Key result
Digoxin treatment in patients with congestive heart failure significantly decreased mean estimated glomerular filtration rate from 65.4 to 57.7 mL/min/1.73m2.
Why the study?
Renal dysfunction is common in CHF, and because digoxin clearance is tied to GFR, its safety and efficacy may vary with renal function.
Does digoxin affect renal function in patients with congestive heart failure?
Observational (n=30)
No
Does digoxin affect renal function in patients with congestive heart failure?
Absolute Event Rate: 57.7% vs 65.4%
p-value: p=0.001
In a small retrospective cohort of patients with congestive heart failure, digoxin treatment was associated with a significant reduction in eGFR and elevations in liver enzymes, suggesting potential adverse effects on renal and hepatic function.
May warrant eGFR monitoring with digoxin in HF; leaves open causality and requires prospective trials.
INTRODUCTION: Renal dysfunction is a common complication among patients with congestive heart failure (CHF) and can significantly impact their management, especially when medications like digoxin are involved. The clearance of digoxin is closely tied to the glomerular filtration rate (GFR), which suggests that the safety and efficacy of digoxin may vary with renal function. Therefore, this study aimed to assess the potential effects of digoxin on renal function in patients diagnosed with CHF at a tertiary hospital in the Asir region of Saudi Arabia. METHODS: A retrospective study examined the records of 30 CHF patients treated with digoxin. Renal function markers like estimated GFR (eGFR), creatinine, blood urea nitrogen (BUN), albumin, and urine levels were compared before and after digoxin treatment. Liver enzymes and other relevant parameters were also examined. A statistical analysis using t-tests was conducted to evaluate the changes in renal function indicators before and after digoxin treatment. RESULTS: after (p = 0.001). Creatinine, BUN, albumin, and urine levels showed no significant changes. Digoxin significantly increased aspartate aminotransferase (AST) from 34.5 ± 11.6 U/L to 53.8 ± 14.6 U/L (p = 0.002), alanine aminotransferase (ALT) from 38.5 ± 12.6 U/L to 55.3 ± 17.6 U/L (p = 0.013), and creatine kinase from 117.7 ± 22.5 U/L to 133.9 ± 15.8 U/L (p = 0.012). Hemoglobin decreased significantly from 12.8 ± 1.4 g/dL to 12.1 ± 1.4 g/dL (p = 0.034). No significant changes occurred in myoglobin, troponin, bilirubin, platelets, potassium, calcium, or chloride levels. Effects on kidney function did not differ significantly by gender or age, except blood urea nitrogen was higher in patients over 50 years (8.3 ± 2.3 vs. 5.6 ± 2.7 mg/dL, p = 0.015). CONCLUSION: This study suggests digoxin may adversely affect renal function in CHF patients, as evidenced by reduced eGFR. However, the small retrospective design limits definitive conclusions. Further prospective research with larger samples is warranted to elucidate digoxin's renal effects in CHF patients.
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Alqahtani et al. (2023) conducted an observational in Congestive heart failure (n=30). Digoxin vs. Baseline (before digoxin treatment) was evaluated on Change in estimated GFR (eGFR) (p=0.001). Digoxin treatment in patients with congestive heart failure significantly decreased mean estimated glomerular filtration rate from 65.4 to 57.7 mL/min/1.73m2.
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