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Published on: April 26, 2019
Clinicopathological Investigation of Medial Smooth Muscle Cell Atrophy in Small Arteries in Kidney Allografts
Noriyuki Kounoue1,2, Hideyo Oguchi3, Masaki Muramatsu1
1Department of Nephrology, Toho University Faculty of Medicine, Tokyo, Japan.
Introduction:
Atrophy of smooth muscle cells (SMCs) in the media of small arteries is occasionally observed, especially in long-term kidney allograft biopsies. The intima-media ratio is used as an index of arteriosclerosis in native kidneys, and medial SMC atrophy suggests severe arteriosclerosis. We aimed to investigate the clinicopathological significance of medial SMC atrophy in small arteries in biopsies from long-term kidney transplants.
Methods:
Samples were obtained from kidney allograft biopsies carried out from January 2016 to December 2019, and biopsies obtained 10 years after transplantation were included in the study. The distal small arteries with the most atrophic SMCs in longitudinal sections in each biopsy specimen were selected (outer diameter <150 µm and ≥60 µm). The outer diameter and width of the media, intima, and lumen of each artery were measured. SMC atrophy was evaluated as the media-outer diameter ratio.
Results:
Fifty biopsies were eligible. The mean media-outer diameter ratio was 0.27 ± 0.11. Donor age and allograft age were significantly inversely correlated with media-outer diameter ratio (rank correlation coefficient -0.3522, p = 0.0141 and -0.3700, p = 0.0096, respectively). After separation into two groups according to the media-outer diameter ratio, donor age and allograft age were both significantly higher and more focal segmental glomerular sclerosis (FSGS) lesions were observed in the low media-outer diameter ratio group. Multivariate analysis revealed that media-outer diameter ratio was significantly related to donor age, allograft age, and FSGS.
Conclusions:
Medial SMC atrophy appears to be related to donor age, allograft age, and FSGS in kidney allografts. Disruption of vascular contraction as a result of medial SMC atrophy in aging allografts may lead to the development of FSGS.

