Background: Chronic kidney disease (CKD) is characterized by high morbidity and mortality rate worldwide, and is considered a major public health problem. Studies have shown that long noncoding RNA (lncRNA)-associated competing endogenous RNA (ceRNA) may be involved in the biological processes of CKD, but the exact mechanisms are still largely unknown. In this study, further analysis of these ceRNA networks will reveal the important role of ceRNAs in the pathogenesis of CKD.Methods: Differentially expressed (DE) lncRNAs in CKD patients and healthy volunteers were identified through high-throughput sequencing. Functional enrichment analysis was performed to examine the key biological functions and pathways involved in CKD. The lncRNA‐associated ceRNA regulatory network was constructed, and a protein-protein interaction (PPI) network analysis was conducted to identify the hub genes involved in the pathogenesis of CKD. Results: In this study, 378 DE lncRNAs were detected, of which 207 were intergenic lncRNAs, 88 were intronic lncRNAs and 83 were exonic lncRNAs. The intergenic lncRNAs have 96 up-regulated lncRNAs and 111 down-regulated lncRNAs. As for intronic lncRNAs, 39 lncRNAs were up-regulated and 49 were down-regulated. Similarly, we also found that 27 exonic lncRNAs were up-regulated and 56 were down-regulated. Functional enrichment analysis was performed based on the prediction of lncRNA‐miRNA-mRNA interactions. GO analysis showed that predicted target gene was highly correlated with the immune response. KEGG analysis revealed that predicted target genes were significantly enriched in regulated pathways such as MAPK signaling pathway. We successfully constructed lncRNA‐associated ceRNA regulatory network involved in the pathogenesis of CKD, and based on this network, a PPI network was established to identify 10 hub genes which participate in the pathogenesis of CKD.Conclusions: Our findings provide a new perspective understanding of the lncRNA‐associated ceRNA network involved in CKD, which may help to elucidate the potential pathogenesis of CKD.