Normoalbuminuric and albuminuric diabetic kidney disease exhibit divergent renal proteomic characteristics: implications for management
Authors' conclusion
Oxidative stress and mitochondrial dysfunction are involved in the progression of NADKD, lesions predominantly located in the tubulointerstitium. The complement pathway participates in the pathogenesis and progression of albuminuric DKD (ADKD).
Study context
- Population
- Biopsy-proven diabetic kidney disease (DKD) patients; proteomics in 5 patients per DKD subgroup and 5 controls295 biopsy-proven DKD
- Participants
- 25 / 26 / 244 / 5
- Comparison
- Normoalbuminuric vs microalbuminuric vs macroalbuminuric DKD vs controls
- Normoalbuminuricn = 25
- Microalbuminuricn = 26
- Macroalbuminuricn = 244
- Controln = 5reference
- Outcome
- Renal glomerular and proximal tubule proteomics
Methodological detailslaser microdissection with mass spectrometry (LMD/MS) proteomics, biopsy-proven
- Laser microdissection with mass spectrometry (LMD/MS) proteomics
- Biopsy-proven
Main finding
As reported in the abstract
- Glomeruli: oxidative stress and metabolic pathways (UQCRC1) upregulated in normoalbuminuric diabetic kidney disease (NADKD)
- Glomeruli: complement and coagulation cascades (C3, C5, C6, C9, CFH, CFHR1) significantly upregulated in microalbuminuric and macroalbuminuric DKD
- Proximal tubule: oxidative phosphorylation-related proteins (SDHA, CYCS, UQCRQ) upregulated in NADKD
- Proximal tubule: collagen I related proteins (COL1A1, COL1A2) significantly upregulated
Original publication
Normoalbuminuric and albuminuric diabetic kidney disease exhibit divergent renal proteomic characteristics: implications for management. Diabetes Res Clin Pract. Published 26 August 2026. doi:10.
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