Abstract: FR-PO1239
Nonrenal Elevation of Cystatin C Mimicking AKI After Allogeneic Stem-Cell Transplantation
Session Information
- Onconephrology: Diagnostic Dilemmas, Therapy-Related Toxicities, and Clinical Cases
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Mahmoud, Saad Abdulrahim Talal, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Jazieh, Hadeel, Blida University, Blida, Algeria
- Almashayekh, Abedalrahman, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Holthoff, Joseph H., University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
Introduction
Cystatin C-based eGFR is increasingly used to assess kidney function, yet non-GFR determinants such as glucocorticoids, inflammation, obesity, and malignancy can falsely elevate cystatin C. We report a critically ill allo-SCT recipient with cystatin C eGFR of 13 mL/min despite preserved kidney function, confirmed by autopsy.
Case Description
A 27-year-old female (BMI 35) with Ph-negative B-ALL underwent matched unrelated donor allo-SCT (Day 0: Feb 6, 2026) after Flu/Cy/fTBI conditioning. Post-transplant course included CMV viremia, suspected aspergillosis, and engraftment syndrome. On Day +22, she developed acute hypoxic respiratory failure requiring intubation, with CT concerning for pulmonary GVHD. She received methylprednisolone, ruxolitinib, tocilizumab, anakinra, and etanercept for refractory cytokine storm.
Nephrology was consulted for non-oliguric AKI with striking discordance among kidney function estimates: creatinine 1.0 mg/dL (CKD-EPI eGFR 79), cystatin C 4.15 mg/L (eGFR 13), combined CKD-EPI eGFR 27, and 24-hr CrCl 41 mL/min, despite adequate urine output (>100 mL/hr).
Multiple non-GFR determinants of cystatin C were present: high-dose glucocorticoids, profound inflammation, obesity, and high cell turnover, supported by concurrently rising LDH (510 IU/L) and ferritin (6,970 ng/mL) paralleling cystatin C elevation while creatinine remained stable. Creatinine-based eGFR was also unreliable due to volume overload and critical illness–associated muscle wasting.
The cystatin C elevation was attributed to non-renal confounders rather than true GFR impairment. The patient expired from complications of acute leukemia. Autopsy revealed no GVHD and no intrinsic kidney pathology, only post-mortem autolytic changes, confirming the discordance was not attributable to kidney disease.
Discussion
Cystatin C-based eGFR can profoundly underestimate kidney function in post–allo-SCT patients when glucocorticoids, inflammation, obesity, and high cell turnover coexist. Autopsy confirmed no intrinsic kidney pathology.
Neither creatinine nor cystatin C-based eGFR was reliable in this critically ill patient; the combined CKD-EPI equation was also misleading due to disproportionate cystatin C elevation.
Clinicians should integrate multiple GFR estimation methods, including measured CrCl, and recognize non-GFR determinants of both biomarkers when assessing kidney function in post-transplant critically ill patients.