Renal ultrasonography predicts worsening renal function in patients with heart failure under tolvaptan administration

Nobukiyo Tanaka; Yoshio Furukawa; Takuya Maeda; Hiroki Ishihara; Kazuhiro Dan; Masanori Teramura; Kei Ichihashi; Tetsuro Takase; Yuya Takahashi; Daichi Tsuzura; Akira Shinoda; Masato Fujii; Hisashi Okada; Fumiharu Itabashi; Tomohiko Teramoto

doi:10.1002/ehf2.14740

Renal ultrasonography predicts worsening renal function in patients with heart failure under tolvaptan administration

ESC Heart Fail. 2024 Mar 12. doi: 10.1002/ehf2.14740. Online ahead of print.

Authors

Affiliation

¹ Department of Cardiovascular Medicine, Ichinomiya Nishi Hospital, 1 Kaimei-hira, Ichinomiya, 494-0001, Japan.

PMID: 38468548
DOI: 10.1002/ehf2.14740

Abstract

Aims: Renal dysfunction in patients with chronic heart failure predicts a poor prognosis. Tolvaptan has a diuretic effect in patients with chronic kidney disease and heart failure without adverse effects on renal function. We aimed to determine the effects of tolvaptan and predictors of worsening renal function in patients with heart failure.

Methods and results: This post hoc analysis was a sub-analysis of a single-centre prospectively randomized trial on the early and short-term tolvaptan administration. We enrolled 201 participants with decompensated heart failure between January 2014 and March 2019 (early group, n = 104; age: 79.0 ± 12.8 years; late group, n = 97; age: 80.3 ± 10.8 years). Renal ultrasonography was performed before and after the administration of tolvaptan. Urine output and oral water intake significantly increased during tolvaptan administration. The difference between water intake and urine volume increased during tolvaptan administration. Changes in body weight, blood pressure, heart rate, and estimated glomerular filtration rate (eGFR) in both groups were comparable. The changes in peak-systolic velocity (PSV), acceleration time (AT) of the renal arteries, and resistance index were comparable. The changes in PSV and end-diastolic velocity (EDV) of the interlobar arteries increased following tolvaptan administration (Δmax PSV: 0.0 ± 14.8 cm/s before tolvaptan vs. 5.6 ± 15.7 cm/s after tolvaptan, P = 0.002; Δmean PSV: 0.4 ± 12.3 vs. 4.9 ± 12.7 cm/s, P = 0.002; Δmax EDV: -0.2 ± 3.5 vs. 1.4 ± 4.0 cm/s, P = 0.001; Δmean EDV: -0.0 ± 3.1 vs. 1.1 ± 3.4 cm/s, P = 0.003). The renal artery AT was negatively correlated with the eGFR (Δmax AT: beta = -0.2354, P = 0.044; Δmean AT: beta = -0.2477, P = 0.035).

Conclusions: Tolvaptan increased the PSV and EDV of the interlobar artery, which may mean tolvaptan increased renal blood flow. The renal artery AT may be a surrogate for worsening renal function.

Keywords: Acceleration time; End-diastolic velocity; Heart failure; Peak-systolic velocity; Renal ultrasonography; Tolvaptan.