Acute renal failure in severely burned patients

Holm, Charlotte; Hörbrand, F.; Donnersmarck, G. Henckel von; Mühlbauer, W.

doi:10.1016/s0305-4179(98)00144-2

Cited by 124 publications

(86 citation statements)

References 28 publications

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“…Our findings support the impression of a number of clinical investigators that patients suffering major trauma or burns can react to a second hit, often a nosocomial infection, several days after the initial injury with an intense and morbid inflammatory response [4,55,56]. This enhanced host response can often lead to MOF with significant mortality.…”

Section: Discussionsupporting

confidence: 85%

Linking the “two-hit” response following injury to enhanced TLR4 reactivity

Murphy

Paterson

Kriynovich

et al. 2004

Journal of Leukocyte Biology

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Severe injury can initiate an exaggerated systemic inflammatory response and multiple organ failure (MOF) if a subsequent immune stimulus, "second hit", occurs. Using a mouse thermal injury model, we tested whether changes in innate immune cell reactivity following injury can contribute to the development of heightened inflammation and MOF. Using high-purity Escherichia coli lipopolysaccharide (LPS) to selectively stimulate Tolllike receptor 4 (TLR4), we demonstrate augmented interleukin (IL)-1␤, tumor necrosis factor ␣ (TNF-␣), and IL-6 production by 1 day but particularly, at 7 days after injury. The in vivo significance of enhanced TLR4 responsiveness was explored by challenging sham or burn mice with LPS at 1 or 7 days after injury and determining mortality along with in vivo cytokine and chemokine levels. Mortality was high (75%) in LPS-challenged burn but not sham mice at 7 days, although not at 1 day, after injury. Death was associated with leukocyte sequestration in the lungs and livers along with increased proinflammatory cytokine and chemokine levels in these organs. Blocking TNF-␣ activity prevented this mortality, suggesting that excessive TNF-␣ production contributes to this lethal response. These findings demonstrate the potential lethality of excessive TLR4 reactivity after injury and provide an explanation for the exaggerated inflammatory response to a second hit, which can occur following severe injury. J. Leukoc. Biol. 77: 16 -23; 2005.

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Section: Discussionsupporting

confidence: 85%

Linking the “two-hit” response following injury to enhanced TLR4 reactivity

Murphy

Paterson

Kriynovich

et al. 2004

Journal of Leukocyte Biology

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“…[37] Oxidative stress accompanied by the increased formation of superoxide anions (O 2 − ), hydrogen peroxide (H 2 O 2 ), and peroxynitrite (ONOO − ) are endogenous inducers of DNA single-strand breakage and is obligatory of PARP activation, leading to cellular dysfunction and necrosis by the rapid depletion of intracellular nicotinamide adenine dinucleotide (NAD + ) and adenosine triphosphate (ATP) pools. [15][16][17] PARP is involved in the repair process of DNA but uses NAD + as a substrate; subsequently, cells utilize ATP to regenerate NAD + stores. [36] The importance of PARP pathway is clearly documented in ischemic acute renal failure.…”

Section: Discussionmentioning

confidence: 99%

“…[12,13] Endotoxemic ARF is associated with the aberrant generation of reactive oxygen species (ROS), which leads to DNA single-strand breaks. [14][15][16][17] The activation of PARP is triggered by single-strand breaks in DNA, but its excessive activation in pathological conditions results in a rapid depletion of intracellular NAD + and ATP. This slows the rate of glycolysis and mitochondrial respiration, eventually leading to cellular dysfunction and death.…”

Section: Introductionmentioning

confidence: 99%

Poly (ADP-Ribose) Polymerase as a Potential Target for the Treatment of Acute Renal Injury Caused by Lipopolysaccharide

