Alterations in Doppler-derived renal venous stasis index during recompensation of right heart failure and fluid overload in a patient with pulmonary hypertension.

Renal congestion is becoming recognized as a potential contributor to cardiorenal syndromes. Adequate control of congestion with simultaneous preservation of renal function has been proposed as a central goal of the management of heart failure. We report our care of a 48-year-old woman suffering from right heart failure and massive fluid overload due to severe pulmonary hypertension secondary to a combination of left-heart disease and status after recurrent pulmonary embolisms. Alterations in Doppler-derived intrarenal venous flow patterns and a novel renal venous stasis index were used to evaluate improvement in renal venous congestion during recompensation. Due to refractory congestion despite optimal medical treatment and continuous veno-venous hemodialysis, a peritoneal dialysis catheter was placed to relieve the massive ascites. The paracentesis of ascites led to a significant loss of weight, normalization of hydration status with subsequent termination of continuous veno-venous hemodialysis, and a significant improvement in clinical and echocardiographic parameters. Renal Doppler ultrasonography showed continuous improvement in intrarenal venous flow patterns and the renal venous stasis index indicative of effective decongestion up to a normal intrarenal venous flow pattern and renal venous stasis index. Furthermore, residual renal function increased during follow-up. This case demonstrates the feasibility of renal Doppler ultrasonography as a simple, non-invasive, and integrative measure of renal congestion. The renal venous stasis index and intrarenal venous flow patterns may be useful to evaluate the treatment response and to guide therapy in patients with right heart failure.
Competing Interests: Dr. Seeger discloses personal fees for consulting from Bayer Pharma AG, Liquidia Technologies, Inc, and United Therapeutics Corporation outside the submitted work. Dr. Gall discloses personal fees and non-financial support from Actelion, AstraZeneca, Bayer, BMS, GlaxoSmithKline, Janssen Cilag, Lilly, MSD, Novartis, Pfizer, and United Therapeutics/OMT outside the submitted work.Dr. Ghofrani discloses grants from German Research Foundation during the work, and personal fees from Actelion, Bayer, GSK, Novartis, Pfizer, Bellerophon Pulse Technologies, and MSD Merck Sharpe & Dohme outside the submitted work. None of the other authors declare a conflict of interest.
(© 2019 Husain-Syed et al. Published by IMR press.)