Effect of Low-Protein Diet and Inulin on Microbiota and Clinical Parameters in Patients with Chronic Kidney Disease.
Study Goal
The researchers aimed to evaluate the effects of a low-protein diet (LPD) with or without the prebiotic inulin on gut microbiota and clinical parameters in chronic kidney disease (CKD) patients.
Results Summary
The LPD modified gut microbiota, increased beneficial bacteria, and improved inflammatory and metabolic markers, with additional benefits observed when combined with inulin, such as reduced serum uric acid and C-reactive protein.
Population
16 CKD patients (9 treated with LPD + inulin, 7 with LPD alone) and 16 healthy controls.
Effective Dosage
LPD (0.6 g/kg/day), inulin (19 g/day).
Duration
6 months.
Interactions
None mentioned.
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
low-protein diet (LPD) (0.6 g/kg/day) | increase | frequencies of Akkermansiaceae and Bacteroidaceae | CKD patients | - | significantly increase | #1 |
low-protein diet (LPD) (0.6 g/kg/day) | decrease | frequencies of Christensenellaceae, Clostridiaceae, Lactobacillaceae, and Pasteurellaceae | CKD patients | - | decrease | #2 |
low-protein diet (LPD) (0.6 g/kg/day) with oral inulin intake (19 g/day) | increase | Bifidobacteriaceae | CKD patients | - | increased | #3 |
low-protein diet (LPD) (0.6 g/kg/day) and inulin (19 g/day) | decrease | serum uric acid (SUA) | patients treated with LPD and inulin | - | significant reduction | #4 |
low-protein diet (LPD) (0.6 g/kg/day) and inulin (19 g/day) | decrease | C-reactive protein (CRP) | patients treated with LPD and inulin | - | significant reduction | #5 |
low-protein diet (LPD) (0.6 g/kg/day) and inulin (19 g/day) | increase | SF-36 (physical role functioning) | patients treated with LPD and inulin | - | improvement | #6 |
low-protein diet (LPD) (0.6 g/kg/day) and inulin (19 g/day) | increase | SF-36 (general health perceptions) | patients treated with LPD and inulin | - | improvement | #7 |
low-protein diet (LPD) (0.6 g/kg/day) | increase | serum bicarbonate | patients treated with LPD | - | significant increase | #8 |
low-protein diet (LPD) (0.6 g/kg/day) and inulin (19 g/day) | increase | serum bicarbonate | patients treated with LPD and inulin | - | significant increase | #9 |
low-protein diet (LPD) (0.6 g/kg/day) and inulin (19 g/day) | decrease | circulating tumor necrosis factor alpha (TNF-α) | patients treated with LPD and inulin | - | significant reduction | #10 |
low-protein diet (LPD) (0.6 g/kg/day) and inulin (19 g/day) | decrease | plasma nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) levels | patients treated with LPD and inulin | - | significant reduction | #11 |
low-protein diet (LPD) (0.6 g/kg/day) with or without inulin | no change | circulating levels of Interleukin (IL)-1β | the two groups | - | did not find a significant difference | #12 |
low-protein diet (LPD) (0.6 g/kg/day) with or without inulin | no change | circulating levels of IL-6 | the two groups | - | did not find a significant difference | #13 |
INTRODUCTION: The gut microbiota has coevolved with humans for a mutually beneficial coexistence and plays an important role in health and disease. A dysbiotic gut microbiome may contribute to progression to chronic kidney disease (CKD) and CKD-related complications such as cardiovascular disease. Microbiota modulation through the administration of prebiotics may represent an important therapeutic target. AIM: We sought to evaluate the effects of a low-protein diet (LPD) (0.6 g/kg/day) with or without the intake of the prebiotic inulin (19 g/day) on microbiota and clinical parameters in CKD patients. MATERIALS AND METHODS: We performed a longitudinal, prospective, controlled, and interventional study on 16 patients: 9 patients treated with LPD (0.6 g/kg/day) and inulin (19 g/day) and 7 patients (control group) treated only with LPD (0.6 g/kg/day). Clinical evaluations were performed and fecal samples were collected for a subsequent evaluation of the intestinal microbiota in all patients. These tests were carried out before the initiation of LPD, with or without inulin, at baseline (T0) and at 6 months (T2). The microbiota of 16 healthy control (HC) subjects was also analyzed in order to identify potential dysbiosis between patients and healthy subjects. RESULTS: Gut microbiota of CKD patients was different from that of healthy controls. The LPD was able to significantly increase the frequencies of Akkermansiaceae and Bacteroidaceae and decrease the frequencies of Christensenellaceae, Clostridiaceae, Lactobacillaceae, and Pasteurellaceae. Only Bifidobacteriaceae were increased when the LPD was accompanied by oral inulin intake. We showed a significant reduction of serum uric acid (SUA) and C-reactive protein (CRP) in patients treated with LPD and inulin (p = 0.018 and p = 0.003, respectively), an improvement in SF-36 (physical role functioning and general health perceptions; p = 0.03 and p = 0.01, respectively), and a significant increase of serum bicarbonate both in patients treated with LPD (p = 0.026) or with LPD and inulin (p = 0.01). Moreover, in patients treated with LPD and inulin, we observed a significant reduction in circulating tumor necrosis factor alpha (TNF-α) (p = 0.041) and plasma nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) (p = 0.027) levels. We did not find a significant difference in the circulating levels of Interleukin (IL)-1β (p = 0.529) and IL-6 (p = 0.828) in the two groups. CONCLUSIONS: LPD, associated or not with inulin, modified gut microbiota and modulated inflammatory and metabolic parameters in patients with CKD. Our results suggest that interventions attempting to modulate the gut microbiome may represent novel strategies to improve clinical outcomes in CKD patients and may provide useful therapeutic effects.