RESUMEN
BACKGROUND: Aerococcus viridans organisms are Gram-positive cocci that are widely distributed in hospital environments and room air. These bacteria have infrequently been encountered as human pathogens causing bacteremia, endocarditis and urinary tract infections. The significance of these bacteria may be overlooked due to their fastidious growth, and they are often confused with other strains of streptococci or staphylococci. CASE REPORT: We present a case of Aerococcus viridans manifesting as cutaneous vasculitis in an immunocompetent patient. A 30-year-old female patient was admitted to hospital after two weeks history of fever, chills and papular rash over the limbs and trunk. The clinical diagnosis of vasculitis was made. Investigations revealed elevated leucocytosis (21.7 × 109/l) with 81% of neutrophils, and an elevated erythrocyte sedimentation rate or 60 mm/h. Serum anti-neutrophil cytoplasmic antibodies (ANCAs) were not found. Blood culture showed growth of Aerococcus viridans. Histopathological assessment of skin biopsy revealed cutaneous vasculitis. CONCLUSIONS: To date, no clinical case report of this kind has been reported implicating Aerococcus viridans in cutaneous vasculitis. Increased awareness and more studies of this genus should lead to the identification of its potential role in human infections.
RESUMEN
Nephrotic syndrome (NS) is one of the common presentations of kidney diseases both in children and adults. NS patients, particularly those with membranous nephropathy, have increased risk of thromboembolic events. Heparin and vitamin K antagonists (VKAs) continue to be commonly used as prophylactic and therapeutic agents, given the experience of use of these agents in NS and nonrenal indications of anticoagulation. The use of direct oral anticoagulants (DOACs) in NS is reported in some case series, conference abstracts, and a few small studies. We report our experience of using DOACs in 11 patients of NS with severe hypoalbuminemia. Out of 11, one patient required change of anticoagulation from DOACs to VKA and the rest of them did well with DOACs. There were no bleeding episodes in our study. We suggest larger studies to be carried out to better understand the use of these agents in NS.
RESUMEN
Rupture of the urinary bladder and extravasation of urine into the peritoneal cavity leading to urinary ascites is an uncommon event, usually caused by blunt trauma to the abdomen. A high index of suspicion is required for early accurate diagnosis, which avoids unnecessary investigations and interventions. The disappearance of ascites following indwelling Foley's catheterization and high peritoneal fluid urea and creatinine compared to serum values are keys for diagnosis. Sometimes, the diagnosis may be delayed as the features are mistaken for intrinsic renal disease. Here, we report a case of pseudo-acute kidney injury caused by urinary ascites due to intraperitoneal bladder rupture following blunt abdominal trauma in an alcoholic patient.
Asunto(s)
Traumatismos Abdominales , Lesión Renal Aguda , Alcoholismo , Heridas no Penetrantes , Humanos , Ascitis/complicaciones , Alcoholismo/complicaciones , Lesión Renal Aguda/diagnóstico , Lesión Renal Aguda/etiología , Lesión Renal Aguda/terapia , Rotura/complicaciones , Vejiga Urinaria/lesiones , Traumatismos Abdominales/complicaciones , Traumatismos Abdominales/diagnóstico , Heridas no Penetrantes/complicaciones , Heridas no Penetrantes/diagnósticoRESUMEN
Guillain-Barre syndrome (GBS) is an acute polyradiculoneuropathy, caused by dysregulated immune response following an infectious or noninfectious event. Although cardiovascular, respiratory, and gastrointestinal systems are commonly involved secondary to neuromuscular paralysis, renal manifestations are rare. Acute kidney injury (AKI) can develop in GBS due to acute tubular necrosis secondary to dysautonomia. Minimal change nephrotic syndrome in GBS may be due to T-cell dysregulation and cytokine release attributed to molecular mimicry. Here, we report the case of GBS with simultaneously developed AKI and nephrotic syndrome during the course of disease, which recovered completely in parallel with neurological improvement without any immunosuppressive medications.