Proteinuria and Activated T-Lymphocytes in Diabetic Nephropathy

  1. GianCarlo Viberti
  1. Unit for Metabolic Medicine, United Medical and Dental Schools (Guy's Campus), and the Department of Immunology, King's College School of Medicine and Dentistry London, England, United Kingdom
  1. Address correspondence and reprint requests to Dr. G.C. Viberti, Unit for Metabolic Medicine, 4th Floor, Hunt's House, Guy's Hospital, London SE1 9RT, UK.

Abstract

The reasons for the presence of activated T-lymphocytes (ATL) in some long-standing insulin-dependent diabetic (IDDM) patients are unknown. These cells have been implicated in the genesis of proteinuria in some forms of immune-mediated renal disease. We measured ATL in 18 IDDM patients with diabetic nephropathy, 10 with nonnephrotic proteinuria (total urinary protein excretion rate >0.5 and <3.5 g/24 h) and 8 with nephrotic proteinuria (total urinary protein excretion rate > 3.5 g/24 h), and in 17 age-, sex-, and duration-of-diabetes–matched diabetic control subjects without clinical proteinuria (total urinary protein <0.5 g/24 h). T-lymphocytes purified from peripheral blood were stained by direct immunofluorescence with the fluorescein-labeled monoclonal antibody anti-HLA-DR. Absolute number and percent of DR-positive T-lymphocytes were significantly higher in patients with nonnephrotic proteinuria (median and range 162 × 106/ml, 40–320 × 106/ml; 13.9%, 8.1–19.4%) compared with nonproteinuric control subjects (81 × 106/ml, 2–240 × 106/ml, P < .05; 6.2%, 0–13.1%, P < .01). In 8 patients with nephrotic proteinuria, absolute and percent DR-positive T-lymphocytes tended to be lower (36 × 106/ml, 14–56 × 106/ml; 3.4%, 1.1–5.4%) than in nonproteinuric control subjects. An increased number of activated T-lymphocytes may be part of an immune-mediated process associated with the development of proteinuria in diabetic nephropathy. In advanced renal disease with nephrotic proteinuria, this immune process may become exhausted.

  • Received March 18, 1987.
  • Revision received October 13, 1987.
  • Accepted October 13, 1987.
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