Copyright: ©Author(s) 2026.
World J Nephrol. Mar 25, 2026; 15(1): 115357
Published online Mar 25, 2026. doi: 10.5527/wjn.v15.i1.115357
Published online Mar 25, 2026. doi: 10.5527/wjn.v15.i1.115357
Table 1 Main uremic toxins and their effect on the kidney
| Compound | Total plasma concentration in CKD | Lowest concentration active on cultured renal cells (μM) | Effects on cultured renal cells | Effects on kidneys in vivo |
| pCS | Median 50; maximum 500 | 100 | Decreased viability, increased oxidative stress, increased inflammatory and profibrotic responses, decreased expression of nephroprotective factors | Progression of CKD, kidney fibrosis, promote epithelial-to-mesenchymal transition. Activate the renal-angiotensin system |
| pCG | Median 0.22; maximum 8 | 25 | Decreased the function of proximal cell membrane transporters (MRP4) | Kidney fibrosis. Promotes epithelial-to-mesenchymal transition |
| IS | Median 221; maximum 1100 | 1000 | Decreased viability, increased oxidative stress, increased inflammatory and profibrotic responses, decreased expression of nephroprotective factors | Accelerated fibrosis and CKD progression. Podocyte injury |
| IAA | Median 5; maximum 50 | 250 | Reduced viability through induction of apoptosis in tubular cells | Accelerated CKD progression |
| TMAO | Median 25; upper quartile > 38 | ND | No data | Kidney tubulointerstitial fibrosis |
- Citation: Salvadori M, Rosso G. Gut-kidney axis: Dysbiosis and renal disease. World J Nephrol 2026; 15(1): 115357
- URL: https://www.wjgnet.com/2220-6124/full/v15/i1/115357.htm
- DOI: https://dx.doi.org/10.5527/wjn.v15.i1.115357