Abstract: FR-PO140

Achieved Mean Arterial Pressure Target and Renal Recovery during Treatment of Hepatorenal AKI

Session Information

Category: Acute Kidney Injury

  • 003 AKI: Clinical and Translational

Authors

  • Velez, Juan Carlos Q., Ochsner Clinic Foundation, New Orleans, Louisiana, United States
  • Rivera de Rosales, Ana Belen, Ochsner Clinic Foundation, New Orleans, Louisiana, United States
  • Hernandez- Montalvo, Edgar, Ochsner Clinic Foundation, New Orleans, Louisiana, United States
  • Leblanc, Bronwyn, Ochsner Clinic Foundation, New Orleans, Louisiana, United States
  • Ledoux, Jason R, Ochsner Clinic Foundation, New Orleans, Louisiana, United States
  • Lukitsch, Ivo, Ochsner Clinic Foundation, New Orleans, Louisiana, United States
Background


We previously reported that a rise in mean arterial pressure (MAP) during treatment of hepatorenal (HR) acute kidney injury (AKI) with vasoconstrictors is associated with improvement in kidney function. However, it remains unclear whether the treatment target should be a specific absolute MAP value or a defined increment in MAP respect to baseline.

Methods


Records from hospitalized adult patients with HR-AKI treated with vasoconstrictors without shock were reviewed. We selected those who achieved ≥ 5-mmHg rise in MAP within 48 hours. The relationship between the mean MAP achieved during the first 72 hours of therapy and the change in kidney function at the end of therapy as determined by serum creatinine (sCr) was examined by analyses of variance for trend and multiple comparisons.

Results


Ninety-two patients with HR-AKI treated for up to 3-7 days with either midodrine/octreotide (M/O, n=73) or norepinephrine (NE, n=19) were identified. Forty-three (47%) of the patients (mean age 52 years, 44% women, mean sCr 3.7 ± 1.3 mg/dL and MELD 33.5) achieved ≥ 5 mmHg rise in MAP by 48 hours [24 (33%) with M/O, 18 (95%) with NE]. When analyzed based on tertiles of absolute value of achieved MAP (65-74, 75-84, ≥ 85 mmHg), there was a significant trend for greater reduction in sCr with higher achieved MAP (p=0.002). Furthermore, those who achieved a MAP of ≥ 85 mmHg had a greater reduction in sCr [-1.76 ± 0.6 mg/dL] compared to those who reached a MAP of 65-74 or 75-84 mmHg [-0.03 ± 0.5 mg/dL (p=0.019) and -0.25 ± 0.6 mg/dL (p=0.02), respectively]. When analyzed based on tertiles of magnitude of MAP increment from baseline (5-9, 10-14, ≥ 15 mmHg), there was a significant trend for greater reduction in sCr with greater rise in MAP (p=0.005). Moreover, those who achieved a MAP increase ≥ 15 mmHg had a greater reduction in sCr [-1.95 ± 0.5 mg/dL] compared to those with either a 5-9 or 10-14 mmHg increment in MAP from baseline [+0.17 ± 0.4 mg/dL (p=0.0004) and -0.58 ± 0.5 mg/dL (p=0.04), respectively].

Conclusion


Achievement of either a target MAP ≥ 85 mmHg or an increment in MAP ≥ 15 mmHg from baseline within the first 3 days of vasoconstrictor therapy is associated with greater reduction in sCr in HR-AKI. These data support the notion of a shift in the renal autoregulatory curve in HR-AKI.