Changes of Cellular Immune Indices and Soluble Interleukin-2 Receptor(sIL-2 R) in Children with Minimal Change Nephrotic Syndrome.
- Author:
Cheol Woo KO
1
;
Byung Ho CHOE
;
Ja Hoon KOO
Author Information
1. Department of Pediatrics, Kyungpook National University, School of Medicine, Taegu, Korea.
- Publication Type:Original Article
- Keywords:
Minimal change nephrotic syndrome;
T-suppressor;
Soluble interleukin-2 receptor
- MeSH:
Antibodies, Monoclonal;
Child*;
Cholesterol;
Cyclophosphamide;
Humans;
Interleukin-2*;
Nephrosis, Lipoid*;
Nephrotic Syndrome;
Recurrence;
Serum Albumin
- From:Korean Journal of Nephrology
1997;16(3):443-448
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
This study was conducted to see the role of cellular immune function in the pathogenesis of minimal change nephrotic syndrome. Study patients consisted of 19 children with biopsy-proven minimal change nephrotic syndrome, aged 2-15 yr. Controls were 10 age-matched healthy children. The proportion of T4 and T8 in peripheral blood were measured with flocytometer using monoclonal antibodies during relapse and 1 month after remission. Serum soluble interleukin-2 receptor(sIL-2 R) was measured using ELIZA kit in both periods. The following results were obtained: (1) No significant change of serum sIL-2 R was noted between relapse and remission period. Both values of serum sIL-2 R did not show any significant change compared to the control value. (2) The proportion of T8 peripheral blood during relapse significantly increased compared to those of controls or remission period(p<0.01). (3) Increased proportion of T8 during relapse was not related to the history of taking immunosuppressive agent such as cyclophosphamide recently, and not correlated with values of serum albumin or cholesterol during relapse. Conclusively, it can be said that increased proportion of T8 in peripheral blood may play an important role in the pathogenesis of minimal change nephrotic syndrome, and this increment of T8 seems not to be the secondary change caused by cytotoxic therapy or nephrotic syndrome itself.
