In this study, we measured the soluble interleukin-2 receptor (sIL-2R)
level to evaluate the cellular immune status in 61 patients with diff
erent types of glomerular diseases; 40 healthy volunteers were used as
control. All patients with glomerular diseases had levels of serum sI
L-2R significantly higher than those of the controls (766 +/- 59 vs 28
0 +/- 23 U/ml; p < 0.05). Even patients with normal renal function sti
ll had higher serum sIL-2R levels than the controls, no matter to whic
h 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 a
nd 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 i
mpaired renal function and showed a significant negative correlation w
ith creatinine clearance (r = -0.56; p < 0.05). Although urinary and s
erum sIL-2R levels were quite well correlated, (r = 0.35; p < 0.05), t
he urinary levels of sIL-2R did not differ in patients with different
disease activity or different renal functions although they had a sign
ificant correlation with 24-hour urinary protein (r = 0.39; p < 0.05).
Patients with nephrotic syndrome also had higher urinary sIL-2R level
s than other patients (529 +/- 106 vs 280 +/- 31 U/ml; p < 0.05). We c
onclude that greater T-cell activation might contribute to the pathoge
nesis of different glomerulonephritis entities, and serum levels of sI
L-2R can serve as a useful clinical marker of glomerulonephritis activ
ity. Renal function influenced the serum levels of sIL-2R significantl
y. 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 pro
tein leak. Further investigation is needed to define the exact excreto
ry pathway of this substance.