that hyponatremia affected 45% of the study participants [Table 2]. It was noted that 12% of the study group had a history of smoking, 35% of patients had hypertension, and 28% of patients had diabetes mellitus [Figure 1]. According to data analysis, AKI finally developed in 63.5% of patients with hyponatremia during a hospital stay, but only 36.5% of individuals without hyponatremia [Table 5].

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Figure 1:

Distribution of characteristics among study patients.

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In comparison to ADHF patients without hyponatremia, those with hyponatremia have a 5.21-fold higher chance of getting AKI (95% CI, 2.20–12.36), and this conclusion was statistically significant (P < 0.001) [Table 6].

After correcting for age, gender, comorbidities, and habits as potential confounders, ADHF patients with hyponatremia are 5.07 times more likely to develop AKI (95% CI, 2.05– 12.55) than ADHF patients without hyponatremia. This finding was statistically significant at P < 0.001 [Table 7].

DISCUSSION

Acute CRS type-1 and ADHF coexistence are a serious condition linked to significantly higher morbidity and mortality in people with HF.^[6-9] The inability to identify patients with a high risk of developing CRS type-1 early enough to start therapies is a significant obstacle to improving clinical outcomes in ADHF patients.

Patients with ADHF often experience hyponatremia. According to Lee et al.,^[10] chronic HF patients who have hyponatremia had increased mortality rates. Patients with ADHF experience this as well.

A 19.7% admission rate for patients with hyponatremia (Na 135 mMoL/L) was found in the analysis of the OPTIMIZE-HF registry. Both registries and clinical trials, such as outcomes of a prospective trial of intravenous milrinone for exacerbations of chronic heart failure^[3] (27%) and ESCAPE^[4] (24%), have similar rates of hyponatremia. When comparing hyponatremia to normal sodium levels, a lower blood sodium concentration is linked to increased mortality during hospitalization and after discharge as well as a higher likelihood of readmission for ADHF after 6 months.

Our study’s key findings were that hyponatremia in HF patients was linked to increased problems during a hospital stay. With ADHF, 45% of patients exhibited hyponatremia (among which 33 patients had AKI, and 12 patients did not have AKI).

Patients with ADHF from a range of age groups, genders, and comorbidities are included in our sample. Some of these variations could play a role in the development of AKI. Even though comorbidities were more prevalent in individuals with AKI, they did not significantly affect the outcomes statistically. Other studies have demonstrated that chronic comorbidities independently increase the mortality rates of patients with newly diagnosed HF^[11] and also in the ambulatory HF population.^[12]

Hyponatremia was found to be a statistically significant (P < 0.001) predictor of increased incidence of AKI in a predetermined group of patients with HF in our study, and ADHF patients with hyponatremia have a 5.21-fold higher risk of developing AKI (95% CI, 2.20–12.36) than ADHF patients without hyponatremia. Future trials with hyponatremic patients and HF should include data on comorbidities to validate the results that we acquired in this study. Older people have more comorbidities, and the percentage of patients with intact ejection fraction is higher.

CONCLUSION

Hyponatremia predicts complications while admission in HF patients like type-I CRS and it has also been shown that comorbidities could play an important role in the presence or absence of hyponatremia and could even influence the length of hospital stay attributed to lower serum sodium levels which need further clinical trials.