Acute Injury Research Articles

More knee reinjuries after ACL reconstruction compared to nonsurgical treatment of the ACL. A 2-year follow-up of the NACOX prospective cohort study.

To describe knee reinjuries and surgeries within 2 years after an acute anterior cruciate ligament (ACL) injury, in patients treated with or without ACL reconstruction (ACLR). Two years follow-up of 275 patients (52% females, mean age 25.2 [SD 7.0] years) about knee reinjuries and surgeries were analysed from the prospective NACOX cohort study, aiming to describe recovery after an acute ACL injury treated according to clinical routine. Knee reinjury was defined as increase or new symptoms due to new trauma. At 2 years after injury, 169 (61%) had undergone an ACLR. Results are presented with descriptive statistics and risk ratios (RR). Thirty-two patients sustained reinjuries within 2 years; 6 in the non-ACLR group, and 26 in the ACLR group (7 before and 19 after ACLR). Twelve patients in the ACLR group sustained a graft rupture and three did an ACL revision. Patients with non-ACLR, aged 21-25 years, had a 5.9-fold higher risk for reinjury than those aged 15-20 years (RR 5.9 [1.3-26.9]; p = 0.012). Twenty-four patients had surgery in the non-ACLR group and 36 patients in the ACLR group (excluding primary ACLR), where six were before ACLR and 30 were after ACLR. Twelve percent sustained a knee reinjury and 21% underwent knee surgery within 2 years after the index ACL injury. There was a higher reinjury incidence in the ACLR group, but no difference in incidence of surgeries. Thus, ACLR did not reduce the risk of traumatic reinjuries or surgeries, which is important for treatment decision considerations. Level I.

Small-molecule mediated MuRF1 inhibition protects from doxorubicin-induced cardiac atrophy and contractile dysfunction

Cancer chemotherapy induces cell stress in rapidly dividing cancer cells to trigger their growth arrest and apoptosis. However, adverse effects related to cardiotoxicity underpinned by a limited regenerative potential of the heart limits clinical application: In particular, chemotherapy with doxorubicin (DOXO) causes acute heart injury that can transition to persisting cardiomyopathy (DOXO-CM). Here, we tested if MuRF1 inhibition (“MuRFi”) was able to attenuate DOXO-CM. To mimic DOXO chemotherapy, we treated mice over four weeks with five DOXO injections, resulting in a cumulative dosage of 25 mg/kg. At day 28, mice had lower body and heart weights, reduced cardiac cross-sectional myofibrillar areas (CSAs), and disturbed functional ejection fractions (EFs) and fractional shortenings (FS) as indicated by echocardiography (ECHO). In contrast, mice with a 1 g/kg Myomed#205 spiked diet, a previously described experimental MuRFi therapy, showed lower DOXO-CM at day 28, and also reduced acute DOXO cardiac injury at day 7 (single DOXO dose; 15 mg/kg). Underlying molecular signatures using Western blot (WB) assays showed at day 28 reduced phospho-AKT (AKTp) and phospo-4EBP1 (4 EBP1p) levels following DOXO that were normalized following MuRFi treatment. Taken together, our data suggest that MuRFi treatment is suitable to attenuate DOXO-CM by preserving AKTp and 4 EBP1p levels in DOXO stressed cardiomyocytes, thereby supporting de novo protein translation and cardiomyocyte survival under translational arrest stress.

A-090 Performance of GFAP and UCH-L1 Biomarkers for Traumatic Brain Injury in the ARCHITECT i1000SR TBI Test

