Mesangial proliferative glomerulonephritis (MsPGN) is one of the most common immune-mediated renal diseases. The mesangium is expanded and hypercellular, immuno-globulin deposits can be found in the mesangium, but the mechanism underlying its cause remains largely unclear. There is a large amount of evidence suggesting that long ﹥200 nucleotide) non-coding RNAs (lncRNA) have important regulatory functions in the epigenetic control of gene expression. Multiple lines of evidence increasingly link mutations and dysregulations of lncRNAs to a diverse number of human diseases. Through microarray expression analysis, tests show that thousands of lncRNAs and protein-coding genes are significantly differentially expressed in IgA-negative MsPGN. Some lncRNAs and their neighboring protein-coding genes are closely related and are cooperatively expressed. This may be part of a potential regulatory mechanism. The malfunction of regulation in the network of lncRNAs may be a possible mechanism for the development of IgA-negative MsPGN. Our observations suggest that some lncRNAs are closely related to IgA-negative MsPGN and may be playing an important role in this disease.