Key result
Lower post-furosemide urine sodium linked to ~12% lower rate of oxygen discontinuation per 10 mmol/L.
Why the study?
Poor natriuresis indicates potential diuretic resistance in dogs with acute CHF, but the relationship between urine sodium concentration and successful decongestion frequency is poorly understood.
Does urine sodium concentration after intravenous furosemide administration predict the duration of supplemental oxygen therapy and successful decongestion in dogs with acute congestive heart failure?
Observational (n=51)
No
Does urine sodium concentration after intravenous furosemide administration predict the duration of supplemental oxygen therapy and successful decongestion in dogs with acute congestive heart failure?
Hazard Ratio: 0.88 (95% CI 0.83–0.95)
p-value: p=<0.001
Spot urine sodium concentration after intravenous furosemide can serve as a quantitative and predictive marker for diuretic responsiveness and decongestion efficacy in dogs with acute congestive heart failure.
Supports urine sodium as a potential diuretic response marker in canine acute CHF; hypothesis-generating and requires prospective validation before adoption.
Background Poor natriuresis is a potential marker of diuretic resistance in dogs with acute congestive heart failure (CHF) but little is known about the relationship between urine sodium concentration (uNa) and frequency of successful decongestion. Supplemental O2 is a common treatment in dogs with severe CHF. The time from start to discontinuation of supplemental O2 therapy (DCSO2) typically reflects the time course and ease of decongestion. Hypothesis/Objectives Urine Na concentration after IV administration of furosemide will be correlated with duration of treatment with supplemental O2 (timeO2) and the cumulative frequency of successful DCSO2 during hospitalization. Animals Fifty-one dogs with acute CHF. Methods Retrospective observational single center study. Results Dogs with low uNa had significantly longer mean timeO2 than dogs with high uNa (uNa <87 mmol/L, 24.2 ± 2.6 hours vs uNa ≥87 mmol/L, 16.6 ± 1.7 hours; P = .02). Low uNa was correlated with lower cumulative frequency of DCSO2 (12 hour, 28%; 24 hour, 42%; 36 hour, 73%) compared to high uNa (12 hour, 28%; 24 hour, 88%; 36 hour, 96%; P = .005). History of PO loop diuretics, low serum chloride concentration (sCl), and high PCV were associated with low uNa. Urine Na concentration outperformed other metrics of diuretic responsiveness including weight loss. Conclusions and Clinical Importance Urine Na concentration after IV furosemide predicted timeO2 and cumulative frequency of DCSO2 in dogs with acute CHF, which likely reflects important aspects of diuretic responsiveness. Urine Na can assess diuretic responsiveness and treatment efficacy in dogs with CHF.
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Convey et al. (2023) conducted an observational in Acute congestive heart failure (n=51). Low urine sodium concentration (<87 mmol/L) after IV furosemide vs. High urine sodium concentration (≥87 mmol/L) after IV furosemide was evaluated on Cumulative frequency of discontinuation of supplemental O2 therapy (DCSO2) (SHR 0.88, 95% CI 0.83-0.95, p=<0.001). Every 10 mmol/L decrease in urine sodium concentration after intravenous furosemide reduced the cumulative frequency of successful supplemental oxygen discontinuation by 12% in dogs with acute congestive heart failure.
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