Abstract Background Traumatic Brain Injury (TBI) has been recognized as an important cause of death and disability and is a growing public health problem. An estimated 69 million people globally experience a TBI annually. The vast majority (80%) of patients evaluated for TBI in the Emergency Department will receive head CT scans, however less than 10% will have findings of acute traumatic abnormalities. This highlights the need for objective, rapid, accurate tools to help clinicians evaluate and triage patients with suspected TBI and reduce unnecessary radiation exposure. Blood based biomarkers such as glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase L1 (UCH-L1) have shown utility to predict acute traumatic intracranial injury on CT scan after TBI. Methods The ARCHITECT TBI test is a panel of in vitro diagnostic chemiluminescent microparticle immunoassays for the measurement of GFAP and UCH-L1 in plasma and serum. A method comparison study was performed to compare the GFAP and UCH-L1 assays on ARCHITECT i1000SR to the FDA cleared Alinity i assays. Performance characteristics such as detection limits, imprecision, linearity, and measuring interval were established following CLSI guidance. Results The analytical measuring interval (AMI) extends from the limit of quantitation (LoQ) to the upper LoQ and is determined by the range that demonstrates acceptable performance for linearity, imprecision, and bias. The AMI is 6.1 to 42,000 pg/mL for GFAP and 26.3 to 25,000 pg/mL for UCH-L1. Within-laboratory imprecision ranged from 2.2 to 6.2% CV for GFAP and 2.2 to 4.5% CV for UCH-L1. The Overall Reproducibility (includes repeatability, between-run, between-day, between-instrument variance components) results ranged from 2.7 to 6.8% CV for GFAP and 2.4 to 3.9 %CV for UCH-L1. The method comparison study evaluated 123 specimens across the range of 6.5-32,548.6 pg/mL for GFAP, and 51.5-24,127.7 for UCH-L1. The correlation coefficients were 1.0, with a slope of 1.03 and 1.06, an intercept of -0.6 and -6.0, for GFAP and UCH-L1, respectively. The results support use of the established GFAP and UCH-L1 cutoffs and clinical performance findings in a multi-site pivotal study which enrolled 1899 mild TBI (Glasgow Coma Scale score 13 to 15) subjects. 116 of the 120 specimens with a positive CT scan had a positive TBI interpretation (Sensitivity 96.7%). Of the 1779 subjects with negative CT scan results, 713 had a negative TBI interpretation (Specificity 40.1%). The negative predictive value (NPV) of the test was 99.4% (713/717). Conclusions The ARCHITECT TBI test performance was evaluated compared to the Alinity i TBI test across a broad concentration range of GFAP and UCH-L1. The results support equivalence of the ARCHITECT TBI test to the Alinity i TBI test. The established cutoffs were evaluated in a prospective cohort of mild TBI subjects and demonstrated high sensitivity and NPV relative to head CT scan results, supporting the utility to rule out the need for CT scan in mild TBI subjects presenting to the emergency department. Funding This work is in collaboration with the US Army Medical Materiel Development Activity, US Army Medical Research and Development Command CRADA 20-1266-CRA.

Proinflammatory factors inhibition and fish oil treatment: A promising therapy for neonatal seizures

Brain injury is one of the most important causes of infant mortality and chronic neurological disabilities. Hypoxia is an acute brain injury which led to various cognitive, behavioral, and memory disorders throughout life. Previous studies reported neuroprotective possibilities for fish oil (FO) in brain-injured situations. In this study, we evaluated the effect of the FO diet during the lactation period on seizure activity, behavioral performance, histomorphometry, and inflammatory changes in the brains of hypoxia rats. Male Wistar rats were randomly divided in to 4 groups: Sham (intact rats), hypoxia, FO and FO+hypoxia groups. Hypoxia was induced by keeping neonate rats at PND12 in a hypoxic chamber (7 % oxygen and 93 % nitrogen intensity) for 15 minutes. In the FO groups, rats received oral FO (1 ml/day) for 12 days during the lactation period. Seizure activity was assessed by measuring the number of tonic-clonic seizures and seizure thresholds. Novel object recognition tests (NORT), rotarod, and open field tests were used to measure behavioral performances. A Histological study was performed to evaluate histomorphometric changes in the hippocampus and cerebellum. The gene expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) was measured using RT-PCR. Findings showed that the number of tonic-clonic seizures, atrophy, and cell death in the hippocampus and cerebellum, the gene expression of TNF-α and IL-1β in the hippocampus, and behavioral disorders were significantly increased in the hypoxia rats compared to the sham group. Administration of FO in the hypoxia groups significantly decreased the gene expression of TNF-α and IL-1β, the number of tonic-clonic seizures, and neuronal cell death in the hippocampus and cerebellum compared to the hypoxia groups. Furthermore, it can improve behavioral tasks and cognitions.

NLRP3 inflammasome-mediated disruption of mitochondrial homeostasis in alveolar macrophages contributes to ozone-induced acute lung inflammatory injury.

