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Journal of Diabetes and Metabolic... Jun 2021Recent trials have demonstrated the possible improvements in lipid profile & anthropometric indices after probiotics supplementation. We aimed to reanalyze the related... (Review)
Review
PURPOSE
Recent trials have demonstrated the possible improvements in lipid profile & anthropometric indices after probiotics supplementation. We aimed to reanalyze the related literature to explore the efficacy of probiotics in Diabetic Nephropathy (DN) patients.
METHODS
PubMed, Embase, Web of science, google scholar, Scopus, and Cochrane Library databases were systematically searched to find the related data on diabetic nephropathy population. All Randomized controlled trials (RCTs) that investigated the effect of probiotics on serum lipid markers (High-Density Lipoprotein [HDL], Triglyceride, Total Cholesterol, TC-to-HDL ratio, Low-Density Lipoprotein, Very Low-Density Lipoprotein) and anthropometric indices (Body Weight, Body Mass Index, waist-to-hip ratio) were included (PROSPERO No.CRD42020186189). Meta-analysis was performed using the random-effect model.
RESULTS
Of 156 studies, seven were eligible for inclusion. Lipid biomarkers had a marginal reduction (except for HDL; WMD = 2.59 mg/dl; 95% CI = -0.28, 5.47; ); whereas anthropometric indices increased in a non-significant manner.
CONCLUSION
There is limited evidence to support the efficacy of probiotics for the modulation of lipid profile and anthropometric indices in DN patients.
GRAPHICAL ABSTRACT
Probiotics did not beneficial effect on lipid profile & anthropometric markers in Diabetic Nephropathy; anyway, more trials should be conducted.
SUPPLEMENTARY INFORMATION
The online version contains supplementary material available at 10.1007/s40200-021-00765-8.
PubMed: 34222095
DOI: 10.1007/s40200-021-00765-8 -
Molecular Biology Reports Aug 2012So far, case-control studies on the association between glucose transporter 1 (GLUT1) gene single nucleotide polymorphisms (SNPs) and diabetic nephropathy (DN) have... (Meta-Analysis)
Meta-Analysis Review
So far, case-control studies on the association between glucose transporter 1 (GLUT1) gene single nucleotide polymorphisms (SNPs) and diabetic nephropathy (DN) have generated considerable controversy. To clarify the linkage of GLUT1 SNPs on the risk of DN, a systematic review and meta-analysis was performed. A comprehensive literature search of electronic databases was conducted to obtain relative studies. Nine case-control studies were included. Significant differences were found between XbaI SNP (rs841853) and increased risk of DN in all genetic models. Subgroup analyses for Caucasians population and DN from both type 1 and type 2 diabetes also revealed positive results. For Enh2-1 SNP (rs841847), Enh2-2 SNP (rs841848) and HaeIII SNP (rs1385129), obvious linkages were demonstrated in recessive model. However, analysis for the association between HpyCH4V SNP (rs710218) and the susceptibility of DN showed no significance. Likewise, negative outcome was also found in the assessment for the influence of XbaI or Enh2-2 SNP on the pathogenesis progress of DN. The evidence currently available shows that XbaI, Enh2 and HaeIII SNPs, but not HpyCH4V SNP, in GLUT1 gene may be genetic susceptibility to DN. However, data does not support the association between either XbaI or Enh2-2 SNP and the severity of DN.
Topics: Alleles; Diabetic Nephropathies; Gene Frequency; Genetic Predisposition to Disease; Genotype; Glucose Transporter Type 1; Humans; Polymorphism, Single Nucleotide; Publication Bias
PubMed: 22707195
DOI: 10.1007/s11033-012-1711-z -
Medicine Apr 2017The existing evidence indicates increased levels of transforming growth factor beta 1 (TGF-β1) in patients with type 2 diabetes mellitus (T2DM) and those with type 2... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
The existing evidence indicates increased levels of transforming growth factor beta 1 (TGF-β1) in patients with type 2 diabetes mellitus (T2DM) and those with type 2 diabetic nephropathy (T2DN); yet no meta-analysis displays a reliable result. Here we conducted a meta-analysis to evaluate characteristic changes of TGF-β1 in T2DM and diabetic nephropathy.
