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Abstract
The cause of INS remains unknown.
Early success in controlling nephrosis with immunosuppressive drugs suggested that the disease was mediated by immunologic mechanisms but evidence for classic mechanisms of immunologic injury has been lacking.
The present study was carried on forty-nine children with idiopathic nephrotic syndrome.
Twenty-seven children were studied during relapse, as well as twenty-two children in remission.
Fifteen apparently healthy child with matched age and sex were chosen to serve as control group.
They were subjected to careful history taking with stress on presence of oedema, its degree, and evidence for an infectious or allergic illness immediately preceding or accompanying the relapse.
Thorough clinical examination was performed as well as laboratory investigations which included complete urine analysis, protein in 24 hrs urine collection, total serum proteins, serum albumin, serum cholestrol, blood urea, serum creatinine, creatinine clearance rate, serum electrolytes Na+, K+, Ca2+ and serum soluble interleukin-2 receptor using an enzyme immunoassay (EIA).
The present study revealed a highly significant increase in serum sIL-2R between case with INS and control group.
Also, there was a highly significant increase in sIL-2R between relapse group and remission group.