Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute kidney injury (AKI) is frequently seen in Hemiscorpius lepturus scorpion stung children. We have previously reported several victims with hemolytic uremic syndrome (HUS) and a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 deficiency. Hence, we conducted this study to identify predictive factors and clinical features of AKI in H. lepturus scorpion stung patients. We included all 215 H. lepturus scorpion stung children with no previous renal diseases in two groups (with and without AKI) and compared them based on their clinical and laboratory findings. AKI was found in 27.4% of patients, they were significantly younger and with lower body weight (P = 0.006, P = 0.011, respectively). There was a significant difference between groups with and without AKI in findings such as fever (P = 0.003), hypertension (P <0.001), hemolytic anemia (P <0.001), thrombocytopenia (P <0.001), massive proteinuria (P <0.001), hemoglobinuria (P <0.001), pyuria (P <0.001), and hematuria (P = 0.004). HUS was in 5.5% and disseminated intravascular coagulation in 14.6% which had a significant association with AKI (P <0.001).There were several independent predictors for AKI in a multivariate regression model including thrombocytopenia (P = 0.002), pyuria (P = 0.01), proteinuria (P =0.01), and fever (P = 0.02). Hemodialysis was performed in four patients but kidney function improved in all patients and there was no findings of renal impairment after three months follow-up. We found several predictors for AKI in children following H. lepturus scorpion sting including younger age, delay in receiving medical care, pigmenturia, microangiopathic hemolytic anemia, proteinuria, and pyuria.
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PMID:Acute kidney injury in Hemiscorpius lepturus scorpion stung children: Risk factors and clinical features. 2775 1

Intravascular hemolysis is relatively rare but can lead to acute kidney injury (AKI), from increased destruction of erythrocytes and release of free hemoglobin. Since hemolysis and hemoglobinuria are known causes of acute kidney injury we sought to define clinicopathologic findings and outcomes of patients with hemolysis-associated hemoglobin cast nephropathy through a retrospective analysis of 27 cases. The mean patient age was 47 years (range 19-79) and the female-to-male ratio was 1.3:1. All patients presented with AKI with a mean serum creatinine of 8.0 (range 2.9-17.0) mg/dL. Etiologies included autoimmune hemolytic anemia (30%), medication (26%), paroxysmal nocturnal hemoglobinuria (7%), procedural/mechanical causes (7%), transfusion of incompatible blood (4%), toxin ingestion (4%), disseminated intravascular coagulation (4%), and hemoglobinopathy (4%). All biopsies showed acute tubular injury and pigmented, proteinaceous casts characterized by positive hemoglobin immunohistochemistry. After a mean follow-up of nine months (range 0.5-26), the mean serum creatinine was 1.3 (range 0.6-3.3) mg/dL, with 78% of patients returning to normal kidney function. Thus, based on our clinicopathologic case series, hemolysis-associated hemoglobin cast nephropathy is an important entity for clinicians and pathologists to recognize as treatment hinges upon elimination of the pathogenic driver of intravascular hemolysis.
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PMID:Hemolysis-associated hemoglobin cast nephropathy results from a range of clinicopathologic disorders. 3166 30

Venous malformations are very commonly encountered in interventional radiologic practice. Indications for therapy are clearly defined based on the lesion's impact on patient's quality of life. Screening laboratory coagulation studies in patients with historical or lesion morphologic risk factors often reveal abnormal coagulation parameters consistent with localized intravascular coagulation or more severe coagulopathic states. These may require chronic or periprocedural medical management to avoid potentially life-threatening disseminated intravascular coagulation or other thromboembolic phenomena. Once a multidisciplinary decision to treat a venous malformation is made, one must decide between percutaneous and/or surgical techniques. Sclerotherapy with adjunctive stasis of efflux (STASE) techniques have become the mainstay of therapy for most venous malformations as they are well-tolerated and effective. STASE techniques work primarily by (i) the administration of sclerosant(s) exerting an inhibitory and/or endotheliocidal effect on venous malformation endothelium leading to thrombosis, involution, and fibrosis, and secondarily via adjunctive outflow occlusion using any combination of local compression, balloons, gelatin, coils, laser, radiofrequency, or adhesives to improve sclerosant penetration and dwell-time in the lesion. Adhesives alone can fill the lesion to facilitate surgical resection in some cases. Common sclerosants in modern practice include sodium tetradecyl sulfate, bleomycin, polidocanol, ethanol, and hypertonic saline. Most agents can be given directly in unmodified or "neat" form or can be mixed with a gas to form a sclerofoam or embolic such as gelatin to form a sclerogel. Choice and method of sclerosant delivery in each patient is based on the intraluminal lesion volume, architecture, vital structure proximity, agent toxicity, viscosity, and level of experience of the interventional radiologist with that particular agent. Multi-session STASE therapy usually reduces symptoms of chronic pain or mass with low risk of known complications of skin or nerve impairment, compartment syndrome, hemoglobinuria, deep venous thrombosis, or pulmonary phenomena.
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PMID:Sclerotherapy with Adjunctive Stasis of Efflux (STASE) in Venous Malformations: Techniques and Strategies. 3186 35


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