METHODS
A systematic search was conducted for eligible studies, which reported the association of TGF-β1 withT2DM and T2DN patients, in PubMed, Wangfang, Chinese-Cqvip, and China National Knowledge Infrastructure database, from February 1, 1991 to December 15, 2015. The association of serum and urine TGF-β1 in T2DM and T2DN patients should be evaluated in case-control studies. The Newcastle-Ottawa Scale was used to access the quality of the included studies, and pooling data were synthesized as standard mean difference (SMD) and 95% confidence interval (CI). The collected data were synthesized according to Cochrane Handbook for Systematic Reviews criteria. Subgroup analysis was conducted by albuminuria and ethnicity. Regression analysis and sensitivity analysis were used to explore the sources of heterogeneity. Publication bias was judged by the Egger test.
RESULTS
Sixty-three case-control studies of 364 T2DM patients (1604 T2DN patients) and 2100 healthy controls were included for meta-analysis. Compared with the controls, the cases had increased TGF-β1 levels in both serum (T2DM: SMD 1.78 μg/L; 95% CI 0.98-2.59, P < .001; T2DN: SMD 4.70 μg/L, 95% CI 3.55-5.85, P < .001) and urine samples (T2DM: SMD 1.27 pg/mg.creatinine, 95% CI 0.16-2.38, P < .001; SMD 1.19 ng/L, 95% CI 0.77-1.62, P < .001; T2DN: SMD 3.14 pg/mg.creatinine, 95% CI 2.15-4.13, P < .001; SMD 4.50 ng/L, 95% CI 3.16-5.83, P < .001). The increase of serum TGF-β1 persisted in patients with either microalbuminuria or macroalbuminuria (all P < .001) in Chinese and non-Chinese population. High heterogeneity exists in some comparisons and small-sample studies.
CONCLUSIONS
Patients with T2DM and those with albuminuria, Chinese or non-Chinese, had increased serum and urine TGF-β1 levels.
Topics: Albuminuria; Biomarkers; Case-Control Studies; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Female; Humans; Male; Prognosis; Transforming Growth Factor beta1
PubMed: 28403088
DOI: 10.1097/MD.0000000000006583 -
Frontiers in Endocrinology 2019This study investigated the relationship strength between hypothyroidism and cardiovascular and renal outcomes in diabetic patients. The electronic databases PubMed,...
This study investigated the relationship strength between hypothyroidism and cardiovascular and renal outcomes in diabetic patients. The electronic databases PubMed, EmBase, and Cochrane library were screened for relevant studies published before November 2018. The outcomes included major cardiovascular events (MACEs), all-cause mortality, cardiac death, stroke, diabetic nephropathy (DN), diabetic retinopathy (DR), and chronic kidney disease (CKD). The pooled results for all outcomes were calculated using random-effects models. A total of eight studies met the inclusion criteria. The summary results indicated that hypothyroidism was not associated with the risk of MACEs (OR:1.21; 95%CI:0.68-2.16; = 0.514), all-cause mortality (OR:1.27; 95%CI:0.93-1.74; = 0.136), cardiac death (OR:1.16; 95%CI:0.89-1.52; = 0.271), stroke (OR:0.96; 95%CI: 0.49-1.88; = 0.915), and DN (OR:1.71; 95%CI:0.37-7.90; = 0.490). There was a significant association between hypothyroidism and the risk of DR (OR:1.73; 95%CI:1.08-2.77; = 0.023) and CKD (OR:1.22; 95%CI:1.10-1.36; < 0.001). These findings indicate that diabetic patients with hypothyroidism have an increased risk of DR and CKD. Additional large-scale prospective studies should be carried out to verify the prognosis of patients with diabetes and hypothyroidism.
