Abstract
Congestion is the primary pathophysiological lesion in most heart failure (HF) hospitalizations. Renal congestion increases renal tubular pressure, reducing glomerular filtration rate (GFR) and diuresis. Because each nephron is a fluid-filled column, renal negative pressure therapy (rNPT) applied to the urinary collecting system should reduce tubular pressure, potentially improving kidney function. We evaluated the renal response to rNPT in congestive HF. Ten anesthetized ∼80-kg pigs underwent instrumentation with bilateral renal pelvic JuxtaFlow catheters. GFR was determined by iothalamate clearance (mGFR) and renal plasma flow (RPF) by para-aminohippurate clearance. Each animal served as its own control with randomization of left versus right kidney to -30 mmHg rNPT or no rNPT. mGFR and RPF were measured simultaneously from the rNPT and no rNPT kidney. Congestive HF was induced via cardiac tamponade maintaining central venous pressure at 20-22.5 mmHg throughout the experiment. Before HF induction, rNPT increased natriuresis, diuresis, and mGFR compared with the control kidney (P < 0.001 for all). Natriuresis, diuresis, and mGFR decreased following HF (P < 0.001 for all) but were higher in rNPT kidney versus control (P < 0.001 for all). RPF decreased during HF (P < 0.001) without significant differences between rNPT treatments. During HF, the rNPT kidney had similar diuresis and natriuresis (P > 0.5 for both) and higher fractional excretion of sodium (P = 0.001) compared with the non-rNPT kidney in the no HF period. In conclusion, rNPT resulted in significantly increased diuresis, natriuresis, and mGFR, with or without experimental HF. rNPT improved key renal parameters of the congested cardiorenal phenotype.
Highlights
Affecting over 1 million Americans annually, acute decompensated heart failure (ADHF) is the most common hospital discharge diagnosis among Medicare beneficiaries and accounts for more than half of all heart failure (HF)-related expenditures [1,2,3]
The increased natriuresis with renal negative pressure therapy (rNPT) was not solely driven by increased sodium filtration, as the FENa was higher with rNPT (15.9 ± 3.3% vs. 12.0 ± 4.2%, P < 0.001)
The benefit appeared to be of potential clinical significance since urine output and sodium excretion during experimental HF with rNPT were similar to the non-rNPT kidney during the no HF period
Summary
Affecting over 1 million Americans annually, acute decompensated heart failure (ADHF) is the most common hospital discharge diagnosis among Medicare beneficiaries and accounts for more than half of all heart failure (HF)-related expenditures [1,2,3]. Since the kidneys are encapsulated and can only minimally expand, congestion increases intrarenal and tubular pressures with an associated worsening of GFR and sodium avidity [10,11,12,13,14,15]. Renal venous congestion diminishes diuretic response, creating a vicious cycle where congestion impedes treatment response and intensifies renal sodium avidity [13, 14, 16]. Loop diuretic therapy exacerbates aberrations in intratubular pressure, potentially intensifying this process [17]. Strategies to reduce intratubular pressure and arrest this positive-feedback cycle warrant investigation.
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