Abstract: TH-PO1143
Intrarenal Vascular Resistance Modifies the Prognostic Meaning of Renal Stiffness for Kidney Risk After Hematopoietic Stem Cell Transplantation
Session Information
- Onconephrology: Emerging Biomarkers, Preclinical Models, Clinical Challenges, and Therapeutic Strategies
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Lee, Chia Ying, National Taiwan University Hospital Hsin-Chu Branch Hsin-Chu Hospital, Hsinchu, Taiwan
- Tsai, Ping-Chi, National Taiwan University Hospital Hsin-Chu Branch Hsin-Chu Hospital, Hsinchu, Taiwan
- Huang, Jenq-wen, National Taiwan University College of Medicine, Taipei City, Taiwan
- Hung, Kuan-Yu, National Taiwan University Hospital Hsin-Chu Branch Hsin-Chu Hospital, Hsinchu, Taiwan
- Su, Chi-Ting, National Taiwan University College of Medicine, Taipei City, Taiwan
Background
Prediction of kidney dysfunction using traditional markers after hematopoietic stem cell transplantation (HSCT) is challenging. Renal resistive index (RI) reflects intrarenal vascular resistance, whereas shear wave elastography (SWE) measures renal parenchymal stiffness. We investigated whether renal SWE and RI improve prediction of post-HSCT acute kidney injury (AKI) and acute kidney disease (AKD).
Methods
We conducted a retrospective study of adult patients receiving their first HSCT between 2023 and 2026. Patients with prior HSCT, end-stage kidney disease or obstructive nephropathy were excluded. RI was measured in kidney interlobular arteries and Young’s modulus (YM) was derived from SWE measured in the renal parenchyma. Cox proportional hazards regression and restricted cubic spline (RCS) models were used to assess risk factors for AKI and AKD.
Results
Among 269 patients, mean YM was 17.4 kPa, mean RI was 0.67, and median follow-up was 258 days. YM and RI were not independently associated with baseline eGFR, indicating that these imaging parameters were not merely surrogates of conventional kidney markers.
During follow-up, 46.8% of patients developed AKI and 35.3% developed AKD. Baseline sCr was independently associated with both AKI and AKD. The phenotype of higher YM with lower RI was independently associated with lower AKD risk. Kaplan–Meier analysis showed significant differences in AKD-free survival across SWE/RI phenotypes.
RCS analyses stratified by RI category suggested divergent YM–outcome relationships. In patients with lower RI, higher YM was associated with lower AKD risk, consistent with preserved renal reserve. In contrast, in patients with elevated RI, higher YM was associated with higher AKI risk, suggesting that renal stiffness may reflect congestion or fibrosis when accompanied by impaired intrarenal hemodynamics. Addition of SWE/RI phenotypes to sCr modestly improved prediction of AKI and AKD, with c-statistics increasing from 0.595 to 0.611 and from 0.616 to 0.634, respectively.
Conclusion
The prognostic meaning of renal stiffness depends on intrarenal vascular resistance, with higher YM and lower RI reflecting preserved renal reserve, whereas higher YM with higher RI may suggest renal vulnerability. Combined SWE/RI assessment may serve as an add-on imaging biomarker for pre-HSCT kidney risk stratification.