PubMed: 31998230
DOI: 10.3389/fendo.2019.00889 -
BMC Endocrine Disorders Aug 2021Diabetic nephropathy (DN) is one of the most serious microvascular complications of diabetes, valsartan and α-lipoic acid alone or in combination has been used for the... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Diabetic nephropathy (DN) is one of the most serious microvascular complications of diabetes, valsartan and α-lipoic acid alone or in combination has been used for the treatment of patients with DN. However, some results in these clinical reports were still controversial. The purpose of this study was to evaluate the efficacy of valsartan combined with α-lipoic acid on renal function in patients with DN.
METHODS
We searched the electronic databases including PubMed, Sciencedirect, EMBASE, Cochrane library, Chinese national knowledge infrastructure (CNKI) and Wanfang databases, and the publication deadline was limited to January 2020. Randomized controlled trials (RCTs) evaluating the effects of valsartan combined with α-lipoic acid in DN patients were included. Pooled estimates were conducted using a fixed or random effect model. The outcomes included urinary albumin excretion rate (UAER), and the level of urinary albumin, β-microglobulin (β-MG), hypersensitive C-reactive protein (hs-CRP) and oxidative stress.
RESULTS
11 studies with 1294 participants were included in this study. The pooled analysis indicated that α-lipoic acid combined with valsartan could remarkably reduce UAER (P < 0.00001, SMD = -1.95, 95%CI = -2.55 to - 1.20; P = 0.03, SMD = -0.85, 95%CI = -1.59 to - 0.1) and the level of urinary albumin (P = 0.001, SMD = -1.48, 95%CI = - 2.38 to - 0.58; P = 0.01, SMD = -1.67, 95%CI = -3.00 to - 0.33), β-MG (P < 0.001,SMD = - 2.59, 95%CI = -3.78 to - 1.40; P = 0.03, SMD = -0.48, 95%CI = -0.93 to - 0.04) when compared with valsartan or lipoic acid monotherapy in patients with DN. However, there was no significant difference in the level of hs-CRP among the three therapies (P = 0.06, SMD = -2.80, 95%CI = -5.67 to 0.07; P = 0.10, SMD = -0.42, 95%CI = - 0.92 to 0.08). In addition, α-lipoic acid combined with valsartan markedly increased the level of SOD (P = 0.03, SMD = 1.24, 95%CI = 0.32 to 1.03; P = 0.0002, SMD = 0.68, 95%CI = 0.32 to 1.03) and T-AOC (P < 0.00001, SMD = 0.89, 95%CI = 0.62 to 1.16; P = 0.02, SMD = 0.58, 95%CI = 0.10 to1.07), and reduced the level of MDA(P = 0.0002, SMD = -1.99, 95%CI = -3.02 to - 0.96; P = 0.0001, SMD = -0.69, 95%CI = -1.04 to - 0.34).
CONCLUSIONS
α-lipoic acid combined with valsartan could significantly reduce the level of urinary albumin and oxidative stress, increase antioxidant capacity and alleviate renal function damage in patients with DN, and this will provide a reference for the selection of treatment drugs for DN.
Topics: Antihypertensive Agents; Antioxidants; Diabetic Nephropathies; Drug Therapy, Combination; Humans; Kidney; Thioctic Acid; Valsartan
PubMed: 34465338
DOI: 10.1186/s12902-021-00844-0 -
Computational Intelligence and... 2022Long noncoding RNA (lncRNA) is involved in the occurrence and development of diabetic kidney disease (DKD). It is necessary to identify the expression of lncRNA from DKD... (Review)
Review
BACKGROUND
Long noncoding RNA (lncRNA) is involved in the occurrence and development of diabetic kidney disease (DKD). It is necessary to identify the expression of lncRNA from DKD patients through systematic reviews, and then carry out silico analyses to recognize the dysregulated lncRNA and their associated pathways.
