Abstract

Recent studies have shown that patients with kidney stone disease, and particularly calcium oxalate nephrolithiasis, exhibit dysbiosis in their fecal and urinary microbiota compared with controls. The alterations of microbiota go far beyond the simple presence and representation of Oxalobacter formigenes, a well-known symbiont exhibiting a marked capacity of degrading dietary oxalate and stimulating oxalate secretion by the gut mucosa. Thus, alterations of the intestinal microbiota may be involved in the pathophysiology of calcium kidney stones. However, the role of nutrition in this gut-kidney axis is still unknown, even if nutritional imbalances, such as poor hydration, high salt, and animal protein intake and reduced fruit and vegetable intake, are well-known risk factors for kidney stones. In this narrative review, we provide an overview of the gut-kidney axis in nephrolithiasis from a nutritional perspective, summarizing the evidence supporting the role of nutrition in the modulation of microbiota composition, and their relevance for the modulation of lithogenic risk.

Highlights

  • The gastrointestinal system plays a pivotal role in the pathophysiology of idiopathic calcium oxalate nephrolithiasis, the most common form of kidney stone disease [1,2,3]

  • Recent studies have shown that calcium kidney stone formers have a different fecal microbiota composition than stone-free individuals, supporting the hypothesis that the microbiota is a major player in the pathophysiology of nephrolithiasis [7,12,13]

  • Not focused on kidney stones, the current literature supports the hypothesis that the beneficial effects of increasing fruit and vegetable (FAV) or juice intake on the risk of kidney stone disease may be at least in part mediated by changes in gut microbiota composition and metabolic function

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Summary

Introduction

The gastrointestinal system plays a pivotal role in the pathophysiology of idiopathic calcium oxalate nephrolithiasis, the most common form of kidney stone disease [1,2,3]. Recent studies have shown that calcium kidney stone formers have a different fecal microbiota composition than stone-free individuals, supporting the hypothesis that the microbiota is a major player in the pathophysiology of nephrolithiasis [7,12,13] These studies have shed light on the gut-kidney axis in nephrolithiasis, but in most cases, failed to provide integration with clinical aspects of nephrolithiasis, and nutrition. Water therapy, adequate consumption of dairy products, FAVs, and low-salt low-animal protein diets are considered the pillars of non-pharmacological prevention of nephrolithiasis [16,17] It is still uncertain how these well-established clinical concepts can be integrated into the novel microbiome-centered acquisitions on the gut-kidney axis, despite the fact that dietary habits are well-known determinants of gut microbiota composition. The aim of this narrative review is to summarize the current knowledge on the relationship between gut microbiota and calcium oxalate kidney stone disease from a nutritional perspective

Before the Microbiota Revolution
MAIN RESULTS
KEY FINDINGS
Beyond the Microbiota Revolution
24 KSF43 controls
MAIN FINDINGS IN STONE FORMERS
The Determinants of Nephrolithiasis-Associated Gut Microbiota Dysbiosis
Salt and Microbiota
Animal Proteins and Microbiota
Oxalate Intake and Microbiota
Calcium Intake and Microbiota
Water Intake and Gut Microbiota
Conclusions and Perspectives
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