ObjectivesMounting evidence suggests that bacterial dysbiosis and immunity disorder are associated with patients with chronic kidney disease (CKD), but the mycobiome is beginning to gain recognition as a fundamental part of our microbiome. We aim to characterize the profile of the mycobiome in the gut of CKD patients and its correlation to serum immunological profiles.Methods and materialsNinety-two CKD patients and sex–age–body mass index (BMI)–matched healthy controls (HCs) were recruited. Fresh samples were collected using sterile containers. ITS transcribed spacer ribosomal RNA gene sequencing was performed on the samples. An immunoturbidimetric test was used to assess the serum levels of immunological features.ResultsThe CKD cohort displayed a different microbial community from that in the HC cohort according to principal coordinate analysis (PCoA). (P=0.001). The comparison of the two cohorts showed that the CKD cohort had significantly higher gut microbial richness and diversity (P<0.05). The CKD cohort had lower abundances of Candida, Bjerkandera, Rhodotorula, and Ganoderma compared to the HC cohort, while it had higher Saccharomyces (P<0.05). However, the microbial community alteration was inconsistent with the severity of kidney damage in patients, as only patients in CKD stage 1~3 had differed microbial community concerning for HCs based on PCoA (P<0.05). The serum concentration of the kappa light chain in CKD patients was positively associated with Saccharomyces, whereas the it was negatively associated with Ganoderma (P<0.05).ConclusionsNot only was gut mycobiome dysbiosis observed in CKD patients, but the dysbiosis was also associated with the immunological disorder. These findings suggest that therapeutic strategies targeting gut mycobiome might be effective.

Background The association between oral dysbiosis and chronic kidney disease (CKD) has gained increasing attention in recent years. Diabetes and hypertension are the most common conditions in CKD. However, a case–control study with matched confounding variables on the salivary microbiome in CKD and the influence of diabetes and hypertension on the microbiome has never been reported. Methods In our study, we compared the salivary microbiome profile between patients with CKD and healthy controls (HC) using 16S ribosomal DNA sequencing and examine its association with diabetes, hypertension, and immunity. Results We observed that the bacterial community was skewed in the saliva of CKD, with increased Lautropia and Pseudomonas, and decreased Actinomyces, Prevotella, Prevotella 7, and Trichococcus. No difference in the bacterial community between the CKD patients complicated with and without diabetes, and between those with and without hypertension. Prevotella 7 declined in CKD patients with/without hypertension with respect to HC, while Pseudomonas increased in CKD patients with/without hypertension. Pseudomonas was negatively associated with immunoglobin G in CKD patients. Both CKD patients with positive and negative antistreptolysin O had declined Prevotella 7 and Trichococcus compared to HC, whereas increased Pseudomonas. Conclusions Our study identifies a distinct bacterial saliva microbiome in CKD patients characterized by alteration in composition. We unravel here that the co-occurrence diseases of diabetes and hypertension are not associated with specific bacterial alterations, suggesting that bacterial dysbiosis in saliva plays a role in renal damage regardless of the occurrence of diabetes and hypertension.

BackgroundTo establish antibiotic preregimes and administration routes for studies on urinary microbiota.Methods and materialsAntibiotics for enteritis (Abx-enteritis) and UTIs (Abx-UTI) were administered via gavage and/or urinary catheterisation (UC) for 1 and/or 2 weeks. The effects of these Abx on the urinary microbiota of rats were examined via 16S rRNA sequencing and urine culture, including anaerobic and aerobic culture. Additionally, the safety of the Abx was examined.ResultsAbx-enteritis/Abx-UTI (0.5 g/L and 1 g/L) administered via gavage did not alter the microbial community and bacterial diversity in the urine of rats (FDR > 0.05); however, Abx-UTI (1 g/L) administered via UC for 1 and 2 weeks altered the urinary microbial community (FDR < 0.05). Rats administered Abx-UTI (1 g/L) via UC for 1 week demonstrated a distinct urinary microbiota in culture. Abx-enteritis/Abx-UTI administered via gavage disrupted the microbial community and reduced bacterial diversity in the faeces of rats (FDR < 0.05), and Abx-UTI administered via UC for 2 weeks (FDR < 0.05) altered the fecal microbiota. Abx-UTI (1 g/L) administered via UC did not alter safety considerations. In addition, we noticed that UC did not induce infections and injuries to the bladder and kidney tissues.ConclusionsAdministration of Abx-UTI via UC for 1 week can be considered a pre-treatment option while investigating the urinary microbiota.

Background High throughput 16S rRNA gene sequencing and enhanced culture methods (e.g., expanded quantitative urine culture, EQUC) have established the existence of the human bladder microbiome. We aim to test the hypothesis that the bladder environment of patients with chronic kidney disease (CKD) differs from that of unaffected controls with associated consequences for the composition of the bladder microbiome. Methods and Materials Females (n=66) and males (n=66) diagnosed with CKD and age-BMI-matched healthy control (HC) females (n=22) and males (n=22) were recruited. Transurethral catheterized urine was collected for 16S rRNA gene sequencing and Expanded Quantitative Urine Culture (EQUC). Fecal samples also were sequenced. Urinary analysis, kidney function and serum cytokines were examined. Results Bladder microbiomes of CKD females and males versus HC females and males differed (FDR<0.05); however, the difference was more obvious in females. In CKD females, sequencing revealed depletion of 5 genera, including Lactobacillus, and enrichment of 14 genera, including Escherichia/Shigella, Bifidobacterium, and several clostridial genera (FDR<0.05), while EQUC detected increased Escherichia and decreased Lactobacillus CKDB(P<0.05). Escherichia-Shigella was positively, whereas Lactobacillus was negatively, associated with CKDB-female serum creatinine (r=0.285, P=0.020; r=-0.337, P=0.006, respectively). Lactobacillus was positively associated with eGFR (r=0.251, P=0.042). Some CKD-related serum cytokines were negatively associated with clostridial genera. In contrast, the fecal microbiomes of CKD and HC females and males did not significantly differ in bacterial diversity or composition. However, bladder and fecal microbiomes of CKD females resembled each other more than those of controls, as assessed by the Bray-Curtis Dissimilarity Index (FDR<0.05). Conclusions CKD bladder microbiomes were dysbiotic, which was more obvious in females. This dysbiosis was associated with kidney damage severity and dysregulation of serum cytokines. The increased similarity between bladder and fecal microbiomes of CKD females suggests possible gut-leakage.