Medullary ray injury in renal allografts
Pathology International, ISSN: 1320-5463, Vol: 60, Issue: 11, Page: 744-749
2010
- 13Citations
- 16Captures
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Metrics Details
- Citations13
- Citation Indexes13
- 13
- CrossRef7
- Captures16
- Readers16
- 16
Article Description
Non-immune injury leading to interstitial fibrosis and tubular atrophy (IF/TA) in renal allografts has various etiologies, but pathological means of verification have yet to be developed. Medullary ray injury (MRI) is a pathological feature of many non-immune injuries inducing IF/TA and pathological determination of calcineurin inhibitor (CNI) toxicity proceeding to striped fibrosis. We investigated the contribution of CNI toxicity to MRI and other non-immune etiologies related to IF/TA. In this study MRI is defined as fibrosis and inflammation localized exclusively to the medullary ray. Thirty-six protocol biopsies showing MRI were analyzed and classified histopathologically as following: MRI related to CNI toxicity; chronic obstruction or reflux nephropathy; and acute or chronic pyelonephritis. The etiology of MRI was CNI toxicity (n= 16, 44.4%), chronic obstruction (n= 13, 36.1%), acute or chronic pyelonephritis (n= 2, 5.6%), and other (n= 5, 13.9%). We performed cystography in seven cases of MRI related to chronic obstruction or reflux nephropathy and six cases showing vesicoureteral reflux. The ci+ct score showed significant progression after one year in 30 of the 36 cases (1.53 ± 1.04 vs. 3.03 ± 1.13, P < 0.01). MRI has various etiologies and may also predict changes in urological complications. The classification of MRI may be useful to determine the non-immune etiology leading to IF/TA. © 2010 The Authors Pathology International © 2010 Japanese Society of Pathology and Blackwell Publishing Asia Pty Ltd.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=77958497546&origin=inward; http://dx.doi.org/10.1111/j.1440-1827.2010.02593.x; http://www.ncbi.nlm.nih.gov/pubmed/20946524; https://onlinelibrary.wiley.com/doi/10.1111/j.1440-1827.2010.02593.x; https://dx.doi.org/10.1111/j.1440-1827.2010.02593.x
Wiley
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