2026-07-01 | Proteomics and human microchips identify Thrombospondin-1 as a potential biomarker for calciphylaxis stem cell therapy.
Calciphylaxis (calcific uremic arteriolopathy, CUA) is a rare, fatal disorder primarily affecting chronic kidney disease patients, characterized by microvascular calcification, thrombosis, and skin necrosis. In a discovery cohort (3 CUA, 10 uremic), plasma proteomics identified Thrombospondin-1 (THBS1) as the top upregulated hub in CUA, significantly reduced after human amnion-derived mesenchymal stem cell (hAMSC) therapy, alongside latent TGF-β binding protein 1, both linked to coagulation and wound healing. In vitro proteomics indicated that THBS1/TGF-β1 blockade impaired CUA serum-induced endothelial adhesion and coagulation. ELISA in combined discovery and validation cohorts (8 CUA, 20 uremic) confirmed this reduction post-treatment (6 patients), independent of systemic inflammation. Multiplex immunofluorescence revealed THBS1 and CD47 co-localized with CD31 and integrin β3 in injured microvessels. A human microvascular chip showed that THBS1 inhibition or hAMSC-conditioned medium alleviates injury. These findings implicate THBS1 as a key factor and potential biomarker in calciphylaxis, suggesting hAMSC therapy as a promising mechanism-based approach.
Open article ↗
2026-05-26 | Proteomics and Microvascular Chip Identify Blood Biomarker Candidates in Calciphylaxis Stem Cell Therapy. Hu et al.
This de-identified dataset encompasses clinical, laboratory, and proteomic data from patients with calciphylaxis, a rare and high-mortality condition also known as calcific uremic arteriolopathy (CUA), who were treated with human amnion-derived mesenchymal stem cells (hAMSCs). This disorder predominantly arises in the context of chronic kidney disease. The dataset further includes information from uremic control subjects, comprising demographics, comorbidities, dialysis history, and medication records across discovery (3 CUA cases and 10 uremic controls) and independent validation (8 CUA cases and 20 uremic controls) cohorts. The data comprise: 1. Proteomics: Static and dynamic proteomic profiles from the discovery cohort, deposited in iProX, identified Thrombospondin-1 (THBS1) as a leading upregulated hub associated with coagulation and wound healing. In vitro proteomic analyses further demonstrated that blockade of the THBS1/TGF-β1 axis attenuates endothelial dysfunction induced by CUA serum (data deposited in iProX). 2. Potential Biomarker Validation (ELISA): Quantitative validation of elevated plasma THBS1 and TGF-β1 levels was conducted using ELISA in both discovery and validation cohorts, confirming a significant reduction three days post-hAMSC therapy. However, in Patient 1 from the discovery cohort, plasma THBS1 and TGF-β1 levels remained low throughout the 15-month follow-up period but increased as the frequency of hAMSC treatment decreased. 3. Microvascular Chip Analysis: Quantitative assessment of integrated density and cell viability using a human microvascular chip to analyze calciphylaxis-associated vascular injury and evaluate the therapeutic effects of hAMSCs in vitro. 4. Clinical Outcomes: Longitudinal evaluations of wound healing utilizing the Bates-Jensen Wound Assessment Tool for CUA (BWAT-CUA), pain measured by the Visual Analog Scale (VAS), and systemic inflammation assessed via high-sensitivity C-reactive protein (hs-CRP). These integrated findings implicate THBS1 as a potential biomarker and therapeutic target, supporting hAMSCs as a mechanism-based treatment for calciphylaxis. All data are anonymized to ensure patient privacy.
Open article ↗
2026-04-27 | Early Calciphylaxis Mimicking Infection in a Patient With End-Stage Renal Disease and Sarcoidosis: A Diagnostic and Wound Management Challenge.
Calciphylaxis is a rare, life-threatening disorder primarily affecting patients with end-stage renal disease (ESRD) on dialysis. Early lesions can mimic infection, leading to delays in diagnosis and wound-directed care. We describe an atypical early presentation of calciphylaxis in a patient with ESRD and sarcoidosis, initially misdiagnosed as cellulitis. Despite early sodium thiosulfate therapy and metabolic control, the patient developed progressive necrotic wounds. This case underscores that calciphylaxis can progress despite controlled mineral metabolism and standard therapy, particularly when potentiated by conditions like sarcoidosis. Early dermatologic evaluation and a high index of suspicion are critical to avoid misdiagnosis.
Open article ↗
