Objectives: The incidence of diabetes significantly increases after kidney transplant, and the associated gut microbiota are closely related to diabetes. However, the gut microbiota of recipients with diabetes after kidney transplant remain unexplored. Materials and Methods: Feces samples from recipients with diabetes 3 months after kidney transplant were collected and analyzed using high-throughput 16S rRNA gene sequencing. Results: Our study included 45 transplant recipients: 23 posttransplant diabetes mellitus recipients, 11 recipients without diabetes mellitus, and 11 recipients with preexisting diabetes mellitus. No significant differences in intestinal flora richness and a diversity were observed among the 3 groups. However, principal coordinate analysis based on UniFrac distance revealed significant differences in ss diversity. At the phyla level, the abundance of Proteobacteria in posttransplant diabetes mellitus recipients decreased (P =.028), whereas that of Bactericide (P =.004) increased. At the class level, the abundance of Gammaproteobacteria (P =.037) decreased, whereas that of Bacteroidia (P =.004) increased. At the order level, the abundance of Enterobacteriales (P =.039) decreased, whereas Bacteroidales (P =.004) increased. At the family level, the abundance of Enterobacteriaceae (P =.039) and Peptostreptococcaceae (P =.008) decreased, whereas Bacteroidaceae (P =.010) increased. At the genus level, the abundance of Lachnospiraceae incertae sedis (P =.008) decreased, whereas Bacteroides (P =.010) increased. Furthermore, KEGG analysis identified 33 pathways, among which the biosynthesis of unsaturated fatty acids was closely related to gut microbiota and posttransplant diabetes mellitus. Conclusions: To our knowledge, this is the first comprehensive analysis of the gut microbiota from posttransplant diabetes mellitus recipients. The microbial composition of stool samples of posttransplant diabetes mellitus recipients was significantly different from recipients without diabetes and with preexisting diabetes. The number of bacteria producing short-chain fatty acids decreased, whereas pathogenic bacteria increased.