Nephrotic syndrome (NS) is a common renal disorder in children. It is attributed to abnormality in the glomerular filtration barrier (GFB) resulting in heavy proteinuria, >3.5g/day in adults and 40mg/m2/h in children, along with hypoalbuminaemia, oedema and hyperlipidaemia. Children with nephrotic syndrome show vast heterogeneity in terms of response to steroids and non-steroidal immune-suppressants, clinical course and outcome which suggests underlying molecular heterogeneity. Many studies have advocated involvement of “circulating factor/humoral substance” in the pathogenesis of NS; however, aetiology of the disease has not been conclusively established. Thus, nephrotic plasma is thought to induce characteristic gene activity leading to structural patterns and functional changes in podocytes. Differential gene expressions in podocytes may be associated with distinct pathobiology and may help in identifying intrinsic sub-types of NS.
Our studies aim to examine the transcriptional responses induced by nephrotic plasma in immortalised podocyte cell line and identify intrinsic subtypes and to develop a novel stratification approach by combining molecular signatures with therapeutic responsiveness and outcome.