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Objectives:To explore the capacity of mutant lactobacilli to remove creatinine (Cr) and urea nitrogen (UN) via the gastrointestinal tract and its effects on renal pathology in the 5/6 nephrectomized rat model of chronic renal failure. Methods:Sixty Sprague–Dawley rats were randomly divided into a Sham group, a Model group, a wide-type Lactobacilli group (L.B group), and a Mutant Lactobacilli group (Mut-L.B group). The rats in the Model, LB and Mut-L.B groups underwent 5/6 nephrectomy. Eight weeks after administration, 24-h urine, orbital blood and digestive secretions were collected to analyze Cr and UN levels. Pathological changes in nephridial tissues were observed by hematoxylin and eosin and Masson trichrome staining, and the expression of TGF-β1 and FN was detected by immunohistochemistry. Results:There were no significant differences in urinary Cr and UN levels among the Sham, L.B and Mut-L.B groups (p > .05), while serum and digestive Cr and UN levels were significantly decreased in the Mut-L.B group (p < .01). Furthermore, renal tubular injury and interstitial fibrosis were significantly reduced and TGF-β1 and FN expression was decreased (p < .05) in the Mut-L.B group. Conclusion:Mutant lactobacilli decreased serum Cr and UN levels, reduced the expression of TGF-β1 and FN in renal tissues and alleviated renal interstitial injury and fibrosis in a rat model of chronic renal failure in a mechanism that may involve decomposition and not just excretion of small molecule toxins in the gastrointestinal tract. [ABSTRACT FROM AUTHOR]

Background/Aims: We aim to obtain a probiotic strain from Lactobacillus bulgaricus by testing its capability to decompose uremic toxins to provide new intestinal bacteria for the treatment of chronic renal failure. Methods: Original L. bulgaricus was cultured with the serum of uremic patients and then mutated by physical (ultraviolet) and chemical (diethyl sulfate) methods repeatedly. Using creatinine decomposition rate as an observed index, we selected the best strains which decreased the most concentration of the creatinine. We then tested its ability to decompose urea, uric acid, serum phosphate, parathyroid hormone, and homocysteine and its genetic stability. Results: After inductive and mutagenic treatment, DUC3-17 was selected. Its decomposition rate of creatinine, urea nitrogen, uric acid, phosphorus, parathyroid hormone, and homocysteine were 17.23%, 36.02%, 9.84%, 15.73%, 78.26%, and 12.69%, respectively. The degrading capacity was sustained over five generations. Conclusions: After directional induction and compound mutation, L. bulgaricus has greater capacity to decompose uremic toxins, with a stable inheritance. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of Shenfushu granule (SFSG) and atropine treatment on microvessels of the kidney and intestine after chronic renal failure (CRF) induced by 5/6 nephrectomy. Methods: Sprague Dawley rats were randomly divided into a sham group, a model group, an SFSG group, and an SFSG + atropine group. SFSG was administered daily 1 week after inducing CRF. Rats were sacrificed at the end of the eighth week. Urinary protein and stool and serum urea nitrogen (UN) and creatinine (Cr) levels were assessed. Hematoxylin and eosin and periodic acid-Schiff staining of the kidney and examination of the vascular endothelial growth factor (VEGF) and microvessel density (MVD) levels in kidney and intestine were performed. Results: The Cr and UN levels were significantly increased in blood and stool of the model group. SFSG significantly improved renal function, and the protective effects were further enhanced with the addition of atropine. Glomerular sclerosis, tubulointerstitial fibrosis, and microvessel loss were observed in CRF rats, and these pathological changes were ameliorated in the two treatment groups ( p < 0.05), especially in the SFSG + atropine group. The expression of VEGF and MVD was decreased in the CRF rats compared with the sham group. SFSG treatment increased the expression of these proteins and reversed the degree of microvessel loss, glomerular sclerosis, and tubulointerstitial fibrosis ( p < 0.05). Co-treatment with atropine enhanced these effects. Conclusions: SFSG alleviated renal function, upregulated the expression of VEGF and MVD in the kidney and intestine, and attenuated the degree of microvessel loss, glomerular sclerosis, and tubulointerstitial fibrosis in the early stages of CRF in rats, and addition of atropine enhanced these effects. [ABSTRACT FROM AUTHOR]