Study rationale: Viral infections, such as CMV, are a risk factor for TA-TMA (transplantation-associated TMA). Viral infections increase interferon (IFN) levels and high IFN levels are associated with thrombotic microangiopathy (TMA). IFNs contribute to TMA pathogenesis through suppression of VEGF transcription. Disruption of the VEGF signalling pathway in the kidney is associated with TMA. Primary objective: To determine the association between IFN levels and the development of biopsy-proven or clinically diagnosed TA-TMA. Secondary objective(s): To explore the relationship between complement activation and IFN in patients with TMA. To explore if high IFN levels are associated with low VEGF-A levels. Endpoint: The study aims to investigate the role of IFN in the pathogenesis of secondary thrombotic microangiopathy (focusing on patients with TA-TMA). It seeks to clarify whether IFN, next to complement dysregulation, is a driver of endothelial damage and TMA in these patients.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
TREATMENT
Masking
NONE
Enrollment
40
blood sampling at designated time points
urine collection at designated time points
Interferon signature
6-gene interferon signature
Time frame: Time point 1: baseline Time point 2: up to week 52
VEGF-A
VEGF-A level
Time frame: Time point 1: baseline Time point 2: up to week 52
Complement analysis (serum)
CH50, AP50, C3, C3d, C4 and C5b-9 at timepoint 1 and C5b-9 at time point 2
Time frame: Time point 1: baseline Time point 2: up to week 52
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