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Objective A kinetic model of the clearance of protein-bound uremic toxins (PBUTs) in maintenance hemodialysis patients is established to evaluate the effects of adding sorbents with different sorption efficiency to dialysate on the clearance rate of PBUTs, and to predict the sorption efficiency of sorbents using the model. Methods The kinetic model was established by integrating the parameters of plasma flow rate (Qp), dialysate flow rate (Qd), free plasma fraction of PBUTs (f1), free dialysate fraction of PBUTs (f2), mass transfer coefficient of dialyzer (K) and surface area of dialysis membrane (A), and using the mass balance equation and Fick's first law. The model was also used to evaluate the relationship between the clearance rate of different PBUTs and the parameters of dialyzer and the sorption efficiency of sorbents. Results The kinetic model of PBUTs clearance (CL):. The model was used to analyze the dialysis parameters of indoxyl sulfate and p-cresol sulfate dialysis.The clearance rate of PBUTs increased with the decrease of its binding capacity to albumin in plasma and the increase of plasma flow rate in dialyzer, dialysate flow rate, mass transfer coefficient of dialyzer, surface area of dialysis membrane, and sorption capacity of sorbents in dialysate. The increasing trend of PBUTs clearance rate was particularly obvious after applying sorbents. Further analysis of the dialysate flow rate and the sorption efficiency of sorbents in the dialysate showed that the increase of the dialysate flow rate could make up for the difference of the sorption efficiency of sorbents. When the dialysate flow rate tended to be infinite, the sorption efficiency of sorbents in the dialysate had no effect on the clearance rate of PBUTs. Conclusion Adding sorbents of PBUTs to the dialysate during dialysis can significantly improve the clearance rate of PBUTs, suggesting a promising clinical application value.
Objective To evaluate the influence of cytomegalovirus (CMV) infection on T cell senescence and cardiovascular disease (CVD) in maintenance hemodialysis (MHD) patients. Methods It was a single center cross sectional study. Patients aged over 18 years old and received hemodialysis for at least 6 months at the Blood Purification Centre of the Department of Nephrology of Zhongshan Hospital Affiliated to Fudan University from January 2021 to April 2021 were enrolled. Demographic, hematological, nutritional and inflammatory markers were obtained. Anti-CMV-IgM and IgG antibodies were detected using the Roche Elecsys assay. CD28- T cell was evaluated by flow cytometry. Mann-Whitney U test or Kruskal-Wallis H test was used for anti-CMV-IgG comparison among groups. Spearman correlation and linear regression were used to assess the relationship between anti-CMV-IgG and CD28- T cell compartment. Logistic regression was used to assess the relationship between anti-CMV-IgG and CVD. Results A total of 438 MHD patients (270 men and 168 women) were enrolled in the study. The median age was 62 (51, 70) years. The median time on hemodialysis was 57 (21, 100) months. The primary diseases included chronic glomerulonephritis [213 cases (48.6%)], diabetic nephropathy [82 cases (18.7%)], polycystic kidney disease [34 cases (7.8%)], hypertensive renal disease [34 cases (7.8%)], etc. Of these patients, 430 (98.2%) were seropositive for anti-CMV-IgG, 206 (47.0%) had anti-CMV-IgG titers exceeding the upper limit of 500 U/ml. Patients aged over 70 years old were 100% seropositive for anti-CMV-IgG. Patients on HD for more than 5 years had a higher seropositive rate of 99.1% than those with shorter HD duration, although these results were not statistically significant. Spearman correlation analysis showed that the anti-CMV-IgG titers in MHD patients were positively correlated with the proportion of CD4+ CD28- T cells and CD8+ CD28- T cells (r=0.316, P<0.001; r=0.272, P<0.001). Multiple linear regression analysis showed that after adjusting for age and gender, lg[CD4+ CD28- T cells(%)] and lg[CD8+ CD28- T