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Abstract: PO1499

Renal Negative Pressure Treatment as a Novel Therapy for Cardiorenal Syndrome

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Asher, Jennifer L., Yale University School of Medicine, New Haven, Connecticut, United States
  • Maulion, Christopher D., Yale University School of Medicine, New Haven, Connecticut, United States
  • Gleason, Olyvia, Yale University School of Medicine, New Haven, Connecticut, United States
  • Meegan, Grace, Yale University School of Medicine, New Haven, Connecticut, United States
  • Ivey-Miranda, Juan B., Yale University School of Medicine, New Haven, Connecticut, United States
  • Fleming, James H., Yale University School of Medicine, New Haven, Connecticut, United States
  • Rao, Veena, Yale University School of Medicine, New Haven, Connecticut, United States
  • Testani, Jeffrey M., Yale University School of Medicine, New Haven, Connecticut, United States
Background

Decongestion is the primary therapeutic objective in acute decompensated heart failure (ADHF). However, congestion itself can worsen renal function and limit diuresis. Renal pelvis negative pressure treatment (rNPT) should reduce tubular pressure, allowing improved kidney function and diuresis. We hypothesized that rNPT would improve diuresis, natriuresis & renal function in a congestion predominate heart failure (HF) model.

Methods

Ten ~80 kg pigs underwent thoracotomy with implantation of a pericardial, Swan Ganz, & bilateral ureteral JuxtaFlow® catheters. High dose furosemide (400mg bolus, then 80mg/hr) was administered since HF clinical use of rNPT will be in conjunction with loop diuretics. Each animal served as its own control with randomization of L vs. R kidney to -30 mmHg rNPT or no rNPT. HF was induced via cardiac tamponade (~200 ml of pericardial 6% hydroxyethyl starch) and IV normal saline. Pericardial pressure was maintained at 20-22.5 mmHg.

Results

Prior to HF induction, rNPT increased urine output (UOP) & creatinine clearance (CrCl) compared to the control kidney during furosemide diuresis (p<0.001 for all, Figure). HF induction achieved the target hemodynamic profile with stable cardiac output & elevated filling pressures (Figure). UOP, sodium excretion, & CrCl decreased during HF (p<0.001 for all, Figure), but were higher consistently in rNPT kidney vs. control (p<0.05 for all, Figure). UOP (p=0.38) was the same in rNPT during HF as control prior to HF (Figure).

Conclusion

rNPT increased UO and CrCl, with & without HF. Notably, rNPT rescued the congested cardio-renal phenotype with equivalent diuresis & natriuresis during HF with rNPT compared to the non-HF period without rNPT.

Funding

  • Commercial Support