Thrombotic Microangiopathy Challenges: Diagnosis and Therapeutics

Mahmoud, Nouha Ben; Salah, Manel Ben; Salem, Meriem Ben; Bchir, Sirine; Hamouda, Mouna; Aloui, Sabra; Letaief, Ahmed; Skhiri, Habib

doi:10.1007/s12098-023-04982-2

Search citation statements

Order By: Relevance

Paper Sections

Select...

Etiology Of Tma In Igan1

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2024

Publication Types

Select...

Article1

Relationship

Self Cite0

Independent1

Authors

Journals

Cited by 1 publication

(1 citation statement)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The pathophysiology underlying TMA in IgAN is complex and multifactorial (24). TMA in IgAN involves endothelial injury triggered by dysregulation of the complement system, exacerbating thrombosis (12,25), Endothelial damage promotes platelet aggregation and activates the coagulation cascade, contributing to TMA (26).…”

Section: Etiology Of Tma In Iganmentioning

confidence: 99%

Thrombotic microangiopathy in IgA nephropathy: pathophysiology, histopathology, and treatment perspectives

Rastegar-Kashkouli,

Jafari,

Shahrokh

et al. 2024

J Nephropathol

View full text Add to dashboard Cite

The current narrative review study aims to provide an overview of thrombotic microangiopathy (TMA) in immunoglobulin A nephropathy (IgAN), with a particular emphasis on its pathophysiology, histopathology, and treatment options. The prevalence and clinical significance of TMA in IgAN may vary across different populations. Estimates suggest that TMA events occur in 2-50% of patients with IgAN. Endothelial injury is a key factor in TMA development in IgAN, triggered by immune complex deposition, complement activation, and potentially hypertension. TMA in IgAN correlates with vascular lesions, including arterial intimal sclerosis, arteriolar lumen reduction, and smooth muscle hypertrophy. Notably, patients with TMA show more intense deposition of C4, C3d, and C5b-9 complements. Treatment involves blood pressure management, immunosuppression, and targeted therapies such as eculizumab.

show abstract