Neointimal hyperplasia in the inferior vena cava of adenine-induced chronic kidney disease rats with aortocaval fistulas.

Clin Exp Nephrol

Department of Nephrology, Shandong Provincial Qianfoshan Hospital, Shandong University, No.16766, Jingshi Road, Jinan, 250014, People's Republic of China.

Published: November 2020

AI Article Synopsis

  • The study focused on using aortocaval fistulas (ACFs) in rats with chronic kidney disease (CKD) to investigate the development of neointimal hyperplasia (NIH) that causes stenosis in arteriovenous fistulas (AVFs).
  • Ten female rats induced with CKD through a special diet underwent ACF surgery, while ten healthy rats acted as controls, with their conditions assessed through scans and tissue analyses.
  • Results showed that CKD rats exhibited higher serum creatinine levels and distinct histological changes, with findings indicating that NIH in these rats parallels the stenosis seen in clinical cases of AVF failures.

Article Abstract

Background: The failure of autologous arteriovenous fistulas (AVFs) occurs primarily due to stenosis in the anastomotic site, which is mainly related to the development of neointimal hyperplasia (NIH). Therefore, we conducted a study to establish a novel approach to create aortocaval fistulas (ACFs) in adenine-induced (AD) chronic kidney disease (CKD) rats to study the NIH in the inferior vena cava.

Methods: Ten adult female rats received a 0.75% adenine-rich diet for 4 weeks to induce CKD and underwent ACF surgery. Ten healthy rats served as controls. A 5-10-mm segment of a vein immediately adjacent to that the portion of the vein used for creating the fistula was surgically removed at the time of creating the fistula, and reconstruction of the failed fistula from the same patient was used as controls. ACF was assessed using duplex scans and histopathological analyses.

Results: At the end of the experiment, AD rats showed higher serum creatinine and urea nitrogen than those of vehicle-treated rats. Remarkable histological changes in kidney tissues demonstrated successful CKD models. Sections of the ACF in AD rats and veins removed at the time of the reconstruction of the failed fistula of the patient demonstrated that the eccentric neointima formation is irregularly thickened, with several small vessels within a more cellular region of the neointima. Immunohistochemistry demonstrated the presence of myofibroblasts, contractile smooth muscle cells and macrophages within the neointima.

Conclusions: Our rat models with ACFs showed typical features of NIH in the formation of fistula stenosis, which can resemble clinical findings in uremic patients.

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Source
http://dx.doi.org/10.1007/s10157-020-01927-3DOI Listing

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