Ozone (O 3), a prevalent atmospheric pollutant, can induce lung injury. However, the molecular mechanisms of O 3-induced acute lung inflammatory injury remain unclear. In this study, we investigate the abnormal changes in and molecular mechanism of mitochondrial homeostasis in alveolar macrophages (AMs) in O 3-induced acute lung inflammatory injury mice. Mitochondria and mitochondrial reactive oxygen species (mtROS) are labeled with Mito-Tracker® Deep Red and MitoSOX Red, respectively. Mitochondrial DNA (mtDNA) in AMs from the bronchoalveolar lavage fluid (BALF) is detected via real-time PCR, and the expressions of mitochondrial fusion/fission-related and biogenesis-related proteins in AMs are determined via immunofluorescence staining. Our data show that in O 3-induced acute lung inflammatory injury mice, the number of AMs and the protein expression of the NLRP3 inflammasome complex in the lung tissue are increased. In AMs from O 3-exposed mice, the number of mitochondria, mtROS, and fission-related protein DRP1 are increased, but the levels of Na +-K +-ATPase, fusion-related protein OPA1, biogenesis-related protein NRF1 and mtDNA are significantly decreased. Compared with that in O 3-exposed WT mice, lung inflammation is attenuated, especially the indicators of mitochondrial homeostatic imbalance in AMs, which are alleviated in NLRP3 ‒/‒ and Caspase-1 ‒/‒ mice after O 3 exposure. These findings indicate that the NLRP3 inflammasome-mediated imbalance in mitochondrial homeostasis in AMs contributes to O 3-induced acute lung inflammatory injury. This study may provide a new target for the prevention of lung inflammation induced by O 3.

Biomarkers of Acute Brain Injury

Introduction: Acute brain injury is one of the most important causes of morbidity, mortality and disability worldwide. Time is the most important aspect of acute brain injury management. In this context, biomarkers could mitigate the limitations of neuroimaging. Neuro-biomarkers could be used both to diagnose intracranial pathology and to predict the effectiveness of treatment applications. Aim: The aim of this review is to describe the role of various and specific markers of brain damage with particular emphasis on acute brain injury and stroke. Results/discussion: The diagnostic and prognostic value of modern biomarkers remains relatively questionable, although grouping biomarkers into panels is improving their usefulness. The groups of biomarkers that will be analyzed include astrocytic, axonal, neuronal as well as extracellular biomarkers. Conclusion: Future studies will demonstrate the utility of neuro-biomarkers in the diagnosis, prognosis and therapeutic monitoring of patients with acute brain injury in the intensive care unit.

Pre- and post-therapy functional MRI connectivity in severe acute brain injury with suppression of consciousness: a comparative analysis to epilepsy features.

Severe acute brain injury (SABI) with suppressed consciousness is a major societal burden, with early prognosis being crucial for life-and-death treatment decisions. Resting-state functional MRI (rs-fMRI) is promising for prognosis and identifying epileptogenic activity in SABI. While established for SABI prognosis and seizure networks (SzNET) identification in epilepsy, the rs-fMRI use for SzNET detection in SABI is limited. This study compared evolution of SzNET and resting-state networks (RSN) pre-to-post treatment in SABI and epilepsy, hypothesizing that changes would align with clinical evolution. Therapies included epilepsy surgery for the epilepsy group and antiseizure medication for the SABI group. Independent component analysis (ICA) was used to identify SzNET and RSNs in all rs-fMRI. High-frequency BOLD (HF-BOLD), an ICA power spectrum-based index, quantified RSN and SzNET changes by the patient. Confidence intervals measured HF-BOLD changes pre-to-post-therapy. Baseline HF-BOLD and HF-BOLD changes were compared using linear-mixed models and interaction tests. Five SABI and ten epilepsy patients were included. SzNET were identified in all SABI's pre-therapy rs-fMRI. The clinical changes in SABI and epilepsy were consistent with rs-fMRI findings across groups. HF-BOLD reduced in the epilepsy group RSN post-therapy (-0.78, 95% CI -3.42 to -0.33), but the evidence was insufficient to determine an HF-BOLD reduction in SABI patients or SzNET. The HF-BOLD change trend in pre-to-post epilepsy surgery scans paralleled the clinical improvement, suggesting that the power spectrum may quantify the degree of abnormality on ICA-derived networks. Despite limitations such as small sample sizes, this exploratory study provides valuable insights into network dysfunction in SABI and epilepsy.

Characterization of Age-Dependent Changes in Skeletal Muscle Repair and Regeneration Using a Mouse Model of Acute Muscle Injury.

