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Pathohistomorphometric and Immuno-Histologic Changes in Early Arteriovenous Fistula Failure in Patients with Chronic
Vladimir Pushevski1,2, Petar Dejanov1,2, Irena Rambabova-Bushljetikj1,2
11University Clinic of Nephrology, Skopje, RN Macedonia.
Insights
Early arteriovenous fistula failure in chronic kidney disease (CKD) patients is complex. Preexisting medial hypertrophy and postoperative neointimal hyperplasia contribute to AVF failure, impacting hemodialysis access.
Area of Science:
- Vascular Surgery
- Nephrology
- Histopathology
Background:
- Arteriovenous fistula (AVF) is the preferred hemodialysis access but frequently fails to mature in chronic kidney disease (CKD) patients.
- Early AVF failure, defined as thrombosis or non-usability within three months, has poorly understood etiologies.
- Neointimal hyperplasia is a key histological finding in AVF failure, yet cellular phenotypes and CKD-related factors require further investigation.
Purpose of the Study:
- To investigate histological, morphometric, and immunohistochemical changes in fistula veins before and after early AVF failure in CKD patients.
- To identify cellular phenotypes and the impact of CKD on AVF failure.
- To elucidate the mechanisms underlying early AVF failure.
Main Methods:
- Eighty-nine stage 4-5 CKD patients undergoing radio-cephalic AVF creation were studied.
- Vein specimens were collected during AVF creation and post-failure surgery.
- Morphometric analysis and immunohistochemistry for Vimentin, TGF, and Ki 67 were performed.
Main Results:
- Histomorphometric analysis revealed significant venous luminal stenosis and endothelial alterations.
- Immunohistologic analysis demonstrated differential expression of cellular markers pre- and post-AVF creation.
- Medial hypertrophy was identified as a significant preexisting lesion, with a shift towards neointimal hyperplasia postoperatively.
Conclusions:
- Early AVF failure in CKD patients is multifactorial, involving vascular remodeling and cellular changes.
- Preexisting medial hypertrophy and postoperative neointimal hyperplasia are critical factors in AVF failure.
- Understanding these vascular alterations is crucial for improving AVF outcomes in CKD patients.
Background:
Hemodialysis is a prevalent treatment for the end-stage chronic kidney disease (CKD) worldwide. The primary arteriovenous fistula (AVF), widely considered the optimal hemodialysis access method, fails to mature in up to two-thirds of the cases. The etiology of the early AVF failure, defined as thrombosis or inability to use within three months post-creation remains less understood, and is influenced by various factors including patient demographics, surgical techniques, and genetic predispositions. Neointimal hyperplasia is a primary histological finding in stenotic lesions leading to the AVF failure. However, there are insufficient data on the cellular phenotypes and the impact of the preexisting CKD-related factors. This study aims to investigate the histological, morphometric, and immunohistochemical alterations in the fistula vein, pre-, peri-, and post-early failure.
Materials And Methods:
Eighty-nine stage 4-5 CKD patients underwent standard preoperative assessment, including the Doppler ultrasound, before a typical radio-cephalic AVF creation. Post-failure, a new AVF was created proximally. The vein specimens were collected during the surgery, processed, and analyzed for morphometric analyses and various cellular markers, including Vimentin, TGF, and Ki 67.
Results:
The study enrolled 89 CKD patients, analyzing various aspects of their condition and AVF failures. The histomorphometric analysis revealed substantial venous luminal stenosis and varied endothelial changes. The immunohistologic analysis showed differential marker expressions pre- and post-AVF creation.
Conclusion:
This study highlights the complexity of the early AVF failures in CKD patients. The medial hypertrophy emerged as a significant preexisting lesion, while the postoperative analyses indicated a shift towards neointimal hyperplasia. The research underscores the nuanced interplay of vascular remodeling, endothelial damage, and cellular proliferation in the AVF outcomes.
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