Resumen:
Phosphate is a key uremic toxin associated with adverse outcomes. As chronic kidney dis ease (CKD) progresses, the kidney capacity to excrete excess dietary phosphate decreases, triggering
compensatory endocrine responses that drive CKD-mineral and bone disorder (CKD-MBD). Eventu ally, hyperphosphatemia develops, and low phosphate diet and phosphate binders are prescribed.
Recent data have identified a potential role of the gut microbiota in mineral bone disorders. Thus,
parathyroid hormone (PTH) only caused bone loss in mice whose microbiota was enriched in the
Th17 cell-inducing taxa segmented filamentous bacteria. Furthermore, the microbiota was required
for PTH to stimulate bone formation and increase bone mass, and this was dependent on bacterial
production of the short-chain fatty acid butyrate. We review current knowledge on the relationship
between phosphate, microbiota and CKD-MBD. Topics include microbial bioactive compounds of
special interest in CKD, the impact of dietary phosphate and phosphate binders on the gut microbiota,
the modulation of CKD-MBD by the microbiota and the potential therapeutic use of microbiota to
treat CKD-MBD through the clinical translation of concepts from other fields of science such as the
optimization of phosphorus utilization and the use of phosphate-accumulating organisms