Impact of acute kidney injury on lung injury

Liu, Kathleen D.

doi:10.1152/ajplung.90541.2008

Cited by 13 publications

(6 citation statements)

References 14 publications

(11 reference statements)

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“…At the molecular level, kidney injury stimulates an increase in lung expression of markers of inflammation, including messenger RNA for tumor necrosis factor-α (TNF-α) and intracellular adhesion molecule-1 [30]. In contrast, neutrophils appeared to be retained in the lung following injury and release of proteases, reactive oxygen and nitrogen species, inflammatory cytokines, and growth factors [27].…”

Section: Discussionmentioning

confidence: 99%

Effect of selenium supplementation on the structure of the lung of adult albino rats subjected to experimentally induced chronic renal failure

Hafez¹

2012

The Egyptian Journal of Histology

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Section: Discussionmentioning

confidence: 99%

Effect of selenium supplementation on the structure of the lung of adult albino rats subjected to experimentally induced chronic renal failure

Hafez¹

2012

The Egyptian Journal of Histology

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“…AKI survivors are also at risk for progression to chronic kidney disease (CKD) [7]. Cross-talk between the kidney and other vital organs has also been demonstrated to harbor deleterious consequences on end organ function and in-hospital morbidity and mortality rates [8, 9], suggesting that AKI-associated mortality is not solely secondary to standard sequelae (e.g., hyperkalemia, acidosis, or uremia). Consistently effective AKI therapy to prevent or limit the disease intensity is lacking, potentially due to delayed recognition of existing and/or ongoing injury.…”

Section: Introductionmentioning

confidence: 99%

Renal angina: an emerging paradigm to identify children at risk for acute kidney injury

et al. 2011

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Acute kidney injury (AKI) leads to high rates of morbidity and independently increases mortality risk. Therapy for AKI is likely limited by the inability to reliably diagnose AKI in its early stages, and, importantly, small changes in serum creatinine may be associated with poor outcomes and severe AKI. Whereas AKI biomarker research seeks to identify more sensitive and timely indices of kidney dysfunction, AKI lacks physical signs and symptoms to trigger biomarker assessment in at-risk patients, limiting biomarker efficacy. Accurate models of AKI prediction are unavailable. Severity of illness (SOI) scoring systems and organ dysfunction scores (OD), which stratify patients by prediction of mortality risk, are AKI reactive, not predictive. Kidneyspecific severity scores do not account for AKI progression, and stratification models of AKI severity are not predictive of AKI. Thus, there is a need for a kidney scoring system that can help predict the development of AKI. This review highlights the concept of renal angina, a combination of patient risk factors and subtle AKI, as a methodology to predict AKI progression. Fulfillment of renal angina criteria will improve the efficiency of AKI prediction by biomarkers, in turn expediting early therapy and assisting in creation of AKIpredictive scoring systems.

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“…Clinically, patients with AKI who develop lung injury suffer worse outcomes than those without antecedent AKI (30). Our work seeks to mimic their clinical condition and present a model by which the mechanistic details of this phenomenon can be explored.…”

Section: Discussionmentioning

confidence: 99%

Antecedent acute kidney injury worsens subsequent endotoxin-induced lung inflammation in a two-hit mouse model

Basu

Donaworth²,

Wheeler³

et al. 2011

American Journal of Physiology-Renal Physiology

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Acute kidney injury (AKI) contributes greatly to morbidity and mortality in critically ill adults and children. Patients with AKI who subsequently develop lung injury are known to suffer worse outcomes compared with patients with lung injury alone. Isolated experimental kidney ischemia alters distal lung water balance and capillary permeability, but the effects of such an aberration on subsequent lung injury are unknown. We present a clinically relevant two-hit murine model wherein a proximal AKI through bilateral renal ischemia (30 min) is followed by a subsequent acute lung injury (ALI) via intratracheal LPS endotoxin (50 g at 24 h after surgery). Mice demonstrated AKI by elevation of serum creatinine and renal histopathological damage. Mice with ALI and preexisting AKI had increased lung neutrophilia in bronchoalveolar lavage fluid and by myeloperoxidase activity over Sham-ALI mice. Additionally, lung histopathological damage was greater in ALI mice with preexisting AKI than Sham-ALI mice. There was uniform elevation of monocyte chemoattractant protein-1 in kidney, serum, and lung tissue in animals with both AKI and ALI over those with either injury alone. The additive lung inflammation after ALI with antecedent AKI was abrogated in MCP-1-deficient mice. Taken together, our two-hit model demonstrates that kidney injury may prime the lung for a heightened inflammatory response to subsequent injury and MCP-1 may be involved in this model of kidney-lung cross talk. The model holds clinical relevance for patients at risk of lung injury after ischemic injury to the kidney.

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Impact of acute kidney injury on lung injury

Cited by 13 publications

References 14 publications

Effect of selenium supplementation on the structure of the lung of adult albino rats subjected to experimentally induced chronic renal failure

Effect of selenium supplementation on the structure of the lung of adult albino rats subjected to experimentally induced chronic renal failure

Renal angina: an emerging paradigm to identify children at risk for acute kidney injury

Antecedent acute kidney injury worsens subsequent endotoxin-induced lung inflammation in a two-hit mouse model

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