Systemic sclerosis & Raynaud's
Kidney spatial multiomics mapping decodes scleroderma renal crisis
Authors' conclusion
This study advances our understanding of SRC beyond histopathology to the molecular and cellular landscape, providing an omics-driven framework to accelerate therapeutic target discovery in this rare, devastating disease.
Study context
- Population
- Patients with scleroderma renal crisis manifesting histopathologically as thrombotic microangiopathy, patients with lupus nephritis, and normal kidneyskidney biopsy samples analysed by spatial transcriptomics (discovery cohort), validation cohort size not stated
- Participants
- 12 / 6 / 3
- Exposure
- Scleroderma renal crisis (SRC) vs lupus nephritis (LN) vs Normal kidneys
- SRCn = 12
- LNn = 6
- Normal kidneysn = 3
- Outcome
- Histopathology on multiplexed imaging
Methodological detailsspatial transcriptomics (discovery cohort), validated in an expanded cohort by multiplexed imaging
- Spatial transcriptomics (discovery cohort)
- Validated in an expanded cohort by multiplexed imaging
Main finding
As reported in the abstract
- Pathological triad of thrombotic microangiopathy (TMA), immune infiltration, and fibrotic remodelling in SRC kidneys
Observational data: associations, not effects.
Further findings
Shared and distinct pathways, SRC vs LN
- SRC and LN shared activation of the complement cascade, type I interferon signalling, and fibrotic remodelling
- SRC exhibited a distinct vascular-hypoxic axis
Spatial organization
- Disease-specific glomerular niches at the interface between renal parenchymal cells and prominent myeloid immune cells
Molecular signatures across lesion stages
- Multiple pathological pathways already upregulated in mild lesions, with selective enrichment in glomerular TMA and arterial injury, converging on injury and remodelling programmes in chronic lesions
Original publication
Kidney spatial multiomics mapping decodes scleroderma renal crisis. Ann Rheum Dis. Published 26 October 2026. doi:10.
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