Probiotics improve renal function, glucose, lipids, inflammation and oxidative stress in diabetic kidney disease: a systematic review and meta-analysis

Abstract

Aims The role of probiotics in the management of diabetic kidney disease (DKD) has been shown. Several current trials are investigating the effect of probiotics, which are widely used to modulate biomarkers of renal function, glucose, lipids, inflammation and oxidative stress in patients with DKD. However, their findings are controversial. This study aimed to systematically evaluate the impact of probiotics on patients with DKD via meta-analysis. Methods PubMed, The Cochrane Library, Web of Science, Scopus, Embase, China National Knowledge Infrastructure, Chinese Wanfang Database and Chinese VIP Database were searched for relevant studies from the establishment of these databases to September 2021. The pooled results evaluated the impact of probiotics on renal function, glucose, lipids, inflammation and oxidative stress indicators in patients with DKD. Additionally, subgroup analysis was performed based on intervention duration, probiotic dose and probiotic consumption patterns, respectively. Results Ten trials that included 552 participants were identified for analysis. Compared with the controls, probiotics significantly decreased serum creatinine (Scr) [WMD = −0.17 mg/dL; 95%CI = −0.29, −0.05; p = 0.004], blood urea nitrogen (BUN) [WMD = −1.36 mg/dL; 95%CI = −2.20, −0.52; p = 0.001], cystatin C (Cys C) [WMD = −29.50 ng/mL; 95%CI = −32.82, −26.18; p < 0.00001], urinary albumin/creatinine ratio (UACR) [WMD = −16.05 mg/g; 95%CI = −27.12, −4.99; p = 0.004] and natrium (Na) [WMD = −0.94 mmol/L; 95%CI = −1.82, −0.05; p = 0.04] in patients with DKD. Enhanced glycemic control was observed in patients with DKD receiving probiotics compared with controls, as demonstrated by reduced levels of fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), homeostasis model of assessment-estimated insulin resistance (HOMA-IR), and increased quantitative insulin sensitivity check index (QUICKI). Probiotics affected lipid metabolism parameters with decreasing triglycerides (TG), total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-c) levels in patients with DKD. Probiotics could also could improve inflammation and oxidative stress by decreasing high-sensitivity C-reactive protein (hs-CRP), plasma malondialdehyde (MDA), total antioxidant capacity (TAC), glutathione (GSH) and nitric oxide (NO). Additionally, subgroup analysis showed that those who received multiple species probiotics had a statistically significant difference in BUN, FPG, HOMA-IR, high-density lipoprotein cholesterol (HDL-c), MDA, TAC, and NO. Meanwhile, Scr, LDL-c, HDL-c, MDA, and TAC were ameliorated when the intervention duration was more than eight weeks and BUN, FPG, HOMA-IR, and MDA were improved when the probiotic dose was greater than four billion CFU/day. Conclusions ...

Renal Health Improvement in Diabetes through Microbiome Modulation of the Gut–Kidney Axis with Biotics: A Systematic and Narrative Review of Randomized Controlled Trials

“…This, coupled with the low number of trials per marker, made the single study that reported significant benefits on serum Cr, BUN, Cys-C, and urine total protein [ 69 ] a large influence on the overall pooled results. In an earlier review, Wang et al [ 70 ] reached similar conclusions to Dai et al [ 34 ], where the team reported that probiotics were beneficial in improving renal function in DN patients by increasing eGFR and decreasing both serum Cr and BUN; however, this contrasts with the previously described findings of Tarrahi et al [ 68 ] concerning eGFR and BUN. Less recent reviews [ 71 , 72 ] included fewer trials and did not show promise with respect to any renal biomarker, likely owing to smaller sample sizes.…”

“…Similar results were found by Tarrahi et al [ 68 ] from their analysis of seven trials administering probiotics in DN patients, revealing significant changes of −0.18 mg/dL (95% CI: −0.26; −0.09) in serum Cr, but no change in BUN or GFR. Contrarily, in their recent meta-analysis of DKD patients, Dai et al [ 34 ] reported that probiotics improved multiple biomarkers of renal injury, including serum Cr, BUN, Cys-C, the Alb/Cr ratio, and sodium, but this analysis stemmed from the exclusion of a study of elderly DN patients by [ 69 ] due to language-based exclusion criteria. This, coupled with the low number of trials per marker, made the single study that reported significant benefits on serum Cr, BUN, Cys-C, and urine total protein [ 69 ] a large influence on the overall pooled results.…”

“…Recently, researchers have also successfully investigated their role in obesity-related kidney disease and hypertension [ 29 , 30 ]. Although other studies have investigated the effect of multiple nutraceuticals on metabolic biomarkers and outcomes in participants with selected renal diseases, there is limited research in the literature providing a qualitative yet comparative summary of all three supplementation types in all diabetic patients [ 31 , 32 , 33 , 34 , 35 ]. This systematic review of randomized controlled trials (RCTs) aims to summarize and analyze whether probiotic, prebiotic, and synbiotic supplementation produces a clinically significant, beneficial effect on biomarkers of renal function in patients with diabetes.…”

Promising Tactics with Certain Probiotics for the Treatment of Nephropathy in Hematopoietic Stem Cell Transplantation

“…Certain therapeutic methods might alter the composition of the gut microbiota and promote the treatment of nephrotoxicity induced by cyclosporine (Figure 2). Altering the gut microbiota by using probiotics can delay the progression of renal injury and reduce inflammation and/or oxidative stress [30]. For example, the administration of Lactobacillus plantarum can decrease the risk of developing a gut-mediated condition in children undergoing HSCT [31].…”

The Effect of Allograft Inflammatory Factor-1 on Inflammation, Oxidative Stress, and Autophagy via miR-34a/ATG4B Pathway in Diabetic Kidney Disease

“…Based on the reports mentioned above, although increasing evidence has suggested that dysregulated autophagy in glomerular and tubular cells is strongly associated with the pathogenesis of DKD, the exact mechanism of autophagy remains to be elucidated. An increasing number of studies have shown that there is an interplay between inflammation, oxidative stress, and autophagy which play an important role in DKD [ 24 , 25 ]. Autophagy as an evolutionarily conserved cellular process protects renal cells from damage by inhibiting oxidative stress and inflammation in DKD [ 26 , 27 ].…”