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• W2800224647 abstract "I thoroughly enjoyed reading the per-protocol analysis of the Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trial performed by Grodin et al.,1 which concluded that ultrafiltration (UF) was associated with more fluid removal compared to diuretic therapy. I commend the authors for undertaking such a rigorous analysis and would like to comment on two important findings in this study. Firstly, the authors rightly point out that the metabolic alkalosis seen with diuretic use is likely because of ‘chloride depletion’ and not ‘volume contraction’ as shown by the fact that patients treated with UF had significantly lower serum bicarbonate levels than those treated with diuretics despite higher volume removal by the former. In the collecting duct of the nephron, a luminal Cl/HCO3- exchanger called pendrin plays a key role in the generation of chloride-depletion metabolic alkalosis (CDA) by retaining more bicarbonate in the setting of chloride loss induced by diuretic therapy. On the other hand, volume depletion alone does not produce the same effect. For example, in a study, diuretic-induced CDA was completely reversed in normal human subjects by oral potassium chloride supplementation despite the presence of negative Na+ balance and plasma volume contraction.2 As there is mounting evidence that hypochloraemia is an independent risk factor for mortality in patients with heart failure,3 this interesting finding merits further investigation in future studies. It would be helpful to measure serial and simultaneous serum and urine chloride levels in patients undergoing UF and diuretic therapy to better understand and interpret CDA in clinical context. Secondly, the findings of higher serum creatinine and renin and lower sodium levels in the UF arm are likely secondary to the activation of renin–angiotensin–aldosterone system and anti-diuretic hormone in the setting of haemodynamic fluctuations from rapid fluid removal ‘relative’ to plasma refill rate in these patients. Moreover, angiotensin II-induced stimulation of thirst mechanism4 could lead to more free water ingestion by the patients, contributing to hyponatraemia. Future studies should consider incorporating more objective techniques such as bioimpedance, bedside ultrasonography (thoracic and inferior vena cava), continuous non-invasive haematocrit monitoring in addition to physical examination to determine the amount of fluid to be removed in patients undergoing UF therapy. This would help us determine the particular subset of patients who would most benefit from this expensive and labour-intensive therapy." @default.
• W2800224647 created "2018-05-17" @default.
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• W2800224647 date "2018-05-03" @default.
• W2800224647 modified "2023-10-18" @default.
• W2800224647 title "Metabolic abnormalities in heart failure patients treated with ultrafiltration versus diuretics" @default.
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• W2800224647 doi "https://doi.org/10.1002/ejhf.1207" @default.
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