METHODS
The study searched Pubmed, Embase, Cochrane Library, WanFang, VIP, CNKI, and CBM to find lncRNA studies on DKD published before March 1, 2021. Systematic review of the literature on this topic was conducted to determine the expression of lncRNA in DKD and non-DKD controls. For the dysregulated lncRNA in DKD patients, silico analysis was performed, and lncRNA2Target v2.0 and starBase were used to search for potential target genes of lncRNA. The Encyclopedia of Genomics (KEGG) pathway enrichment analysis was performed to better identify dysregulated lncRNAs in DKD and determine the associated signal pathways.
RESULTS
According to the inclusion and exclusion criteria, 28 publications meeting the eligibility criteria were included in the systematic evaluation. A total of 3,394 patients were enrolled in this study, including 1,238 patients in DKD group, and 1,223 diabetic patients, and 933 healthy adults in control group. Compared with the control, there were eight lncRNA disorders in DKD patients (MALAT1, GAS5, MIAT, CASC2, NEAT1, NR_033515, ARAP1-AS2, and ARAP1-AS1). In addition, five lncRNAs (MALAT1, GAS5, MIAT, CASC2, and NEAT1) participated in disease-related signal pathways, indicating their role in DKD. . This study showed that there were eight lncRNAs in DKD that were persistently dysregulated, especially five lncRNAs which were closely related to the disease. Although systematic review included 28 studies that analyzed the expression of lncRNA in DKD-related tissues, the potential of these dysregulated lncRNAs as biomarkers or therapeutic targets for DKD remains to be further explored. Trial registration. PROSPERO (CRD42021248634).
Topics: Adult; Biomarkers; Diabetes Mellitus; Diabetic Nephropathies; Female; Humans; Male; RNA, Long Noncoding; Signal Transduction
PubMed: 35528328
DOI: 10.1155/2022/8400106 -
BMC Nephrology Jul 2023
PubMed: 37495940
DOI: 10.1186/s12882-023-03274-3 -
The Cochrane Database of Systematic... Sep 2018Diabetes is the commonest cause of chronic kidney disease (CKD). Both conditions commonly co-exist. Glucometabolic changes and concurrent dialysis in diabetes and CKD... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Diabetes is the commonest cause of chronic kidney disease (CKD). Both conditions commonly co-exist. Glucometabolic changes and concurrent dialysis in diabetes and CKD make glucose-lowering challenging, increasing the risk of hypoglycaemia. Glucose-lowering agents have been mainly studied in people with near-normal kidney function. It is important to characterise existing knowledge of glucose-lowering agents in CKD to guide treatment.
OBJECTIVES
To examine the efficacy and safety of insulin and other pharmacological interventions for lowering glucose levels in people with diabetes and CKD.
SEARCH METHODS
We searched the Cochrane Kidney and Transplant Register of Studies up to 12 February 2018 through contact with the Information Specialist using search terms relevant to this review. Studies in the Register are identified through searches of CENTRAL, MEDLINE, and EMBASE, conference proceedings, the International Clinical Trials Register (ICTRP) Search Portal and ClinicalTrials.gov.
SELECTION CRITERIA
All randomised controlled trials (RCTs) and quasi-RCTs looking at head-to-head comparisons of active regimens of glucose-lowering therapy or active regimen compared with placebo/standard care in people with diabetes and CKD (estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m) were eligible.
DATA COLLECTION AND ANALYSIS
Four authors independently assessed study eligibility, risk of bias, and quality of data and performed data extraction. Continuous outcomes were expressed as post-treatment mean differences (MD). Adverse events were expressed as post-treatment absolute risk differences (RD). Dichotomous clinical outcomes were presented as risk ratios (RR) with 95% confidence intervals (CI).
