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Updated: Feb 11, 2026

Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease
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Complement activation in patients with diabetic nephropathy.

X-Q Li1, D-Y Chang1, M Chen1

  • 1Renal Division, Department of Medicine, Peking University First Hospital, Peking University Institute of Nephrology, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, No 8, Xishiku Street, Xicheng District, 100034 Beijing, China.

Diabetes & Metabolism
|May 7, 2018
PubMed
Summary
This summary is machine-generated.

The complement system is activated in diabetic nephropathy (DN), with lectin and alternative pathway activation linked to kidney damage. Complement component levels in plasma and urine correlate with DN severity and clinical markers.

Keywords:
ComplementComplement activation pathwayDiabetic nephropathy

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Area of Science:

  • Nephrology
  • Immunology
  • Complement System Biology

Background:

  • The complement system plays a role in diabetic nephropathy (DN) pathogenesis.
  • Specific complement activation pathways and their clinical relevance in DN are not fully understood.

Purpose of the Study:

  • To investigate complement component levels in plasma and urine of DN patients.
  • To correlate these levels with clinicopathological parameters in DN.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) was used to measure seven complement components (C1q, MBL, Bb, C4d, C3a, C5a, sC5b-9).
  • Plasma and urine samples from 68 biopsy-proven DN patients were analyzed.
  • Associations between complement levels and clinicopathological parameters were examined.

Main Results:

  • Plasma and urinary levels of most complement components were elevated in DN patients compared to controls.
  • Urinary C3a, C5a, and sC5b-9 correlated with markers of kidney function and damage (serum creatinine, urinary protein, eGFR).
  • Urinary MBL, Bb, C4d, and C3a correlated with urinary protein and glomerular lesion classification.

Conclusions:

  • The complement system is activated in DN.
  • Activation of the lectin and alternative complement pathways is associated with renal damage in DN.