Acute skeletal muscle injury initiates a process of necrosis, debris clearance, and ultimately tissue regeneration via myogenesis. While skeletal muscle stem cells (MuSCs) are responsible for populating the proliferative myogenic progenitor pool to fuel muscle repair, recruited and resident immune cells have a central role in the regulation of muscle regeneration via the execution of phagocytosis and release of soluble factors that act directly on MuSCs to regulate myogenic differentiation. Therefore, the timing of MuSC proliferation and differentiation is closely linked to the populations and behaviors of immune cells present within skeletal muscle. This has important implications for aging andmuscle repair, as systemic changes in immune system function contribute to a decline in muscle regenerative capacity. Here, we present adapted protocols for the isolation of mononuclear cells from skeletal muscles for the quantification of immune cell populations using flow cytometry. We also describe a cardiotoxin skeletal muscle injury protocol and detail the expected outcomes including immune cell infiltration to the injured sites and formation of new myocytes. As immune cell function is substantially influenced by aging, we extend these approaches and outcomes to aged mice.

Total alkaloids of Aconitum carmichaelii Debx alleviate cisplatin-induced acute renal injury by inhibiting inflammation and oxidative stress related to gut microbiota metabolism

BackgroundCisplatin-induced acute kidney injury (AKI) is a complex and serious clinical issue, representing a major cause of hospital-acquired AKI. Alkaloids are the main active constituents of Aconitum carmichaelii Debx, which exhibit protective effects in several kidney disease models and against other acute organ injuries. However, its activity and mechanism of action in AKI treatment remain unclear. PurposeThis study aimed to elucidate the effect of Aconitum carmichaelii Debx (ACA) in a model of cisplain-induced AKI and comprehensively investigate its underlying mechanisms. MethodsThe major alkaloids in ACA were analyzed using high-performance liquid chromatography. Blood urea nitrogen (BUN) and serum creatine levels were measured using automated biochemical instruments. 16S rRNA sequencing, short-chain fatty acid (SCFA) analysis, fecal microbiota transplantation (FMT), non-targeted metabolomics, and transcriptomics were performed to systematically identify prospective biomarkers after ACA treatment. Anti-inflammatory and anti-oxidative stress activities were monitored using ELISA and western blotting. ResultsFour main compounds (fuziline, neoline, talatisamine, and songorine) were identified in ACA. ACA significantly alleviated cisplatin-induced AKI by reducing (BUN) and serum creatine levels and improving histopathological scores. Moreover, ACA balanced cisplatin-mediated confoundments in microbial composition and function, including decreasing the levels of Escherichia-Shigella, Clostridium, and Ruminococcus, as well as increasing Ligilactobacillus, Anaerotruncus, Bacteroides and Desulfovibrio levels, accompanied by uremic toxin reduction, and augmenting serum SCFAs. The FMT experiments further confirmed that ACA exerts anti-AKI effects by affecting gut microbiota. A multi-omics study has shown that ACA regulates glutathione and tryptophan metabolism and mediates pathways that trigger inflammatory responses. Finally, ACA reduced serum levels of inflammatory factors (IL-1β, IL-6, and TNF-α), restored enzymes of the antioxidative system (SOD and CAT) and GSH values, and decreased monoester diterpene alkaloid levels in the kidney by inhibiting the expression of NF-κB pathway-related proteins and increasing Nrf2/HO-1 pathway-related protein expression. ConclusionACA protects against cisplatin-induced AKI through its anti-inflammatory and antioxidant functions, which may be associated with the restoration of gut microbiota metabolism. ACA is a potential drug for AKI and other forms of organ damage related to the disruption of the gut microbiota.

AKR7A5 knockout promote acute liver injury by inducing inflammatory response, oxidative stress and apoptosis in mice.

