The kidney in acute renal failure: innocent bystander, victim or still a suspect?

Groesdonk, Heinrich V.; Heringlake, Matthias

doi:10.1007/s00134-009-1741-8

Cited by 4 publications

(3 citation statements)

References 17 publications

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“…[14][15][16][17] For a long period, the kidney was viewed as a victim or an innocent bystander thought to merely reflect disease severity in critically ill patients. 18 However, advanced evidence indicates that acute kidney injury is a critical protagonist in acute illnesses, including sepsis, rather than simply a victim or bystander. 19 While there is some understanding of how the kidney and liver impact and are impacted by sepsis, understanding liver-kidney comorbidity in sepsis is still in an early stage.…”

Section: Introductionmentioning

confidence: 99%

“…Besides the liver, the kidney is another main target of sepsis because it is responsible for excreting toxic metabolites and maintaining the balance of fluid and electrolytes 14–17 . For a long period, the kidney was viewed as a victim or an innocent bystander thought to merely reflect disease severity in critically ill patients 18 . However, advanced evidence indicates that acute kidney injury is a critical protagonist in acute illnesses, including sepsis, rather than simply a victim or bystander 19 .…”

Section: Introductionmentioning

confidence: 99%

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Proteome characterization of liver–kidney comorbidity after microbial sepsis

Gui,

Yu,

Wang

et al. 2024

The FASEB Journal

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Sepsis is a life‐threatening condition that occurs when the body responds to an infection but subsequently triggers widespread inflammation and impaired blood flow. These pathologic responses can rapidly cause multiple organ dysfunction or failure either one by one or simultaneously. The fundamental common mechanisms involved in sepsis‐induced multiple organ dysfunction remain unclear. Here, employing quantitative global and phosphoproteomics, we examine the liver's temporal proteome and phosphoproteome changes after moderate sepsis induced by cecum ligation and puncture. In total, 4593 global proteins and 1186 phosphoproteins according to 3275 phosphosites were identified. To characterize the liver–kidney comorbidity after sepsis, we developed a mathematical model and performed cross‐analyses of liver and kidney proteome data obtained from the same set of mice. Beyond immune response, we showed the commonly disturbed pathways and key regulators of the liver–kidney comorbidity are linked to energy metabolism and consumption. Our data provide open resources to understand the communication between the liver and kidney as they work to fight infection and maintain homeostasis.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Proteome characterization of liver–kidney comorbidity after microbial sepsis

Gui,

Yu,

Wang

et al. 2024

The FASEB Journal

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“…Mit zunehmender Einschränkung der Nierenfunktion werden akute Nierenschä-digungen jedoch durch komplexe Auswirkungen urämischer Sekundär effekte und Inflammation (z. B. Aktivierung immunkompetenter Zellen, Freisetzung humoraler Mediatoren wie Zytokine) zum "Täter" und beeinflussen dann negativ die Prognose kritisch kranker Patienten [15,17]. [28].…”

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Die akute Nierenschädigung

Schmid

Schiffl

Lederer

2012

Med Klin Intensivmed Notfmed

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Acute kidney injury plays a pivotal role in intensive care medicine and exerts crucial adverse effects on the course of the disease and overall prognosis of the critically ill patient. Intensive renal support, including initiation of earlier dialysis or maximal uremic toxin removal by higher dosage and frequency of renal replacement therapy, and individualized selection of modality were not able to decrease excessive mortality in this population. Systemic acute inflammation, mediated, at least in part, by cytokines, and not secondary uremic side effects, seems to have a major impact on nonrenal organ damage. Assessment of short-term outcome in critically ill patients who develop acute kidney injury may underestimate the true burden of disease. The overall survival at 5 years in patients discharged alive after severe acute kidney injury necessitating renal replacement therapy is only 20-30%, comparable to cancer patients. In addition, acute renal damage was identified as an independent risk factor for progression of chronic renal insufficiency. Current research focuses on strategies for the prevention of acute kidney injury and on the establishment of effective biomarkers for the early recognition and accurate diagnosis of subclinical renal damage.

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