HLA-DR Display by Renal Tubular Epithelium and Phenotype of Infiltrate in Interstitial Nephritis

• Published in: Nephrology, dialysis, transplantation dialysis, transplantation, 1989, Vol.4 (3), p.205-215
• Main Authors: Cheng, H.-F., Nolasco, F., Cameron, J. S., Hildreth, G., Neild, Gillian, Hartley, B.
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Aged; Anti-Inflammatory Agents, Non-Steroidal - adverse effects; Antibodies, Monoclonal; Biological and medical sciences; Child; Epithelium - immunology; Extracellular Space - immunology; Female; HLA-DR; HLA-DR Antigens - analysis; Humans; Interstitial nephritis; Kidney Glomerulus - immunology; Kidney Tubules - immunology; Leukocytes, Mononuclear - analysis; Male; Medical sciences; Middle Aged; Monocytes; Nephritis, Interstitial - immunology; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Non-steroidal anti-inflammatory drugs; Phenotype; Renal tubule; T-lymphocytes; T-Lymphocytes - analysis; Tubulointerstitial nephritis
• ISSN: 0931-0509; 1460-2385
• DOI: 10.1093/oxfordjournals.ndt.a091857

Renal tubular display of HLA-DR was estimated semi-quantitatively in 28 biopsies from 27 patients with various forms of tubulointerstitial nephritis (10 following use of non-steroidal anti-inflammatory drugs) using a monoclonal anti-MHC class II non-polymorphic antibody (DK-22). Normal donor kidneys and biopsies from patients with minimal-change nephrotic syndrome were examined as controls. The phenotype of infiltrating cells was also studied quantitatively, using monoclonal antibodies on frozen biopsy tissue; the number of cells infiltrating the interstitium was counted per tubular cross-section. Display of H LA-DR was seen in up to 5% of control tubular cells, but up to 100% expressed HLA-DR in tubulointerstitial nephritis biopsies. There was a correlation between the expression of HLA-DR and the severity of both tubular atrophy and tubulointerstitial fibrosis judged semi-quantitatively by optical microscopy. In controls up to 50 leucocytes per tubular cross-section were evident, but in patients with tubulointerstitial nephritis up to 1500 were observed, approximately 50% being T-lymphocytes, the majority expressing the helper phenotype except in early, active drug-induced tubulointerstitial nephritis; the remainder were mostly monocytes. There were no qualitative differences between the different causes of tubulointerstitial nephritis. Tubular DR expression correlated with the number of DR-positive cells in the interstitium, but not with total leucocytes or T-lymphocytes. HLA-DR tubular expression was greater in the early stages than late stages of NSAID-induced tubulointerstitial nephritis, but this relationship was not present in the group as whole. HLA-DR expression by renal tubular epithelial cells may play a role in localising or amplifying tubular injury in tubulo-interstitial nephritis.