Alcohol liver disease has become a worldwide critical health problem. The ingested alcohol could be converted into acetaldehyde or combined with free fatty acids to induce the endoplasmic reticulum oxidative stress in the liver. Coincidentally, AKR7A5 has both aldehyde detoxification and antioxidant effects. Therefore, we discuss the possible role and mechanism of AKR7A5 in the acute alcohol injury of mice liver. There were four experiment groups, the C57BL/6 mice of wild-type mice (WT) or AKR7A5-/- mice (KO) were intragastrically administrated with saline or 50% ethanol at 14 mL/kg, respectively. Compared to the WT + alcohol group, abnormal liver function, disordered hepatic cord, severe congestion in the hepatic sinus and the space of the hepatic cord, occurrence of oxidative stress, DNA damage and different expressions of apoptosis-related proteins were detected in the KO + alcohol group. Meanwhile, the biological process enrichment analysis showed that the down-regulated proteins were related to the metabolism of fatty acid, the up-regulated proteins positive regulation of reactive oxygen species metabolic process, negative regulation of coagulation and haemostasis. In conclusion, single ethanol binge combined with the absence of AKR7A5 caused more severe inflammatory response, oxidative stress, apoptosis of endogenous pathways, abnormal lipids metabolism and disordered coagulation in mice liver.

Severe acute liver disease in adults: Contemporary role of histopathology.

Liver biopsies have consistently contributed to our understanding of the pathogenesis and aetiologies of acute liver disease. As other diagnostic modalities have been developed and refined, the role of biopsy in the management of patients with acute liver failure (ALF), acute-on-chronic liver failure (ACLF) and acute hepatitis, including acute liver injury (ALI), has changed. Liver biopsy remains particularly valuable when first-line diagnostic algorithms fail to determine aetiology. Despite not being identified as a mandatory diagnostic tool in recent clinical guidelines for the management of ALF or ACLF, many centres continue to undertake biopsies given the relative safety of transjugular biopsy in this setting. Several studies have demonstrated that liver biopsy can provide prognostic information, particularly in the context of so-called indeterminate hepatitis, and is extremely useful in excluding conditions such as metastatic tumours that would preclude transplantation. In addition, its widespread use of percutaneous biopsies in cases of less severe acute liver injury, for example in the establishment of a diagnosis of acute presentation of autoimmune hepatitis or confirmation of a probable or definite drug-induced liver injury (DILI), has meant that many centres have seen a shift in the ratio of specimens they are receiving from patients with chronic to acute liver disease. Histopathologists therefore need to be equipped to deal with these challenging specimens. This overview provides an insight into the contemporary role of biopsies (as well as explant and autopsy material) in diagnosing acute liver disease. It outlines up-to-date clinical definitions of liver injury and considers recent recommendations for the diagnosis of AIH and drug-induced, autoimmune-like hepatitis (DI-AIH).

Xiaobugan decoction prevents CCl4-induced acute liver injury by modulating gut microbiota and hepatic metabolism

BackgroundThe liver plays a crucial role in detoxification and metabolism. When its capacity to metabolize foreign substances is exceeded, it can lead to acute liver injury (ALI). Therefore, preventing liver disease and maintaining daily liver health are of utmost importance. Xiaobugan Decoction (XBGD), a traditional Chinese medicine (TCM) formula, is recorded in ‘Fuxingjue’, is used in folk practice to promote liver health and regulate respiration. However, the hepatoprotective mechanisms of XBGD remained unclear. PurposeWe investigated the prophylactic and hepatoprotective effects of XBGD and explored its related molecular mechanisms using a mouse model of carbon tetrachloride (CCl4)-induced ALI. Study design and methodsXBGD composition was determined using analytical methods, and the main compounds were identified using ultra-high-performance liquid chromatography coupled with Q-Exactive focus mass spectrum (UHPLC-QE-MS) and high-performance liquid chromatography (HPLC). A CCl4-induced L02 cell injury model was employed to explore the protective effects of XBGD on liver cells, and a CCl4-induced ALI mouse model was used to investigate the hepatoprotective effects of XBGD. ResultsCellular experiments demonstrated that XBGD had a protective function against L02 cell damage by increasing cell viability, restoring alanine aminotransferase (ALT), aspartate aminotransferase (AST), and superoxide dismutase (SOD) levels, reducing malondialdehyde (MDA) content, and improving mitochondrial membrane potential (ΔΨm). In the mouse ALI model, XBGD prevented ALI by reducing ALT, AST, and alkaline phosphatase (ALP) levels and inhibiting oxidative stress. Quantitative real-time polymerase chain reaction (qPCR), immumohistochemical staining and western blotting results revealed that XBGD exerted hepatoprotective effects by reducing inflammatory responses and inhibiting cell apoptosis. Furthermore, 1H-NMR metabolomics indicated that XBGD regulates hepatic and intestinal metabolism, whereas 16S rDNA sequencing demonstrated the regulatory effects of XBGD on the gut microbiota. Correlation analysis highlighted the close relationship among gut microbiota, metabolites, and ALI indicators. ConclusionsXBGD is a promising TCM for the prevention of CCl4-induced ALI via regulation of microbiota and metabolism. This study provides a new perspective on the development of hepatoprotective measures and the prevention of liver disease in daily life.

