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To investigate if toll-like receptor (TLR) 4/nuclear factor-kappa B (NF-κB) signaling pathways mediated crush injury induced acute kidney injury (AKI) in rats, and if TAK-242 (a specific inhibitor of TLR4) attenuates the injury through inhibiting the signaling pathways.
This study was divided into two parts: (1) Establish the crush injury model: 50 rats were randomly divided into control group and four crush injury groups (n = 10/group). Crush injury groups were given 3kg pressure for eight hours and were sacrificed at the time points of 0h, 6h, 12h, and 24h after relieving pressure. And (2) Select the most obvious injury group (12h group) for drug intervention group. Thirty rats were randomly divided into control group, 12h group, and 12h+TAK-242 group (n = 10/group). Two parts detection were as follows: pathological changes of kidney tissues were observed in Haematoxylin and Eosin (HE) staining. Serum creatinine, blood urea nitrogen (BUN), myoglobin (Mb), and blood potassium were examined by automatic biochemical analysis instrument. Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured by enzyme-linked immunosorbent assay (ELISA). The TLR4 messenger ribonucleic acid (mRNA), TLR4, and P65 were detected by real-time polymerase chain reaction (PCR), western blot, immunohistochemistry staining.
Compared with the control group, kidney tissues were damaged in crush injury groups, and most obvious in the 12h group. The level of serum creatinine, BUN, Mb, blood potassium, IL-6, TNF-α, and TLR4mRNA were increased in the crush injury groups and significantly increased in the 12h group (P <.05). The TLR4 and P65 were significantly increased in the 12h group (P <.05). Compared with the 12h group, kidney tissue damage was significantly reduced in the TAK-242 group (P <.05). The level of serum creatinine, BUN, Mb, blood potassium, IL-6, TNF-α, TLR4mRNA, TLR4, and P65 in the TAK-242 group were significantly reduced (P <.05).
The present findings conclude that TLR4/NF-κB signaling pathways mediated crush injury induced AKI in rats, and TAK-242 attenuates the injury through inhibiting the signaling pathways.
Dialysis patients may not have access to conventional renal replacement therapy (RRT) following disasters. We hypothesized that improvised renal replacement therapy (ImpRRT) would be comparable to continuous renal replacement therapy (CRRT) in a porcine acute kidney injury model.
Following bilateral nephrectomies and 2 hours of caudal aortic occlusion, 12 pigs were randomized to 4 hours of ImpRRT or CRRT. In the ImpRRT group, blood was circulated through a dialysis filter using a rapid infuser to collect the ultrafiltrate. Improvised replacement fluid, made with stock solutions, was infused pre-pump. In the CRRT group, commercial replacement fluid was used. During RRT, animals received isotonic crystalloids and norepinephrine.
There were no differences in serum creatinine, calcium, magnesium, or phosphorus concentrations. While there was a difference between groups in serum potassium concentration over time (P < 0.001), significance was lost in pairwise comparison at specific time points. Replacement fluids or ultrafiltrate flows did not differ between groups. There were no differences in lactate concentration, isotonic crystalloid requirement, or norepinephrine doses. No difference was found in electrolyte concentrations between the commercial and improvised replacement solutions.
The ImpRRT system achieved similar performance to CRRT and may represent a potential option for temporary RRT following disasters.
A systematic literature review (SLR) was performed to elucidate the current triage and treatment of an entrapped or mangled extremity in resource scarce environments (RSEs).
A lead researcher followed the search strategy following inclusion and exclusion criteria. A first reviewer (FR) was randomly assigned sources. One of the 2 lead researchers was the second reviewer (SR). Each determined the level of evidence (LOE) and quality of evidence (QE) from each source. Any differing opinions between the FR and SR were discussed between them, and if differing opinions remained, then a third reviewer (the other lead researcher) discussed the article until a consensus was reached. The final opinion of each article was entered for analysis.
Fifty-eight (58) articles were entered into the final study. There was 1 study determined to be LOE 1, 29 LOE 2, and 28 LOE 3, with 15 determined to achieve QE 1, 37 QE 2, and 6 QE 3.
This SLR showed that there is a lack of studies producing strong evidence to support the triage and treatment of the mangled extremity in RSE. Therefore, a Delphi process is suggested to adapt and modify current civilian and military triage and treatment guidelines to the RSE.
Crush syndrome, of which little is known, occurs as a result of compression injury to the muscles. This syndrome is characterized by systemic manifestations such as acute kidney injury (AKI), hypovolemic shock, and hydroelectrolytic variations. This pathology presents high morbidity and mortality if not managed aggressively by prehospital care.
A 40-year-old worker was rescued after being buried underground in a ditch for 19 hours. The patient was administered early resuscitation with isotonic solutions and monitored during the entire rescue operation. Despite having increased plasma levels of total creatine kinase (CK), the patient did not develop AKI or hydroelectrolytic variations.
Aggressive early management with isotonic solutions before hospital arrival is an effective option for nephron-protection and prevention of crush syndrome.
MardonesA, ArellanoP, RojasC, GutierrezR, OliverN, BorgnaV. Prevention of Crush Syndrome through Aggressive Early Resuscitation: Clinical Case in a Buried Worker. Prehosp Disaster Med. 2016;31(3):340–342.