• Vol. 39 No. 9, 705–713
  • 15 September 2010

Urotensin 2 and Retinoic Acid Receptor Alpha (RARA) Gene Expression in IgA Nephropathy

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ABSTRACT

Introduction: IgA nephropathy is a disease where the pathogenesis is still poorly understood. Deoxyribonucleic acid (DNA) microarray technique allows tens of thousands of gene expressions to be examined at the same time. Commercial availability of microarray genechips has made this powerful tool accessible for wider utilisation in the study of diseases.

Materials and Methods: Seven patients with IgA nephropathy, 6 with minimal change nephrotic syndrome (MCNS) as patient controls and 7 normal healthy subjects were screened for the differential expression of genes, genome-wide. The Human Genome U133 Plus 2.0 Arrays (Affymetrix, USA) were used to quantitate the differential expression of 38,500 well-characterised human genes.

Results: A total of 7761 gene expressions were identified that have an IgAN/Normal gene expression ratio of 0.06-fold to 5.58-fold. About 35% of the altered gene expressions have no gene title or just a hypothetical protein label such as FLJ30679. Most of the remaining 65% are identified proteins where their importance to IgAN is not immediately apparent at this time. Among the 30 most upregulated and 30 most downregulated genes are Urotensin 2 (upregulated 3.09-fold, P <0.05 ) and Fatty-acid binding protein 6 (downregulated to 0.12-fold, P < 0.005). Taqman real-time polymerase chain reaction (PCR) for urotensin 2 and retinoic acid receptor alpha (RARA) were performed on 20 patients with IgA nephropathy and 11 with Minimal Change Disease and the data correlated with various clinical indices.

Conclusions: The findings suggest that there may be a therapeutic role for retinoic acid receptor alpha (RARA) in IgA nephropathy and a clinical monitoring role for Urotensin 2 in Minimal Change Disease.


IgA nephropathy (IgAN) is the most common primary glomerulonephritis in Singapore1 and in many parts of the world, contributing significantly to the pool of end-stage renal failure patients annually. Despite more than 3 decades of research, the pathogenesis of the disease is still poorly understood.

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