Stat5b SNP Reduces Sexual Dimorphism of Renal Gene Expression and Protects against Acute Injury

Stat5b SNP Reduces Sexual Dimorphism of Renal Gene Expression and Protects against Acute Injury

A Case of Fanconi Syndrome with Biopsy-Proven Acute Proximal Tubular Injury Induced by a Dietary Supplement, Benikoji

A Case of Fanconi Syndrome with Biopsy-Proven Acute Proximal Tubular Injury Induced by a Dietary Supplement, Benikoji

Guideline of Management of Acute Smoke Inhalation Injury: Systematic Review and Meta-Analysis of Last 10 Years

Guideline of Management of Acute Smoke Inhalation Injury: Systematic Review and Meta-Analysis of Last 10 Years

Secondary Syphilis Can Simultaneously Mimic Cholestatic Liver Injury and Glomerular Nephropathy

ABSTRACT Syphilis, a disease affecting millions, still poses challenges for men who have sex with men in high-income countries and often presents in varying ways. It is exceedingly rare for syphilis to simultaneously cause an acute liver injury and nephropathy. This case describes the concomitant clinical presentation of these abnormalities and also describes a liver injury that mimicked cholestatic disease. Treatment of syphilis led to complete resolution of the liver and kidney injury. This case demonstrates a need to exclude syphilis in patients with high-risk behaviors who present with cholestatic liver injury in atypical fashions.

LGR6 protects against myocardial ischemia-reperfusion injury via suppressing necroptosis

Regulated necrosis (necroptosis) and apoptosis are important biological features of ischemia-reperfusion (I/R) injury. However, the molecular mechanisms underlying myocardial necroptosis remain elusive. Leucine rich repeat containing G protein-coupled receptor 6 (LGR6) has been reported to play important roles in various cardiovascular disease. In this study, we aimed to determine whether LGR6 suppresses I/R-induced myocardial necroptosis and the underlying molecular mechanisms. We generated LGR6 knockout mice and used ligation of left anterior descending coronary artery to produce an in vivo I/R model. The effects of LGR6 and its downstream molecules were subsequently identified using RNA sequencing and CHIP assays. We observed significantly downregulated LGR6 expression in hearts post myocardial I/R and cardiomyocytes post hypoxia and reoxygenation (HR). LGR6 deficiency promoted and LGR6 overexpression inhibited necroptosis and acute myocardial injury after I/R. Mechanistically, in vivo and in vitro experiments suggest that LGR6 regulates the expression of STAT2 and ZBP1 by activating the Wnt signaling pathway, thereby inhibiting cardiomyocyte necroptosis after HR. Inhibiting STAT2 and ZBP1 effectively alleviated the aggravating effect of LGR6 deficiency on myocardial necroptosis after I/R. Furthermore, activating LGR6 with RSPO3 also effectively protected mice from acute myocardial I/R injury. Our findings reveal that RSPO3-LGR6 axis downregulates the expression of STAT2 and ZBP1 through the Wnt signaling pathway, thereby inhibiting I/R-induced myocardial injury and necroptosis. Targeting the RSPO3-LGR6 axis may be a potential therapeutic strategy to treat myocardial I/R injury.

7023 Hypoinsulinemic Hypoglycemia in a Severely Malnourished Patient with an Acute Liver Injury: A Marker of Poor Outcome!

7023 Hypoinsulinemic Hypoglycemia in a Severely Malnourished Patient with an Acute Liver Injury: A Marker of Poor Outcome!

Concordance of Prebiopsy and Postbiopsy Diagnosis in Patients with Suspected Acute Interstitial Nephritis or Acute Tubular Injury

Concordance of Prebiopsy and Postbiopsy Diagnosis in Patients with Suspected Acute Interstitial Nephritis or Acute Tubular Injury

S4536 The Use of N-Acetylcysteine (NAC) in Cocaine-Induced Acute Liver Injury: A Case Report

S4536 The Use of N-Acetylcysteine (NAC) in Cocaine-Induced Acute Liver Injury: A Case Report