Abstract: TH-PO038
Porto-Pulmonary Hypertension and Decongestion in Norepinephrine-Treated Hepatorenal Syndrome Type 1
Session Information
- AKI: Biomarkers, Risk Factors, Treatments, Outcomes
November 03, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical‚ Outcomes‚ and Trials
Authors
- Wickman, Terrance Joseph, Ochsner Medical Center, New Orleans, Louisiana, United States
- Yousuf, Adil, Ochsner Medical Center, New Orleans, Louisiana, United States
- Mohamed, Muner, Ochsner Medical Center, New Orleans, Louisiana, United States
- Velez, Juan Carlos Q., Ochsner Medical Center, New Orleans, Louisiana, United States
Group or Team Name
- Ochsner Nephrology
Background
Porto-pulmonary hypertension (PoPHTN) is a complication of cirrhosis that can lead to venous congestion. Contrary to traditional dogma, we previously reported that in patients with acute kidney injury (AKI) due to hepatorenal syndrome type 1 (HRS-1), addition of IV furosemide (FURO) to vasoconstrictor therapy with norepinephrine (NE) results in enhanced diuresis without worsening the course of AKI. We aimed to examine the relationship between PoPHTN and AKI course and response to FURO in NE-treated HRS-1.
Methods
We searched records of patients with HRS-1 treated with NE as a vasoconstrictor who during the course of AKI underwent echocardiography with an estimate of pulmonary artery systolic pressure (PASP) over a 3-year period. PoPHTN was defined as echo-based PASP > 35 mmHg and absence of reduced left ventricular ejection fraction (rLVEF) or left ventricular diastolic dysfunction (LVDD). Outcomes examined were association of PoPHTN with need for dialysis (AKI-RRT) and influence of PoPHTN on the correlation between NE-induced MAP rise and FURO-enhanced diuresis.
Results
Among 39 patients with HRS-1 treated with NE, 26 had echo-based PASP, 9 (35%) had PoPHTN (5 confirmed by right heart catheterization); 4 had reduced right ventricular systolic function, 1 rLVEF and 1 LVDD. Five of 9 (55%) of those with PoPHTN reached AKI-RRT compared to 4 of 17 (24%) without PoPHTN (p=0.11). Of the 26 patients, 19 received FURO [median 160 (80-240) mg q 12 (8-24) hrs] for decongestion. Urine output (UOP) response correlated with NE-induced MAP rise (r=0.62, p=0.004). The correlation between UOP and MAP rise among those with PoPHTN (n=9, median PASP 45, r=0.84, p=0.009) was stronger than that observed in those without PoPHTN (n=10, median PASP 27, r=0.53, p=0.09). Furthermore, PoPHTN with concomitant estimated central venous pressure (CVP) 8-15 mmHg (n=4) was associated with greater UOP response to MAP rise compared to absence of PoPHTN with CVP 3 mmHg (n=4) (252 vs 101 ml/mmHg, p=0.0008).
Conclusion
PoPHTN may be present in 1/3 of patients with HRS-1 and it is associated with greater dependence of the UOP response to FURO to the NE-induced MAP rise. Presence of PoPHTN should be assessed to guide decongestive strategies in the management of AKI due to HRS-1.