MAIN RESULTS
Forty-four studies (128 records, 13,036 participants) were included. Nine studies compared sodium glucose co-transporter-2 (SGLT2) inhibitors to placebo; 13 studies compared dipeptidyl peptidase-4 (DPP-4) inhibitors to placebo; 2 studies compared glucagon-like peptide-1 (GLP-1) agonists to placebo; 8 studies compared glitazones to no glitazone treatment; 1 study compared glinide to no glinide treatment; and 4 studies compared different types, doses or modes of administration of insulin. In addition, 2 studies compared sitagliptin to glipizide; and 1 study compared each of sitagliptin to insulin, glitazars to pioglitazone, vildagliptin to sitagliptin, linagliptin to voglibose, and albiglutide to sitagliptin. Most studies had a high risk of bias due to funding and attrition bias, and an unclear risk of detection bias.Compared to placebo, SGLT2 inhibitors probably reduce HbA1c (7 studies, 1092 participants: MD -0.29%, -0.38 to -0.19 (-3.2 mmol/mol, -4.2 to -2.2); I = 0%), fasting blood glucose (FBG) (5 studies, 855 participants: MD -0.48 mmol/L, -0.78 to -0.19; I = 0%), systolic blood pressure (BP) (7 studies, 1198 participants: MD -4.68 mmHg, -6.69 to -2.68; I = 40%), diastolic BP (6 studies, 1142 participants: MD -1.72 mmHg, -2.77 to -0.66; I = 0%), heart failure (3 studies, 2519 participants: RR 0.59, 0.41 to 0.87; I = 0%), and hyperkalaemia (4 studies, 2788 participants: RR 0.58, 0.42 to 0.81; I = 0%); but probably increase genital infections (7 studies, 3086 participants: RR 2.50, 1.52 to 4.11; I = 0%), and creatinine (4 studies, 848 participants: MD 3.82 μmol/L, 1.45 to 6.19; I = 16%) (all effects of moderate certainty evidence). SGLT2 inhibitors may reduce weight (5 studies, 1029 participants: MD -1.41 kg, -1.8 to -1.02; I = 28%) and albuminuria (MD -8.14 mg/mmol creatinine, -14.51 to -1.77; I = 11%; low certainty evidence). SGLT2 inhibitors may have little or no effect on the risk of cardiovascular death, hypoglycaemia, acute kidney injury (AKI), and urinary tract infection (low certainty evidence). It is uncertain whether SGLT2 inhibitors have any effect on death, end-stage kidney disease (ESKD), hypovolaemia, fractures, diabetic ketoacidosis, or discontinuation due to adverse effects (very low certainty evidence).Compared to placebo, DPP-4 inhibitors may reduce HbA1c (7 studies, 867 participants: MD -0.62%, -0.85 to -0.39 (-6.8 mmol/mol, -9.3 to -4.3); I = 59%) but may have little or no effect on FBG (low certainty evidence). DPP-4 inhibitors probably have little or no effect on cardiovascular death (2 studies, 5897 participants: RR 0.93, 0.77 to 1.11; I = 0%) and weight (2 studies, 210 participants: MD 0.16 kg, -0.58 to 0.90; I = 29%; moderate certainty evidence). Compared to placebo, DPP-4 inhibitors may have little or no effect on heart failure, upper respiratory tract infections, and liver impairment (low certainty evidence). Compared to placebo, it is uncertain whether DPP-4 inhibitors have any effect on eGFR, hypoglycaemia, pancreatitis, pancreatic cancer, or discontinuation due to adverse effects (very low certainty evidence).Compared to placebo, GLP-1 agonists probably reduce HbA1c (7 studies, 867 participants: MD -0.53%, -1.01 to -0.06 (-5.8 mmol/mol, -11.0 to -0.7); I = 41%; moderate certainty evidence) and may reduce weight (low certainty evidence). GLP-1 agonists may have little or no effect on eGFR, hypoglycaemia, or discontinuation due to adverse effects (low certainty evidence). It is uncertain whether GLP-1 agonists reduce FBG, increase gastrointestinal symptoms, or affect the risk of pancreatitis (very low certainty evidence).Compared to placebo, it is uncertain whether glitazones have any effect on HbA1c, FBG, death, weight, and risk of hypoglycaemia (very low certainty evidence).Compared to glipizide, sitagliptin probably reduces hypoglycaemia (2 studies, 551 participants: RR 0.40, 0.23 to 0.69; I = 0%; moderate certainty evidence). Compared to glipizide, sitagliptin may have had little or no effect on HbA1c, FBG, weight, and eGFR (low certainty evidence). Compared to glipizide, it is uncertain if sitagliptin has any effect on death or discontinuation due to adverse effects (very low certainty).For types, dosages or modes of administration of insulin and other head-to-head comparisons only individual studies were available so no conclusions could be made.
