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Soluble interleukin-2 receptor in patients with glomerular diseases.
  1. H. S. Chen,
  2. M. S. Wu,
  3. T. S. Yen,
  4. W. Y. Chen
  1. Department of Internal Medicine, National Taiwan University Hospital, Taipei, Republic of China.

    Abstract

    In this study, we measured the soluble interleukin-2 receptor (sIL-2R) level to evaluate the cellular immune status in 61 patients with different types of glomerular diseases; 40 healthy volunteers were used as control. All patients with glomerular diseases had levels of serum sIL-2R significantly higher than those of the controls (766 +/- 59 vs 280 +/- 23 U/ml; p < 0.05). Even patients with normal renal function still had higher serum sIL-2R levels than the controls, no matter to which subgroups they belonged (primary glomerulonephritis, lupus nephritis or diabetic nephropathy). Serum sIL-2R levels were similar among the three subgroups. The serum levels of sIL-2R correlated well with age and were significantly higher in older patients, although this was not observed in the control group. Serum sIL-2R levels were significantly higher in patients with active urinary sediment and in patients with impaired renal function and showed a significant negative correlation with creatinine clearance (r = -0.56; p < 0.05). Although urinary and serum sIL-2R levels were quite well correlated, (r = 0.35; p < 0.05), the urinary levels of sIL-2R did not differ in patients with different disease activity or different renal functions although they had a significant correlation with 24-hour urinary protein (r = 0.39; p < 0.05). Patients with nephrotic syndrome also had higher urinary sIL-2R levels than other patients (529 +/- 106 vs 280 +/- 31 U/ml; p < 0.05). We conclude that greater T-cell activation might contribute to the pathogenesis of different glomerulonephritis entities, and serum levels of sIL-2R can serve as a useful clinical marker of glomerulonephritis activity. Renal function influenced the serum levels of sIL-2R significantly. This factor must be considered when we interpret the data. Urinary sIL-2R levels did not reflect the disease activity as well. This might be due to the secondary influence of the extent of the glomerular protein leak. Further investigation is needed to define the exact excretory pathway of this substance.

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