Advancements of aquaporin 1 in ultrafiltration failure secondary to peritoneal dialysis

TL;DR

This paper explores how aquaporin 1 (AQP1) influences ultrafiltration failure in peritoneal dialysis patients and how corticosteroids may help.

Contribution

The paper highlights new insights into AQP1's role in peritoneal dialysis and its potential as a therapeutic target.

Findings

AQP1 accounts for up to 50% of ultrafiltration in peritoneal dialysis.

AQP1 genotype variation affects water transport and patient prognosis in PD.

Corticosteroids may regulate AQP1 to improve ultrafiltration in PD patients.

Abstract

For patients undergoing long-term peritoneal dialysis (PD), exposure to biologically incompatible PD solutions and the consequent peritoneal structure change can lead to progressive angiogenesis and fibrosis, and ultimately result in ultrafiltration failure (UFF). Peritoneal transport studies in aquaporin 1 (AQP1) knockout mice indicate that water transport across the peritoneum is mediated by AQP1, which accounts for up to 50% of ultrafiltration. Another recent study on a large cohort of PD patients with kidney failure further substantiated the impact of AQP1 genotype variation on water channel expression in the peritoneal membrane, influencing water transport, ultrafiltration, and patient prognosis. High-dose corticosteroid therapy in both patients and mice seems to be effective in regulating AQP1 to improve ultrafiltration. At present, increasing evidence suggests that AQP1 is relevant for the process of PD water osmotic transport and ultrafiltration. Despite a great deal of research having been done on the structure and function of aquaporin proteins, many fundamental issues remain unresolved.

A higher resolution version of the Graphical abstract is available as Supplementary information

A higher resolution version of the Graphical abstract is available as Supplementary information

The online version contains supplementary material available at 10.1007/s00467-024-06626-9.

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