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Abstract: SA-PO780

Alterations in Kidney Venous Flow in the Prognosis of Heart Failure

Session Information

  • Hypertension and CVD: Mechanisms
    November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Hypertension and CVD

  • 1503 Hypertension and CVD: Mechanisms

Authors

  • Husain-Syed, Faeq, University of Virginia, Charlottesville, Virginia, United States
  • Singam, Sharma, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Viehman, Jason K., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Schulte, Philip, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Bauer, Pascall, Universitatsklinikum Giessen und Marburg GmbH, Giessen, Hessen, Germany
  • Tello, Khodr, Universitatsklinikum Giessen und Marburg GmbH, Giessen, Hessen, Germany
  • Richter, Manuel, Universitatsklinikum Giessen und Marburg GmbH, Giessen, Hessen, Germany
  • Seeger, Werner, Universitatsklinikum Giessen und Marburg GmbH, Giessen, Hessen, Germany
  • Gall, Henning, Universitatsklinikum Giessen und Marburg GmbH, Giessen, Hessen, Germany
  • Ghofrani, Ardeschir, Universitatsklinikum Giessen und Marburg GmbH, Giessen, Hessen, Germany
  • Birk, Horst-Walter, Universitatsklinikum Giessen und Marburg GmbH, Giessen, Hessen, Germany
  • Kashani, Kianoush, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Ronco, Claudio, Azienda Ospedale Universita Padova, Padova, Veneto, Italy
Background

Doppler-derived kidney venous flow (KVF) has gained interest as a potential surrogate marker of kidney congestion and adverse outcomes in heart failure (HF). The clinical importance of changes in KVC from baseline remains unclear.

Methods

216 inpatients with HF comprising the whole left ventricular ejection fraction spectrum and diuretic-resistant volume overload were enrolled and underwent spectral Doppler at baseline and after one month. 4 KVF patterns (i.e., continuous, pulsatile, biphasic, and monophasic venous flows) and the kidney venous stasis index (KVSI) were defined. In addition, echocardiography, intra-abdominal pressure (only baseline), kidney function, hormones, and hydration status were assessed on the day of kidney Doppler ultrasonography. We evaluated HF-related morbidity using the cause-specific Cox proportional hazard model for the composite outcome of HF progression (hospitalization for worsening HF, outpatient HF decompensation) and all-cause mortality for 18-months post-discharge.

Results

During follow-up, the morbidity/mortality outcome occurred in 126 patients and was independently predicted by baseline KVSI (per 0.1 increase: HR 1.18 [95% CI 1.03–1.35; p=0.020]) and KVF patterns (per one pattern increase: HR 1.42 [95% CI 1.04–1.94; p=0.026]), respectively. Both an increase of 0.1 in the change from Doppler 1 to 2 KVSI and a single increase in the individual KVF pattern in the change from Doppler 1 to 2 were associated with higher risk of the composite outcome (HR 2.99 [95% CI 2.08–4.32; p<0.0001] and HR 6.73 [95% CI 3.27–13.86; p<0.0001], respectively).

Conclusion

Serial assessment of KVF provides additional prognostic information on worsening HF and death risk-stratification. Changes in KVF may provide a basis for enhanced clinical making in patients with HF.