cells(%)] were positively correlated with lg[anti-CMV-IgG titers (U/ml)], respectively (β=0.455, t=8.315, P<0.001; β=0.412, t=7.282, P<0.001). In analyzing the relationship between anti-CMV-IgG titers and CVD, patients were divided into six groups according to age and anti-CMV-IgG level. Group 1 included young patients with a lower anti-CMV-IgG titers (age ≤55 years old, anti-CMV-IgG <400 U/ml); Group 2 included young patients with a higher anti-CMV-IgG titers (age≤55 years old, anti-CMV-IgG ≥400 U/ml); Group 3 included middle-aged patients with a lower anti-CMV-IgG titers (55<age≤65 years old, anti-CMV-IgG<400 U/ml); Group 4 included middle-aged patients with a higher anti-CMV-IgG titers (55<age≤65 years old, anti-CMV-IgG≥400 U/ml); Group 5 included old aged patients with a lower anti-CMV-IgG titers (age >65 years old, anti-CMV-IgG<400 U/ml); Group 6 included old aged patients with a higher anti-CMV-IgG titers (age>65 years old, anti-CMV-IgG≥400 U/ml). The incidence of CVD was significantly different among the six groups (χ2=18.780, P=0.002) and patients aged over 55 years old with higher anti-CMV-IgG level had a higher CVD incidence compared with group 1 (P<0.05). Multivariate logistic regression analysis showed that increased age (OR=1.020, 95% CI 1.002-1.038, P=0.033), male (OR=1.855, 95% CI 1.161-2.965, P=0.010), history of diabetes (OR=1.867, 95% CI 1.145-3.046, P=0.012), increased lg[NT-proBNP(μg/L)] (OR=2.848, 95% CI 1.816-4.467, P<0.001) and lg[anti-CMV-IgG (U/ml)] (OR=3.183, 95% CI 1.582- 6.405, P=0.001) were independent factors associated with CVD in MHD patients. Conclusions CMV infection is extremely common in MHD patients. Increased anti-CMV-IgG is related to T cell senescence and CVD complications in MHD patients.
Objective To determine the impact of early serum sodium concentrations on the survival prognosis in maintenance hemodialysis (MHD) patients. Methods It was a retrospective cohort study. The newly admitted hemodialysis patients who were included in the registration system of Zhejiang Province Dialysis Quality Control Center from January 1, 2010 to December 31, 2019 were identified. Follow-up was conducted until December 31, 2020. Baseline data were collected for the first three months of dialysis, in which the mean level of serum sodium was defined as early serum sodium. Patients were divided into five groups based on early serum sodium level. Restricted cubic spline (RCS) was used to fit the relationship between long-term serum sodium level and risk of death. Kaplan-Meier model and Log-rank test were used to compare the survival rates of different groups. Multivariable Cox regression was used to analyze the correlation between early serum sodium level and death. Results A total of 26 309 MHD patients were included in this study, and their ages were (59.07±15.41) years (ranging from 18 to 100 years). Among them, 13 643 (51.9%) were over 60 years old and 15 843 (60.2%) were males. Among the primary diseases of chronic renal failure, chronic glomerulonephritis was the first [13 703 cases (52.1%)], followed by diabetic nephropathy [6 460 cases (24.6%)], hypertensive nephropathy [1 293 cases (4.9%)], polycystic kidney disease [1 164 cases (4.4%)], etc. According to early serum sodium level, 12 883 patients (49.0%) had hyponatremia (serum sodium <135 mmol/L), of which 4 001 patients (15.2%) had serum sodium ≤130 mmol/L; 1 529 patients (5.8%) had hypernatremia (serum sodium >145 mmol/L). Patients were divided into the following 5 groups: 4 001 cases (15.2%) in group 1 (serum sodium ≤130 mmol/L), 8 882 cases (33.8%) in group 2 (130 <serum sodium <135 mmol/L), 8 231 cases (31.3%) in group 3 (135≤serum sodium ≤140 mmol/L), 3 666 cases (13.9%) in group 4 (140 < serum sodium≤145 mmol/L) and 1 529 cases (5.8%) in group 5 (>145 mmol/L). Among them, patients in the Na≤130 mmol/L group had a slightly older age, a higher proportion of diabetes and cardiovascular disease, a lower level of blood uric acid, albumin, hemoglobin, and a higher level of alkaline phosphatase and leukocytes, while patients in the Na >145 mmol/L