AUTHORS' CONCLUSIONS
Evidence concerning the efficacy and safety of glucose-lowering agents in diabetes and CKD is limited. SGLT2 inhibitors and GLP-1 agonists are probably efficacious for glucose-lowering and DPP-4 inhibitors may be efficacious for glucose-lowering. Additionally, SGLT2 inhibitors probably reduce BP, heart failure, and hyperkalaemia but increase genital infections, and slightly increase creatinine. The safety profile for GLP-1 agonists is uncertain. No further conclusions could be made for the other classes of glucose-lowering agents including insulin. More high quality studies are required to help guide therapeutic choice for glucose-lowering in diabetes and CKD.
Topics: Cause of Death; Diabetes Mellitus; Diabetic Nephropathies; Dipeptidyl-Peptidase IV Inhibitors; Glipizide; Glucagon-Like Peptide 1; Glycated Hemoglobin; Humans; Hypoglycemic Agents; Insulin; Randomized Controlled Trials as Topic; Renal Insufficiency, Chronic; Sitagliptin Phosphate; Sodium-Glucose Transporter 2; Sodium-Glucose Transporter 2 Inhibitors; Thiazolidinediones
PubMed: 30246878
DOI: 10.1002/14651858.CD011798.pub2 -
International Journal of Clinical... Nov 2021Diabetic nephropathy (DN) is one of the microvascular complications of diabetes, leading to renal failure. In this study, we sought to systematically investigate the... (Meta-Analysis)
Meta-Analysis
AIM
Diabetic nephropathy (DN) is one of the microvascular complications of diabetes, leading to renal failure. In this study, we sought to systematically investigate the cytokine gene polymorphisms association with DN.
METHODS
A structured bibliographic search on PubMed, Scopus, and EMBASE databases has been performed to identify related papers. The odds ratio and corresponding 95% confidence intervals (CIs) were calculated to estimate the association.
RESULTS
Overall, the pooled results showed that the dominant models of TNF-α rs1800629, IL-1β rs16944, IL-8 rs4073, and IL-10 rs1800896 were associated with increased susceptibility to DN. Also, the pooled analyses of the mutant allele vs wild allele of TNF-α rs1800629, rs1799964, IL-1β rs16944, and IL-8 rs4073 were associated with increased susceptibility to DN. Rs1800629, rs16944, rs4073, and rs1800896 polymorphisms were significantly associated with DN susceptibility, suggesting its potential use as a genetic risk marker in the population.
Topics: Cytokines; Diabetes Mellitus; Diabetic Nephropathies; Genetic Predisposition to Disease; Humans; Polymorphism, Single Nucleotide; Tumor Necrosis Factor-alpha
PubMed: 34309136
DOI: 10.1111/ijcp.14634 -
Frontiers in Pharmacology 2023Diabetic nephropathy (DN) is the main cause of chronic kidney disease (CKD) and end-stage renal failure (ESRF), and the control of disease progression and adverse...
