Highlights
- •Patients with heart failure exhibit lower perfusion of the kidney compared to patients without heart failure.
- •Patients with heart failure have larger transrenal renin-angiotensin-aldosterone system marker gradients compared to controls without heart failure.
- •Such renal origin of neurohormonal activation may be associated with renal vasoconstriction and lower perfusion of the kidney in patients with heart failure.
ABSTRACT
Objective
Understanding cardiorenal pathophysiology in heart failure (HF) is of clinical importance.
We sought to characterize the renal hemodynamic function and the transrenal gradient
of the renin-angiotensin-aldosterone system (RAAS) markers in patients with HF and
in controls without HF.
Methods
In this post hoc analysis, the glomerular filtration rate (GFRinulin), effective renal plasma flow (ERPFPAH) and transrenal gradients (arterial-renal vein) of angiotensin converting enzyme
(ACE), aldosterone, and plasma renin activity (PRA) were measured in 47 patients with
HF and in 24 controls. Gomez equations were used to derive afferent (RA) and efferent (RE) arteriolar resistances. Transrenal RAAS gradients were also collected in patients
treated with intravenous dobutamine (HF, n = 11; non-HF, n = 11) or nitroprusside
(HF, n = 18; non-HF, n = 5).
Results
The concentrations of PRA, aldosterone and ACE were higher in the renal vein vs the
artery in patients with HF vs patients without HF (P < 0.01). In patients with HF, a greater ACE gradient was associated with greater
renal vascular resistance (r = 0.42; P 0.007) and greater arteriolar resistances (RA: r = 0.39; P = 0.012; RE: r = 0.48; P = 0.002). Similarly, a greater aldosterone gradient was associated with lower GFR
(r = –0.51; P = 0.0007) and renal blood flow (RBF), r = –0.32; P = 0.042) whereas greater PRA gradient with lower ERPF (r = –0.33; P = 0.040), GFR (r = –0.36; P = 0.024), and RBF (r = –0.33; P = 0.036). Dobutamine and nitroprusside treatment decreased the transrenal gradient
of ACE (P = 0.012, P < 0.0001, respectively), aldosterone (P = 0.005, P = 0.030) and PRA (P = 0.014, P = 0.002) in patients with HF only.
Conclusions
A larger transrenal RAAS marker gradient in patients with HF suggests a renal origin
for neurohormonal activation associated with a vasoconstrictive renal profile.
Key Words
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Article info
Publication history
Published online: September 03, 2021
Accepted:
August 17,
2021
Received in revised form:
July 19,
2021
Received:
April 29,
2021
Footnotes
Toronto and Ottawa, Ontario, Canada; New Haven, Connecticut; and Sao Paolo, Brazil
Identification
Copyright
© 2021 Elsevier Inc. All rights reserved.