group had an older age and a higher proportion of cardiovascular disease. After follow-up of (55.67±33.58) months, a total of 4 954 patients (18.8%) died, 1 537 patients (5.8%) underwent kidney transplantation, 128 patients (0.5%) were converted to peritoneal dialysis. Of the deaths, 990 (20.0%) were due to cardiovascular diseases, 498 (10.1%) to cerebrovascular diseases and 400 (8.1%) to infections, and cardiovascular disease was the main cause of death. RCS curve fitting of the relationship between serum sodium level and risk of death found that the all-cause mortality hazard ratio (HR) increased with decreasing or increasing serum sodium, and the optimal serum sodium was between 135 mmol/L and 140 mmol/L. Kaplan-Meier survival curve showed that the risk of all-cause death (Log-rank test, χ2=66.5, P<0.001), the risk of cardiovascular death (Log-rank test, χ2=31.5, P<0.001) and the risk of infection death (Log-rank test, χ2 =28.6, P<0.001) were significantly different among five groups. The 10-year cumulative survival rate was 63.0%, 71.5%, 72.5%, 67.8% and 61.4% in groups with different serum sodium levels from low to high, and the 10-year cumulative cardiovascular mortality rate was 9.6%, 6.2%, 5.5%, 7.3% and 11.7%, and the 10-year cumulative infection mortality rate was 4.9%, 3.2%, 1.7%, 2.8% and 3.9%. Multivariable Cox regression showed early serum sodium level >145 mmol/L was an independent relevant factor for all-cause death in MHD patients (HR=1.237, 95% CI 1.045-1.465, P=0.013). Conclusions MDH patients are more likely to develop hyponatremia in the early stage of dialysis. The cumulative survival rate of all-cause death, cardiovascular death and infection death in patients with predialysis serum sodium ≤130 mmol/L and >145 mmol/L within three months after initiation of dialysis is significantly lower than those in other levels. Early serum sodium >145 mmol/L is associated with higher mortality in MHD patients.
Objective To explore the relationship between prognostic nutritional index (PNI) and cognitive impairment (CI) in maintenance hemodialysis (MHD) patients. Methods It was a multicenter cross-sectional study that included adult patients who received MHD treatment at 18 hemodialysis centers in Guizhou province from June to October 2020 as the study subjects. Cognitive function was assessed with the mini-mental state examination score. According to the scale score, the patients were divided into CI group (≤27 scores) and non-CI group (>27 scores), and the differences between the two groups were compared. The patients were divided into Q1 (PNI<38.0), Q2 (38.0≤PNI<40.4), Q3 (40.4≤PNI<43.0), and Q4 (PNI≥43.0) groups based on the PNI quartiles. The PNI was estimated based on the serum albumin and lymphocyte count. Multivariate logistic regression analysis was used to analyze the correlation between PNI and CI, and subgroup analysis was conducted. Results A total of 1 740 MHD patients were enrolled in the study, with 1 021 males (62.9%) and 719 females (37.1%). The age was (55±15) years old. There were 411 patients (23.6%) with CI. The age, C-reactive protein, and the proportions of females, current smoking/drinking and diabetes in the CI group were significantly higher than those in the non-CI group, and the education level, blood lymphocyte count, blood prealbumin, serum albumin, serum creatinine, blood uric acid and PNI were significantly lower than those in the non-CI group (all P<0.05). The risk of CI in Q1 group was 1.88 times higher than that of Q4 group after adjusting for confounding factors such as sex, age, body mass index, education level, comorbidities, current smoking/drinking, dialysis age and C-reactive protein (OR=1.88, 95% CI 1.17-2.30, P=0.008). Subgroup analysis showed that there was an interaction between age and PNI on CI (P=0.040for interaction). Q1 group in the patients aged 18 to 45 years old had a higher risk of CI compared to Q4 group (OR=3.30, 95% CI 1.19-9.10). Conclusions Low PNI significantly increases the risk of CI in MHD patients, in particularly in the patients aged <45 years old.
