The AKI-to-CKD Transition: The Role of Uremic Toxins

• Published in: International journal of molecular sciences Vol. 24; no. 22; p. 16152
• Main Authors: André, Camille, Bodeau, Sandra, Kamel, Saïd, Bennis, Youssef, Caillard, Pauline
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 10.11.2023; MDPI
• Subjects: Acute Kidney Injury; Apoptosis; Cardiovascular disease; Chronic kidney failure; Development and progression; Diabetes; Humans; Hypertension; Kidney; Kidney diseases; Kinases; Life Sciences; Metabolites; Mortality; Patients; Plasma; Proteins; Renal Insufficiency, Chronic - complications; Risk factors; Toxicity; Toxins, Biological; Uremic Toxins; Urine; France; AKI-to-CKD transition; chronic kidney disease; acute kidney injury; uremic toxins; Uremic toxins; Chronic kidney disease; Acute kidney injury
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms242216152

After acute kidney injury (AKI), renal function continues to deteriorate in some patients. In a pro-inflammatory and profibrotic environment, the proximal tubules are subject to maladaptive repair. In the AKI-to-CKD transition, impaired recovery from AKI reduces tubular and glomerular filtration and leads to chronic kidney disease (CKD). Reduced kidney secretion capacity is characterized by the plasma accumulation of biologically active molecules, referred to as uremic toxins (UTs). These toxins have a role in the development of neurological, cardiovascular, bone, and renal complications of CKD. However, UTs might also cause CKD as well as be the consequence. Recent studies have shown that these molecules accumulate early in AKI and contribute to the establishment of this pro-inflammatory and profibrotic environment in the kidney. The objective of the present work was to review the mechanisms of UT toxicity that potentially contribute to the AKI-to-CKD transition in each renal compartment.