We describe a case of rapid onset of vascular calcification coincident with the initiation of warfarin therapy in a kidney transplant patient. Calcification developed within the media of the blood vessel wall, with relative intimal sparing. Medium and small sized arteries were affected, but the aorta was mostly free of calcifications, suggesting a differential response to warfarin between the intima and media as well as between different vascular beds. In addition, unlike the highly calcified native kidney's vessels, the kidney allograft was not calcified, suggesting local, genetically determined, mechanisms in preventing vascular calcification. Distal subcutaneous necrosis ultimately lead to the patient's demise. Index wordsvascular calcification; warfarin; hemodialysis; MGP Vascular calcification is a major contributor to the morbidity and mortality of end-stage renal disease (ESRD) patients. Whereas atherosclerosis typically involves the vessel intima, ESRD patients are particularly susceptible to a form of vascular calcification involving the media and elastic lamina of large and medium sized arteries. Recently, vitamin K dependent proteins have gained recognition as important components in this process. 1 MGP (matrix Gla protein) acts as a potent vascular calcification inhibitor, and Gas6 (growth arrestspecific 6) controls vascular smooth muscle cell death and calcification. Both are produced by vascular smooth muscle cells, and undergo post-translational carboxylation in order to become biologically active, a process requiring sufficient levels of reduced vitamin K, as well as several important enzymes, including vitamin K epoxide reductase and gammaglutamylcarboxylase. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Financial Disclosure: The authors declare that they have no relevant financial interests. NIH Public Access Author ManuscriptAm J Kidney Dis. Author manuscript; available in PMC 2011 December 1. Warfarin, widely used as an anticoagulant, interferes with the post-translational modification of vitamin K dependent proteins, rendering them inactive. Although its anticoagulant effect has gained widespread therapeutic use, less is known about its potential side effect on vitamin K dependent proteins within the vasculature. In animal models, warfarin administration, albeit at supraphysiological doses, induces widespread medial vascular calcification 2 . Its clinical use has been associated with the development of calciphylaxis 3 , a form of metastatic small vessel calcification, aortic valve and coronary calcification 4 , and stroke 5 .We describe a cas...
Herein we present a case of a patient with systemic lupus erythematosus (SLE) and a sterile empyematous pleural effusion, a complication not generally associated with SLE. A discussion of the diagnostic and treatment dilemmas follows the case presentation. Keywords empyema; nephritis; systemic lupus erythematosus Case presentationA 26-year-old woman from Cape Verde presented to the Beth Israel Deaconess Medical Centre with severe shortness of breath and chest pain. Several months prior to her presentation, the patient developed fever, progressive dyspnea on exertion, arthralgias, fatigue, weight loss (6 kg over 7 months) and a periorbital rash. One month prior to her presentation, she was found to have large bilateral pleural effusions and acute renal failure. Laboratory evaluation disclosed that she had positive anti-dsDNA antibodies and low complement levels; she was started on 60 mg oral prednisone daily. One week prior to admission to our hospital, she underwent leftsided thoracentesis in a hospital at Cape Verde. The laboratory tests from the pleural fluid demonstrated a glucose level less than 10 mg/dL, lactate dehydrogenase (LDH) of 2054 IU/L and a pH of 5.0 (Table 1). Bacterial cultures were negative. No antibiotics were administered.Following this treatment the patient came to the United States for further care. Three days prior to presentation she stopped taking prednisone. Upon presentation to the BIDMC emergency department the patient complained of chest and left flank pain. On physical examination, she was tachycardic, tachypneic and had a temperature of 100.6 °F. She had mild periorbital erythema, dullness to percussion over both lung bases with decreased breath sounds bilaterally and tenderness to palpation over the right flank. She received one tablet of levofloxacin 750 mg for empiric treatment of pneumonia and was admitted to the hospital. Initial laboratory evaluations are shown in Tables 2 and 3. Chest X-ray and computed tomography revealed left greater than right pleural effusions with loculated air (Figure 1 On hospital day one, she underwent thoracentesis of her left-sided effusion and chest tube placement. Pleural fluid laboratory tests and cultures are shown in Table 1. The patient was empirically started on a 14-day course of intravenous Vancomycin 1000 mg every 12 h and piperacillin-tazobactam 4.5 g every 8 h after the procedure. She was also started on prednisone 60 mg, hydroxychloroquine 200 mg and lisinopril 5 mg daily. On hospital day two, she underwent thoracentesis of the right pleural effusion, which was consistent with lupus pleuritis (Table 1). On hospital day five, a renal biopsy was performed. Multiple blood cultures remained negative despite continued fevers on broad-spectrum antibiotics. On hospital day six, she underwent a video-assisted thoracoscopy with total pulmonary decortication. Differential diagnosisPleuritis is the most common manifestation of serositis in patients with systemic lupus erythematosus (SLE). 1,2 Pleural effusions in patients with SLE can als...
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