Objective To explore the relationship between geriatric nutritional risk index (GNRI) and modified creatinine index (mCI) and all-cause mortality in maintenance hemodialysis (MHD) patients. Methods It was a prospective cohort study. The MHD patients aged≥50 years old at hemodialysis centers of eleven hospitals in Beijing from April to June 2017 were selected as subjects. Baseline clinical data of the patients were collected. The patients were divided into high GNRI group (≥98) and low GNRI group (<98), and high mCI group (≥20.16 mg·kg-1·d-1) and low mCI group (<20.16 mg·kg-1·d-1), and further divided into 4 groups: G1 group (high GNRI and high mCI), G2 group (high GNRI and low mCI), G3 group (low GNRI and high mCI) and G4 group (low GNRI and low mCI). The differences of clinical characteristics among the four groups were compared. The patients were followed-up until June 2018 or death or loss, and the endpoint event was all-cause mortality. Kaplan-Meier survival analysis was used to compare the differences of the cumulative survival rates among the four groups. A multivariate Cox regression model was used to analyze the relationship between GNRI and mCI and all-cause mortality. Results A total of 613 patients were included in the study, aged (63.65±7.78) years old (ranged from 50 to 81 years old), with 355 males (57.91%). The GNRI and mCI were (99.35±5.75) and (20.16±2.79) mg·kg-1·d-1, respectively. There were 232 patients (37.85%) in the G1 group, 177 patients (28.87%) in the G2 group, 95 patients (15.50%) in the G3 group, and 109 patients (17.78%) in the G4 group. There were statistically significant differences in age, sex, proportion of diabetes, proportion of coronary heart disease, body mass index, serum albumin and serum creatinine among the four groups (all P<0.05). A total of 69 patients (11.26%) died during a median follow-up time of 52(4, 52) weeks. Kaplan-Meier survival curve results showed that the mortality of patients with low GNRI was higher than that of patients with high GNRI (log-rank χ2 =26.956, P<0.001), and the mortality of patients with low mCI was higher than that of patients with high mCI (log-rank χ2 =25.842, P<0.001). The mortality was 3.45% in group G1, 10.73% in group G2, 9.47% in group G3, and 30.28% in group G4, and the differences among the four groups were statistically significant (log-rank χ2 =57.153, P<0.001). Multivariate Cox regression analysis results showed that as continuous variables, GNRI (HR=0.911, 95% CI 0.882-0.941, P<0.001) and mCI (HR=0.873, 95% CI 0.797-0.956, P=0.003) were correlated with all-cause death. As categorical variables, compared with high GNRI group and high mCI group, patients with low GNRI (HR=3.469, 95% CI 2.125-5.665, P<0.001) and low mCI (HR=3.255,95% CI 1.879-5.640, P<0.001) had higher risks of death. Compared with G1 group, patients in G2 group (HR=2.488, 95% CI 1.079-5.738, P=0.033) and G4 group (HR=9.449, 95% CI 4.362-20.470, P<0.001) had higher risks of death. Conclusions GNRI and mCI are independent predictive factors of all-cause mortality in MHD patients. The combination of GNRI and MCI can more accurately predict the risk of all-cause death in middle-aged and elderly MHD patients.
Objective To explore the association between increasing ultrafiltration rate before a long interdialytic interval and hospitalization risk in maintenance hemodialysis (MHD) patients. Methods A retrospective study was conducted to collect and analyze the demographic characteristics, disease-related, and laboratory indicators of MHD patients in the hemodialysis center of the Third Affiliated Hospital of Guangzhou Medical University from August to November 2020. The actual ultrafiltration rate higher than the planned ultrafiltration rate was defined as increased ultrafiltration rate. The patients were divided into increased ultrafiltration rate group and control group, and the differences of clinical data between the two groups were compared. The actual ultrafiltration rate >13 ml·kg-1·h-1 was defined as high filtration rate. Multivariate logistic regression analysis was used to assess the association between high ultrafiltration rate, increased ultrafiltration rate in MHD patients and occurrence of hospitalization (all cause, cardiovascular, and heart failure events). The receiver-operating characteristic curve was performed to evaluate the best cut point value of actual ultrafiltration rate and percentage of additional ultrafiltration rate for predicting intradialytic hypotension. Results A total of 126 MHD patients were included in the study, with age of (57.48±13.81) years old, including 67 males (53.2%) and 59 females (46.8%). There were 69 patients (54.8%) in the increased ultrafiltration rate group, and 57 patients (45.2%) in the control group. During 2-year follow-up period, there were 69 patients (54.8%) of all cause hospitalization, 37 patients (29.4%) of cardiovascular hospitalization, 25 patients (19.8%) of heart failure hospitalization, and 43 patients (34.1%) of intradialytic hypotension. The