Related Experiment Video

Updated: Jan 9, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

843

Nicotinamide Attenuates Complement and Coagulation Pathways and Resultant Renal Fibrosis

Saori Kin1, Yuji Oe1, Taku Obara2

  • 1Department of Nephrology, Graduate School of Medicine, Tohoku University, Sendai, Japan.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 1, 2025
PubMed

Insights

Chronic kidney disease (CKD) involves excessive coagulation and complement activity. Nicotinamide (NAM) effectively modulated these pathways, suggesting therapeutic potential for kidney disease.

Area of Science:

  • Nephrology
  • Immunology
  • Hematology

Background:

  • Coagulation and complement pathways interact, influencing inflammation and thrombosis.
  • Their specific roles in chronic kidney disease (CKD) pathogenesis are not fully understood.

Purpose of the Study:

  • To investigate the association between coagulation and complement systems in CKD.
  • To explore the therapeutic potential of nicotinamide (NAM) in modulating these pathways in CKD.

Main Methods:

  • Analysis of CKD patient cohorts for coagulation markers (fibrinogen, prothrombin time) and complement levels (C3, C4).
  • Gene expression analysis in CKD renal tissues and adenine/folic acid-induced nephropathy mouse models.
  • RNA sequencing and KEGG pathway analysis to evaluate NAM's effects on coagulation and complement cascades.

Main Results:

  • Elevated fibrinogen and shortened prothrombin time correlated with higher C3 and C4 levels in CKD patients.
  • Upregulation of coagulation factors (tissue factor, fibrinogen) and C3 observed in fibrotic kidneys of mouse models.
  • NAM administration significantly inhibited coagulation and complement cascades in adenine-induced nephropathy, suppressing inflammasome and neutrophil extracellular trap formation.

Conclusions:

  • Excessive coagulation and complement activation are implicated in CKD pathogenesis.
  • Nicotinamide (NAM) demonstrates therapeutic potential by modulating these pro-thrombotic and inflammatory pathways in CKD.

Keywords:
NAD+inflammasomeneutrophil extracellular trapthrombosis

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