Ventilation-induced acute kidney injury in acute respiratory failure: Do PEEP levels matter?

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dc.article.number130
dc.catalogadorpva
dc.contributor.authorBenites, Martín H.
dc.contributor.authorSuarez-Sipmann, Fernando
dc.contributor.authorKattan Tala, Eduardo José
dc.contributor.authorCruces, Pablo
dc.contributor.authorRetamal Montes, Jaime
dc.date.accessioned2025-03-28T12:44:28Z
dc.date.available2025-03-28T12:44:28Z
dc.date.issued2025
dc.date.updated2025-03-23T01:03:29Z
dc.description.abstractAcute Respiratory Distress Syndrome (ARDS) is a leading cause of morbidity and mortality among critically ill patients, and mechanical ventilation (MV) plays a critical role in its management. One of the key parameters of MV is the level of positive end-expiratory pressure (PEEP), which helps to maintain an adequate lung functional volume. However, the optimal level of PEEP remains controversial. The classical approach in clinical trials for identifying the optimal PEEP has been to compare “high” and “low” levels in a dichotomous manner. High PEEP can improve lung compliance and significantly enhance oxygenation but has been inconclusive in hard clinical outcomes such as mortality and duration of MV. This discrepancy could be related to the fact that inappropriately high or low PEEP levels may adversely affect other organs, such as the heart, brain, and kidneys, which could counteract its potential beneficial effects on the lung. Patients with ARDS often develop acute kidney injury, which is an independent marker of mortality. Three primary mechanisms have been proposed to explain lung-kidney crosstalk during MV: gas exchange abnormalities, such as hypoxemia and hypercapnia; remote biotrauma; and hemodynamic changes, including reduced venous return and cardiac output. As PEEP levels increase, lung volume expands to a variable extent depending on mechanical response. This dynamic underlies two potential mechanisms that could impair venous return, potentially leading to splanchnic and renal congestion. First, increasing PEEP may enhance lung aeration, particularly in highly recruitable lungs, where previously collapsed alveoli reopen, increasing lung volume and pleural pressure, leading to vena cava compression, which can contribute to systemic venous congestion and abdominal organ impairment function. Second, in lungs with low recruitability, PEEP elevation may induce minimal changes in lung volume while increasing airway pressure, resulting in alveolar overdistension, vascular compression, and increased pulmonary vascular resistance. Therefore, we propose that high PEEP settings can contribute to renal congestion, potentially impairing renal function. This review underscores the need for further rigorous research to validate these perspectives and explore strategies for optimizing PEEP settings while minimizing adverse renal effects.
dc.fechaingreso.objetodigital2025-03-23
dc.format.extent15 páginas
dc.fuente.origenBiomed Central
dc.identifier.citationCritical Care. 2025 Mar 21;29(1):130
dc.identifier.doi10.1186/s13054-025-05343-5
dc.identifier.issn1364-8535
dc.identifier.urihttps://doi.org/10.1186/s13054-025-05343-5
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/103017
dc.information.autorucEscuela de Medicina; Benites, Martín H.; S/I; 1246778
dc.information.autorucEscuela de Medicina; Kattan Tala, Eduardo José; 0000-0002-1997-6893; 172152
dc.information.autorucEscuela de Medicina; Retamal Montes, Jaime; 0000-0002-6817-3659; 175147
dc.issue.numero1
dc.language.isoen
dc.nota.accesocontenido completo
dc.publisherSpringer Nature
dc.revistaCritical Care
dc.rightsacceso abierto
dc.rights.holderThe Author(s)
dc.rights.licenseAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectAcute respiratory failure
dc.subjectAcute kidney injury
dc.subjectPositive end‑expiratory pressure
dc.subjectVenous congestion
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleVentilation-induced acute kidney injury in acute respiratory failure: Do PEEP levels matter?
dc.typeartículo
dc.volumen29
sipa.codpersvinculados1246778
sipa.codpersvinculados172152
sipa.codpersvinculados175147
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