body mass index (t=4.343, P<0.001) and actual ultrafiltration rate (t=4.694, P<0.001) in the increased ultrafiltration rate group were higher than those in the control group. Multivariate logistic regression analysis results showed that high ultrafiltration rate was an independent related factor of cardiovascular hospitalization after adjusting for age, gender and cardiovascular disease (OR=2.871, 95% CI 1.202-6.854, P=0.018), and increasing ultrafiltration rate was an independent related factor of heart failure hospitalization after adjusting for age and serum albumin in the MHD patients (OR=0.302, 95% CI 0.112-0.812, P=0.018). When the actual ultrafiltration rate was ≤13 ml·kg-1·h-1, increasing ultrafiltration rate was correlated with the reduced risk of heart failure hospitalization (after adjusting for serum albumin, OR=0.044, 95% CI 0.005-0.360, P=0.004) and cardiovascular hospitalization (after adjusting for age, OR=0.052, 95% CI 0.010-0.259, P<0.001) in the MHD patients. Receiver-operating characteristic curve analysis results showed that the area under the curve of actual ultrafiltration rate for predicting the risk of intradialytic hypotension in MHD patients was 0.734 (95% CI 0.633-0.835, P<0.001) with the best cut point of 13.8 ml·kg-1·h-1, and the sensitivity and specificity of 0.488 and 0.951, respectively. When the actual ultrafiltration rate was ≤13 ml·kg-1·h-1, the area under the curve of percentage of additional ultrafiltration rate for predicting the risk of intradialytic hypotension in MHD patients was 0.746 (95% CI 0.603-0.889, P=0.001), with the best cut point of 26.0%, and the sensitivity and specificity of 0.579 and 0.914, respectively. Conclusions Increasing ultrafiltration rate before a long interdialytic interval and reduced risk of heart failure and cardiovascular hospitalization in MHD patients with the ultrafiltration rate ≤13 ml·kg-1·h-1 during 2-year follow-up period.
Objective To establish a conditional knockout mouse model of polycystic kidney disease 1 (Pkd1) gene based on CRISPR/Cas9 and Cre-loxP gene editing technology, and to provide an animal model for in-depth research on the role of Pkd1 gene in the development of polycystic kidney disease. Methods In-Fusion technology was used to construct a targeting vector. Corresponding gRNAs, Cas9 mRNAs, and donor vectors carrying the loxP site were prepared based on the Pkd1 gene, and injected into the fertilized eggs of C57BL/6N mice. The fertilized eggs were transferred to the fallopian tubes of female mice with pseudopregnancy. After the newborn mice were identified by PCR and sequencing analysis, Pkd1flox/flox F0 generation positive mice were selected. The F0 generation positive mice were bred with wild-type mice, and F1 generation heterozygous mice with Pkd1flox/+ genotype were selected for offspring. F2 generation homozygous mice with Pkd1flox/flox genotype were obtained through internal expansion, and then hybridized with Cre positive Ggt1/Cre mice. F3 generation mice with Pkd1flox/+Ggt1Cre genotype were obtained. F4 generation mice with Pkd1flox/flox Ggt1Cre genotype were obtained by self crossing or backcrossing with F2 generation Pkd1flox/flox, namely kidney-specific Pkd1 gene knockout mice (Ggt1-cKO mice). PCR method was used to identify the genotype of mice, and then the mice were divided into wild-type control (WT) group (n=6), Pkd1 homozygous control (PKD) group (n=6), and Ggt1-cKO knockout validation (CKO) group (n=6) according to the gene identification results. Real-time fluorescence quantitative PCR (RT-qPCR) was used to detect the expression of Pkd1 mRNA in the kidneys and other organs of mice in each group. HE staining was used to detect the pathological changes in renal tissues of mice in each group. The automatic biochemical detector was used to detect the blood urea nitrogen and serum creatinine levels of mice, and the kidney coefficient was calculated. Results The PCR detection results showed that the genotype of offspring mice in CKO group was consistent with Pkd1floxflox Ggt1Cre . Pkd1 gene was only specifically expressed in the kidney, but not in other tissues. The RT-qPCR results showed that the relative expression of Pkd1 mRNA in the renal medulla of CKO group was significantly lower than that of WT and PKD groups. The kidney volume of the CKO group had increased by about twice compared to the WT group. Under the microscope, it could be observed that there were multiple vacuoles of varying sizes and shapes in the kidneys of the CKO group, and there was a significant increase in the interstitial space of the medullary tissue. The kidney coefficient, blood urea nitrogen, and serum creatinine in the CKO group were significantly higher than those in the WT and PKD groups (all P<0.05). Conclusion Based on CRISPR/Cas9 and Cre-loxP gene editing technology, Pkd1 gene kidney conditional knockout mice can be successfully constructed, providing an animal model for further studying the action mechanism of Pkd1 gene in polycystic kidney disease.
