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Updated: Jun 16, 2026

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells
Published on: June 20, 2018
A tubulointerstitial nephritis antigen gene defect causes childhood-onset chronic renal failure
Yutaka Takemura1, Machiko Koshimichi, Keisuke Sugimoto
1Department of Pediatrics, Kinki University School of Medicine, 377-2 Ohno-higashi, Osaka-Sayama, 589-8511, Japan.
Abstract:
Tubulointerstitial nephritis antigen (TIN-ag), which has been localized to the renal tubular basement membrane, is a target antigen in some forms of TIN. Physiologically, TIN-ag is thought to be important in maintaining the structure of renal tubular basement membrane. Here we describe a child with chronic renal failure showing a human TIN-ag gene (hTIN-ag) deletion. Immunohistochemical examination using an antihuman TIN-ag monoclonal antibody showed attenuation or lack of TIN-ag staining along the renal tubular basement membrane, whereas nephrocystin staining was normal in renal tubules. Polymerase chain reaction detected no amplification band corresponding to hTIN-ag in this patient. Testing for a deletion in this gene showed nearly complete deletion. By using array-comparative genomic hybridization method, large deletion of a gene mapped on chromosome 6p11-6p12 was demonstrated, corresponding to the locus where hTIN-ag is located. Therefore, an hTIN-ag defect may be a potent cause of end-stage renal failure in childhood.
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