Abstract

Indoxyl sulfate (IS) is involved in the progression of chronic kidney disease (CKD) and in its cardiovascular complications. One of the approaches proposed to decrease IS is the administration of synbiotics. This work aimed to search for a probiotic strain capable to decrease serum IS levels and mix it with two prebiotics (inulin and fructooligosaccharide (FOS)) to produce a putative synbiotic and test it in a rat CKD model. Two groups of Sprague-Dawley rats were nephrectomized. One group (Lac) received the mixture for 16 weeks in drinking water and the other no (Nef). A control group (C) included sham-nephrectomized rats. Serum creatinine and IS concentrations were measured using high-performance liquid chromatography with diode array detector (HPLC-DAD). Optical microscopy and two-photon excitation microscopy was used to study kidney and heart samples. The Lac group, which received the synbiotic, reduced IS by 0.8% while the Nef group increased it by 38.8%. Histological analysis of kidneys showed that the Lac group increased fibrotic areas by 12% and the Nef group did it by 25%. The synbiotic did not reduce cardiac fibrosis. Therefore, the putative synbiotic showed that function reducing IS and the progression of CKD in a rat model, but no heart protection was observed.

Highlights

  • Chronic kidney disease (CKD) is considered a permanent alteration of the kidney structure, its function or, in the most severe cases, both

  • Isolation of Strains Capable to Reduce Indoxyl sulfate (IS) In Vitro

  • Strains were cultured in MRS broth supplemented with 2.8 mM IS during 48 h and IS was measured by high-performance liquid chromatography (HPLC)

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Summary

Introduction

Chronic kidney disease (CKD) is considered a permanent alteration of the kidney structure, its function or, in the most severe cases, both. The intensified surveillance and the awareness in the population has increased CKD diagnoses reaching, for example, to be determined that a 15% of the USA population is affected by this pathology [3]. The progression of the disease, as well as the effects of the above mentioned metabolites, have a serious impact in multiple systems of the body, including the cardiovascular and the gastrointestinal systems, being the presence of these metabolites associated to an increased mortality in the former and affecting assimilation, motility, and permeability in the latter [4,5]. The gastrointestinal alterations provoke an increased absorption of metabolites in the intestine contributing to sustain a systemic inflammation which, in turn, affects the composition of the normal microbiota and its metabolic functions and may cause intestinal dysbiosis [6]

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