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Updated: May 28, 2026

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
Structural damage in diabetic nephropathy is associated with TNF-α system activity
José Manuel Fernández-Real1, Joan Vendrell, Isabel García
1Department of Diabetes, Endocrinology and Nutrition, and CIBEROBN Fisiopatología de la Obesidad y Nutrición, University Hospital of Girona Dr. Josep Trueta, Carretera de França s/n, 17007, Girona, Spain. jmfernandezreal.girona.ics@gencat.cat
Tumour necrosis factor-alpha (TNF-α) system activity, particularly plasma sTNFR1, is linked to kidney damage in type 2 diabetes patients. This finding suggests potential therapeutic targets for diabetic nephropathy.
Area of Science:
- Nephrology
- Immunology
- Endocrinology
Background:
- Tumour necrosis factor-alpha (TNF-α) plays a role in diabetic kidney disease in animal models.
- Antibodies targeting TNF-α have shown promise in improving kidney lesions.
Purpose of the Study:
- To investigate the association between TNF-α system activity and renal histological changes in patients with type 2 diabetes.
Main Methods:
- Prospective, cross-sectional study of 22 type 2 diabetes patients.
- Measured plasma concentrations of soluble TNF-α receptors 1 and 2 (sTNFR1, sTNFR2) as surrogates of TNF-α activity.
- Assessed glomerular filtration rate (GFR), albumin excretion rate (AER), and performed renal biopsies.
Main Results:
- Albumin excretion rate (AER) did not directly correlate with histological damage (mesangial expansion, interstitial fraction).
- After adjusting for GFR, AER showed a significant correlation with sTNFR1.
- sTNFR1 levels significantly correlated with age, mesangial expansion, and interstitial fraction, independent of other clinical factors.
Conclusions:
- The TNF-α system, specifically plasma sTNFR1, is associated with structural kidney damage in type 2 diabetes.
- sTNFR1 may serve as a biomarker for kidney damage progression in diabetic nephropathy.
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