Abstract: FR-PO0931
Raynaud Phenomenon as a Manifestation of Sorafenib-Induced Thrombotic Microangiopathy: A Case Report
Session Information
- Glomerular Case Reports: Lupus, FSGS, Complement, and More
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Alagla, Nahlah Abdullah, KFSHRC, Riyadh, Riyadh, Saudi Arabia
- Alqarni, Khaled Abdullah, KFSHRC, Riyadh, Riyadh, Saudi Arabia
Introduction
Thrombotic microangiopathy (TMA) is a rare complication of stem cell transplantation, often linked to TKIs like Sorafenib. While typically renal-limited, systemic signs may be underrecognized. We report a case of Sorafenib-associated TMA with refractory Raynaud phenomenon that improved with Eculizumab, suggesting Raynaud may represent a systemic TMA manifestation and highlighting complement inhibition as a potential therapy.
Case Description
A 42-year-old man with diabetes and hypertension underwent allogeneic PBSCT for FLT3-positive AML in January 2023, receiving TBI, chemotherapy, and Sorafenib (200 mg BID from March 2023). In July, he developed erythematous follicular papules; biopsy confirmed chronic GVHD, which responded to steroids, Ruxolitinib, and phototherapy.
By August 2024, he presented with 2 months of leg edema and subnephrotic proteinuria. BP was 160/70. Labs: Hb 109, Plt 128, Cr 111, Alb 33, urine PCR 273 mg/mmol. Workup: normal complement, HbA1c 5.3, negative ANCA, anti-PLA2R, and APS; kappa/lambda ratio normal. Renal biopsy showed chronic TMA with glomerular double contours, arteriolar hyalinosis, and severe IFTA; no immune deposits. ADAMTS13 was preserved; no schistocytes or hemolysis. Managed conservatively with RAAS blockade and SGLT2i, with improving proteinuria (PCR 131, then 57 mg/mmol).
In October, he developed cold-induced fingertip pain, bluish discoloration, and ulcers—diagnosed as Raynaud phenomenon, without scleroderma features. ANA nucleolar 1:1280, dsDNA 254, normal complements. CBC: macrocytic anemia, Plt 115, stable Cr. Adalat was started. Creatinine rose to 160 with flank pain; Doppler negative. Anticardiolipin IgG transiently elevated; APS unlikely.
Sorafenib was stopped in November due to worsening renal function (Cr 170) and Raynaud symptoms. Eculizumab was initiated in December (900 mg weekly ×4, then 1200 mg biweekly). Raynaud resolved within weeks. By January 2025, renal function stabilized, proteinuria improved, and vasospastic symptoms resolved.
Discussion
The findings supported that Raynaud phenomenon in this patient likely represented a systemic manifestation of sorafinib-induced TMA. The resolution of symptoms with Eculizumab highlights the potential role of complement inhibition in such cases and underscores the importance of recognizing Raynaud as a possible complication of TKI.