Gut dysbiosis in endocrine and metabolic derangements of chronic kidney disease: mechanisms, controversies, and perspectives
This narrative review maps mechanisms linking gut dysbiosis to endocrine-metabolic derangements in CKD but provides no original data to quantify direction or magnitude of effect.
| Outcome | Grade | Direction | Effect | Studies |
|---|---|---|---|---|
| CKD-mineral and bone disorder | D | — Insufficient | não reportado | — |
| Insulin resistance | D | — Insufficient | não reportado | — |
| Protein-energy wasting | D | — Insufficient | não reportado | — |
| Renal anaemia | D | — Insufficient | não reportado | — |
| Vascular calcification | D | — Insufficient | não reportado | — |
| Cognitive dysfunction | D | — Insufficient | não reportado | — |
| CKD progression | D | — Insufficient | não reportado | — |
Context
CKD affects approximately 10% of the global population and is associated with endocrine-metabolic complications that increase cardiovascular mortality. The gut-kidney axis has emerged as a pathophysiological target, but the field lacks clinical trials testing microbiota-directed interventions on hard endpoints. Critical synthesis of available mechanisms informs research priorities.
What the study showed
The study presents no primary data and no formal meta-analysis; it is a narrative mini-review. It describes that in CKD there is expansion of proteolytic, uremic-toxin-generating taxa (e.g., indoxyl sulfate, p-cresol sulfate, TMAO) and depletion of SCFA producers, mechanistically linked to systemic inflammation, oxidative stress, intestinal barrier dysfunction, insulin resistance, vascular calcification, and anaemia. No absolute numbers, 95% CIs, or effect sizes are reported.
How it was done
Narrative mini-review published in 2026 (Frontiers in Endocrinology). No registered protocol, inclusion/exclusion criteria, systematic search strategy, or risk-of-bias assessment (AMSTAR-2 not applicable due to absence of systematic methods). The evidence base consists of literature selected by the authors without explicit quantification of included studies.
Effect magnitude
Not quantifiable. No effect size, 95% CI, or absolute/relative differences are reported for any outcome.
Limitations
Narrative design without systematic methodology: no protocol, eligibility criteria, search strategy, or risk-of-bias assessment (AMSTAR-2 inapplicable). High susceptibility to selection and confirmation bias. Causal relationships inferred from mechanistic, observational, and preclinical studies; reverse causality is not ruled out. Direct clinical applicability is limited by the absence of efficacy data for microbiota interventions on hard endpoints in CKD.
In clinical practice
Clinicians should not modify practice based on this review alone. The text supports the gut-kidney axis hypothesis but does not provide evidence that microbiota interventions (prebiotics, probiotics, synbiotics) improve hard clinical outcomes in CKD. Monitor for adequately powered RCTs testing these interventions.
What is still missing
Adequately powered RCTs with sufficient follow-up to assess the impact of gut microbiota modulation on hard CKD outcomes (progression to ESRD, cardiovascular mortality, bone events). A standardised operational definition of CKD-specific dysbiosis is a prerequisite.