A case of syphilis-related membranous proliferative glomerulonephritis is reported, presenting with fever, rash, generalized lymphadenopathy, and peripheral hypocytosis as the initial symptoms. The patient was admitted to the hospital and underwent various examinations to rule out lymphoma and other diseases. Subsequently, the patient developed edema with proteinuria. The toluidine red unheated serum test (TRUST) was 1∶4 (+) and the treponema pallidum particle agglutination (TPPA) test was >1∶160 (+). The pathological results of renal biopsy revealed membranous proliferative glomerulonephritis. The diagnosis of the patient was considered syphilitic nephropathy. Treatment with penicillin resulted in improvement of the condition. The coexistence of syphilitic nephropathy and membranous proliferative glomerulonephritis is rare and should be given careful attention in clinical practice. Antisyphilitic treatment improves the prognosis.
Atypical hemolytic uremic syndrome (aHUS) is characterized by non-immune microangiopathic hemolytic anemia, thrombocytopenia and acute kidney injury. IgA nephropathy (IgAN) is a common primary glomerular disease, while aHUS combined with IgAN is rare, and has been reported rarely in the past. This paper reported a case of children with aHUS combined with IgAN. In the acute stage, she was treated with plasma therapy and glucocorticoid. After remission, she was treated with glucocorticoid combined with immunosuppressants. During the follow-up period, aHUS did not recur, the renal function was normal, and urinary protein decreased to weakly positive.
The child was a 9-year-old girl, and sought medical advice due to "proteinuria for over a month". Renal biopsy result showed focal segmental glomerulosclerosis with diffuse vacuolization of glomerular podocytes and tubular epithelial cells. The child was diagnosed as type Ⅱ sialidosis with a compound heterozygote mutation in neuraminidase 1 gene for c.239C>T(p.Pro80Leu), c.220G>C(p.Val74Leu) and c.205A>G(p.Arg69Gly). Her father was proved to carry the first mutation, and her mother carried the other two, respectively. The report aims to improve the clinician's understanding of the rare disease. Early diagnosis can help avoid overuse of immunosuppressants, guide treatment reasonably and improve prognosis.
Alport syndrome (AS), also known as "eye-ear-kidney syndrome or hereditary nephritis", is a common hereditary disorder. AS is caused by pathogenic mutations of type Ⅳ collagen genes (COL4α3, COL4α4 and COL4α5), leading to defects in the basement membrane of glomeruli, cochlea, and ocular lens. Patients present with hematuria, proteinuria, and progressive renal failure. With the redefinition of AS and the clinical application of high-throughput sequencing technology, the prevalence of AS may be much higher than the previously recognized. The specific pathogenic mechanism of AS is unknown. Recent studies have showed that type Ⅳ collagen gene mutation may lead to kidney injury by causing abnormal basement membrane components, lipid deposition, energy metabolism disorders, endoplasmic reticulum stress, inflammation and fibrosis. Renin-angiotensin system inhibitor is the main therapy of AS, but the effect is not satisfactory. The new therapeutic strategies mainly include inhibition of abnormal collagen signal transduction, reduction of endoplasmic reticulum stress in podocytes, regulation of energy metabolism, antioxidant stress, anti-inflammation and fibrosis, gene and stem cell therapy. The paper reviewed the research progress on pathogenesis and new therapies of AS.
Chronic kidney disease (CKD) is a serious health problem worldwide, whereas there is still no efficient cure. The gut microbiota plays a crucial role in maintaining human health and disease resistance, and multiple studies have confirmed that the gut microbiota is closely related to the occurrence and development of CKD. Starting from the "gut-kidney axis" theory, this article provides a systematic review of the changes in gut microbiota composition and function in patients with CKD, such as a decrease in the abundance of butyrate-producing bacteria Roseburia and Faecalibacterium prausnitzii. Besides that, the article explores the mechanisms by which the gut microbiota affects CKD progression, such as inflammation and immunity, and also describes the application methods of using the gut microbiota as a therapeutic target for CKD, such as fecal microbiota transplantation, microecologics, and dietary therapy, in order to provide microbial- based targets for the clinical diagnosis and treatment of CKD.
