Renal Negative Pressure Treatment as a Novel Therapy for Heart Failure Induced Renal Dysfunction
Congestion is the primary pathophysiologic 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 L vs. R kidney to -30mmHg 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 20-22.5mmHg throughout the experiment. Prior to 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 vs. 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 cardio-renal phenotype.