Sa. Hulton et al., LYMPHOCYTE SUBPOPULATIONS, INTERLEUKIN-2 AND INTERLEUKIN-2 RECEPTOR EXPRESSION IN CHILDHOOD NEPHROTIC SYNDROME, Pediatric nephrology, 8(2), 1994, pp. 135-139
Abnormal T lymphocyte function and reduced interleukin-2 (IL-2) produc
tion have been implicated in the pathogenesis of the nephrotic syndrom
e (NS). We investigated: (1) lymphocyte subpopulations and expression
of IL-2 receptor (IL-2R) on T cells using two-colour flow cytometry, (
2) serum IL-2 and (3) the soluble component of IL-2R (sIL-2R) in serum
, using enzyme-linked immunosorbent assay, in 38 children with NS. All
children, except those in remission, had marked proteinuria. They wer
e divided into groups according to renal pathology: (1) steroid-sensit
ive NS (SSNS) not receiving prednisolone therapy, (2) SSNS on predniso
lone, (3) focal segmental glomerulosclerosis (FSGS), (4) SSNS in remis
sion and not receiving prednisolone therapy, (5) congenital NS (CNS).
Results were compared with 26 age-matched controls. Total T lymphocyte
s (CD3) were reduced in groups 1 and 2; CD4 count was reduced in group
s 1-4; CD8 count increased in groups 2 and 3; CD8 and CD19 (B lymphocy
tes) were significantly reduced in group 5. Increased IL-2R expression
(CD25) on CD4 lymphocytes was noted in groups 1, 2 and 3 implying act
ivation of these cells. In patients with SSNS, increased serum sIL-2R
was recorded during relapse (1,273 +/- 497 U/l vs. 913 +/- 401 U/l in
remission, P <0.005) but free serum IL-2 was not detectable at any sta
ge. The specific alterations in lymphocyte subpopulations in SSNS and
FSGS would imply an involvement of the immune system distinct from tha
t in CNS.