Diabetic nephropathy (DN) is the main cause of chronic kidney disease (CKD) and end-stage renal failure (ESRF), and the control of disease progression and adverse events during treatment needs to be improved. This study aimed to systematically evaluate the clinical efficacy and safety of Niaoduqing granules (NDQG) in the treatment of diabetic kidney disease (DKD). Randomized controlled trials (RCTs) of NDQG for DKD from Chinese and English databases up to 31 August 2022 were included. The quality of the literature was assessed using the risk of bias tool of the Cochrane Handbook. At a 95% confidence interval (CI), relative risk (RR) and Cohen's d were used for the categorical and continuous variables, respectively, and Stata 16.0 software was used for statistical analysis. A funnel plot and Egger's tests were used to assess publication bias. A total of 4,006 patients were included in 52 RCTs, including 1,987 cases in the control group and 2,019 cases in the treatment group. Compared with conventional treatment (CT), combined NDQG therapy is more effective in improving clinical efficiency [RR = 1.23, 95% confidence interval (1.17, 1.29), < 0.001, = 53.17%], kidney function (urinary albumin excretion rate [SMD = -0.90, 95% CI (-1.14, -0.66), < 0.001, = 78.19%], 24hUTP levels [SMD = -0.81, 95% CI (-1.08, -0.55), < 0.001, = 87.08%], blood urea nitrogen [SMD = -0.54, 95% CI (-0.69, -0.39), < 0.01, = 77.01%], SCr [SMD = -0.68, 95% CI (-0.90, -0.45), < 0.001, = 89.97%], CCr [SMD = 0.76, 95% CI (0.10,1.42), = 0.02, = 95.97%], and Cys-C [SMD = -1.32, 95% CI (-2.25, -0.40), = 0.01, = 93.44%]), the level of glucose metabolism (fasting blood glucose [SMD = -0.18, 95% CI (-0.38, 0.03), = 0.10, = 71.18%] and HbA1c [SMD = -0.42, 95% CI (-0.86, -0.02), = 0.06, = 81.64%]), the level of lipid metabolism (total cholesterol [SMD = -0.70, 95% CI (-1.01, -0.39), < 0.001, = 86.74%] and triglyceride [SMD = -0.61, 95% CI (-0.87,-0.36), < 0.001, = 80.64%]), inflammatory factors (Hs-CRP [SMD = -1.00, 95% CI (-1.54, -0.46), < 0.001, = 86.81%], IL-18 [SMD = -1.25, 95% CI (-1.58, -0.92), < 0.001, = 0], and TNF-α [SMD = -1.28, 95% CI (-1.64, -0.91), < 0.001, = 75.73%]), and indicators of oxidative stress (malondialdehyde [SMD = -0.88, 95% CI (-1.22, -0.54), < 0.001, = 66.01%] and advanced oxidation protein products [SMD = -0.92, 95% CI (-1.85, 0.00), < 0.001, = 90.68%]). In terms of improving uric acid [SMD = -1.59, 95% CI (-3.45, 0.27), = 0.09, = 94.67%], 2hPG [SMD = -0.04, 95% CI (-0.61, 0.53), = 0.89, = 84.33%], HDL-C [SMD = 0.71, 95% CI (0.02, 1.40), = 0.04, = 87.43%], Hb [SMD = 0.11, 95% CI (-0.10, 0.32), = 0.32, = 0.00]), and superoxide dismutase [SMD = 1.32, 95% CI (0.44, 2.20), < 0.001, = 93.48%], the effect is not obvious. Adjuvant treatment with NDQG did not increase the incidence of adverse reactions in the control group [SMD = 0.98, 95% CI (0.71, 1.34), = 0.89, = 1.59%]. Obvious publication bias was detected by funnel plot and Egger's test. Our meta-analysis showed that adjuvant treatment with NDQG has more advantages than conventional treatment alone in the DKD treatment, which could improve clinical efficiency, kidney function, the level of glucose metabolism, the level of lipid metabolism, inflammatory factors, and oxidative stress indicators. At the same time, it also showed that NDQG are relatively safe. However, more high-quality studies are needed to provide more reliable evidence for clinical use. : https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42022373726, identifier CRD42022373726.
PubMed: 37475716
DOI: 10.3389/fphar.2023.1180751