Taşatargil¹,

Aksoy²,

Dalaklıoğlu³

et al. 2008

Renal Failure

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Recent studies have clearly reported that there is a relationship between endotoxemia and acute renal injury. The aim of this study was to investigate whether treatment with the new potent PARP inhibitor PJ34 could prevent the acute renal injury induced by lipopolysaccharide (LPS). Endotoxemia was induced by LPS injection (10 mg/kg, i.v.). LPS increased blood urea nitrogen (BUN) levels from 22 ± 0.54 mg/dL to 45.7 ± 5.79 mg/dL (p < 0.05). The plasma creatinine levels were 0.38 ± 0.02 mg/dL and 0.47 ± 0.03 mg/dL for the control and LPS groups, respectively. In addition, urinary excretion of N-acetyl-β-dglucosaminidase (NAG, a marker of renal tubular damage) was increased after LPS injection. By light microscopy, structural renal damage was observed in the LPS-treated group. However, PJ34 treatment (10 mg/kg, i.p.) attenuated LPS-induced renal injury, as indicated by plasma BUN and creatinine levels, urinary NAG excretion, and renal histology. These results indicated that the overactivation of the PARP pathway may have a role in LPSinduced renal impairment. Hence, pharmacological inhibition of this pathway might be an effective intervention to prevent endotoxin-induced acute renal injury.

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“…The study designs included 32 case series , 16 cohort studies (11,(45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55)(56)(57)(58)(59), and 4 case control studies (60 -63 ), for a total of 2399 subjects. Of the 52 studies, 16 measured uMb in only a portion of their study group.…”

Section: Study Characteristicsmentioning

confidence: 99%

“…Twenty studies looked at drugs or toxins (therapeutic/drugs of abuse, alcohol, insect venoms, snake venoms, heavy metals) (13, 14, 16, 18, 20 -23, 27, 28, 32, 33, 38, 43, 44, 52, 55, 56, 59, 63 ), 20 referred to trauma (crush injuries, motor vehicle accidents, surgery, physical torture and abuse, long-term confinement without changing position) (11, 21, 24 -26, 27, 29, 30, 34 -36, 38, 42, 44, 45, 48, 53, 54, 56, 59 ), 17 to infection (11,15,17,23,26,27,29,35,38,40,41,43,44,47,55,56,62 ), 12 to physical exertion (strainful muscle exercise, excessive muscle activity, seizures, longdistance running) (11, 23, 25-27, 30, 31, 38, 39, 43, 44, 49 ), 11 to metabolic disturbance (metabolic syndromes, endocrine disorders, electrolytes imbalances) (11,15,19,23,27,35,41,43,44,55,56 ), 9 to burns (thermal injury, high-voltage electrical injury, lightning) (19,26,35,38,46,48,50,57,58 ), 7 to asphyxiation (19,21,35,…”

Section: Study Characteristicsmentioning

confidence: 99%

Utility of Urine Myoglobin for the Prediction of Acute Renal Failure in Patients with Suspected Rhabdomyolysis: A Systematic Review

et al. 2009

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Background: Urine myoglobin continues to be used as a marker of rhabdomyolysis, particularly to assess risk of developing acute renal failure and evaluate treatment success. We sought to determine the predictive validity of urine myoglobin (uMb) for acute renal failure (ARF) in patients with suspected rhabdomyolysis. Methods: We performed a broad systemic review of the literature from January 1980 to December 2006 using the search terms myoglobin$ AND (renal OR ARF OR kidney). Only primary studies published in English where uMb measurement was related to ARF were included. Results: Of 1602 studies screened, 52 met all selection criteria. The studies covered a wide spectrum of etiologies for rhabdomyolysis, dissimilar diagnostic criteria for ARF and rhabdomyolysis, and various methods of uMb measurement and were mostly case series (n = 32). There was poor reporting on the uMb method, and 17 studies failed to provide any information about the method. The reporting of clinical criteria for ARF with respect to timing, description, performance, and interpretation also lacked adequate detail for replication. Eight studies (total 295 patients) had data for 2-by-2 tables. Sensitivity of the uMb test was 100% in 5 of the 8 studies, specificity varied widely (15% to 88%), and CIs around these measures were high. Pooling of data was not possible because of study heterogeneity. Conclusions: There is inadequate evidence evaluating the use of uMb as a predictor of ARF in patients with suspected rhabdomyolysis.

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Acute renal failure in severely burned patients

Cited by 124 publications

References 28 publications

Linking the “two-hit” response following injury to enhanced TLR4 reactivity

Linking the “two-hit” response following injury to enhanced TLR4 reactivity

Poly (ADP-Ribose) Polymerase as a Potential Target for the Treatment of Acute Renal Injury Caused by Lipopolysaccharide

Utility of Urine Myoglobin for the Prediction of Acute Renal Failure in Patients with Suspected Rhabdomyolysis: A Systematic Review

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