RESUMEN
BACKGROUND: Preeclampsia (PE) refers to the development of hypertension and new-onset proteinuria or progressive organ damage (especially kidney) in a previously normotensive pregnant women after 20 weeks of gestation. Thus, new-onset nephrotic syndrome due to PE before 20 weeks of gestation seems to be rare, making its diagnosis difficult in this time period. CASE PRESENTATION: A 28-year-old woman presented with a new-onset nephrotic syndrome at 16 weeks of gestation. A high dose of oral glucocorticoids (prednisolone, 40 mg) was initiated for presumed glomerulonephritis since she presented with severe nephrotic syndrome before 20 weeks of gestation, however, the treatment was not effective. At 21 weeks of gestation, we confirmed that the soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PlGF) ratio was very high (sFlt-1, 13,400 pg/mL; PlGF, 21.9 pg/mL; serum sFlt-1/PlGF ratio 611.9). Therefore, we diagnosed nephrotic syndrome due to PE, and oral glucocorticoids were discontinued. After she underwent a cesarean section at 24 weeks & 3 days, we performed a kidney biopsy. Focal segmental sclerotic lesions with epithelial cell hyperplasia and foam cells in the tubular poles were seen on light microscopy. On immunofluorescence tests, C4d staining showed linear peripheral patterns in the glomeruli. Electron microscopy revealed diffuse subendothelial edema with focal foot process effacement. The histological diagnosis was severe glomerular endotheliosis with focal segmental glomerulosclerosis. Furthermore, the histology of placenta was consistent with PE. Eight months after delivery, her proteinuria disappeared completely. CONCLUSIONS: We not only confirmed an abnormal serum sFlt-1/PlGF ratio but also presented the histology compatible with pure PE in the kidney and placenta in a case of nephrotic syndrome before 20 weeks of gestation. The serum sFlt-1/PlGF ratio may be useful in determining the treatment strategy for atypical cases of pregnant women with nephrotic syndrome, particularly before 20 weeks of gestation.
Asunto(s)
Glomeruloesclerosis Focal y Segmentaria/patología , Síndrome Nefrótico/diagnóstico , Preeclampsia/diagnóstico , Adulto , Antihipertensivos/uso terapéutico , Cesárea , Edema/fisiopatología , Femenino , Furosemida/uso terapéutico , Glomeruloesclerosis Focal y Segmentaria/fisiopatología , Glucocorticoides/uso terapéutico , Humanos , Síndrome Nefrótico/patología , Síndrome Nefrótico/fisiopatología , Síndrome Nefrótico/terapia , Factor de Crecimiento Placentario/sangre , Derrame Pleural/fisiopatología , Preeclampsia/sangre , Preeclampsia/fisiopatología , Preeclampsia/terapia , Prednisolona/uso terapéutico , Embarazo , Segundo Trimestre del Embarazo , Recuperación de la Función , Albúmina Sérica Humana/uso terapéutico , Inhibidores del Simportador de Cloruro Sódico y Cloruro Potásico/uso terapéutico , Receptor 1 de Factores de Crecimiento Endotelial Vascular/sangreRESUMEN
CASE PRESENTATION: A 60-year-old woman presented with acute-onset, progressively worsening shortness of breath and pleuritic chest pain for 3 days. She also complained of a dry cough, but no fever or chills. There was no history of swelling of the feet; nor was there a history of nausea or diarrhea. She was a lifelong nonsmoker and had no history of recent travel or sick contacts. Her medical history included hypertension and ulcerative colitis. The ulcerative colitis was in remission and she had not been taking medications for this for over 7 years. Her home medications included alendronate, amlodipine, aspirin, atenolol, and vitamin D3 supplements. She had no allergies.
Asunto(s)
Antiinflamatorios/administración & dosificación , Dolor en el Pecho , Colitis Ulcerosa , Disnea , Derrame Pericárdico , Derrame Pleural , Tórax/diagnóstico por imagen , Dolor en el Pecho/diagnóstico , Dolor en el Pecho/etiología , Colitis Ulcerosa/complicaciones , Colitis Ulcerosa/diagnóstico , Diagnóstico Diferencial , Disnea/diagnóstico , Disnea/etiología , Ecocardiografía/métodos , Femenino , Humanos , Persona de Mediana Edad , Gravedad del Paciente , Derrame Pericárdico/diagnóstico por imagen , Derrame Pericárdico/etiología , Derrame Pericárdico/fisiopatología , Derrame Pericárdico/terapia , Derrame Pleural/diagnóstico por imagen , Derrame Pleural/etiología , Derrame Pleural/fisiopatología , Derrame Pleural/terapia , Serositis/diagnóstico , Serositis/etiología , Toracocentesis/métodos , Tomografía Computarizada por Rayos X/métodos , Resultado del TratamientoRESUMEN
Enternal nutritional support, a frequently applied technique for providing nutrition and energy, played a pivotal role in the treatment of high risk patients. However, severe complications induced by malposition of nasogastric tube caused great danger and even death to the patients. In this case report, we present a patient with severe acute respiratory distress syndrome (ARDS) induced by bronchopleural fistula (BPF) due to malposition of nasogastric tube. Repeated lung lavage combined with extracorporeal membrane oxygenation (ECMO) was performed after transferring to the ICU of our hospital. Finally, the patient recovered and discharged 7 days after admission.
Asunto(s)
Fístula Bronquial/etiología , Lavado Broncoalveolar , Oxigenación por Membrana Extracorpórea , Intubación Gastrointestinal/efectos adversos , Errores Médicos/efectos adversos , Derrame Pleural/etiología , Síndrome de Dificultad Respiratoria/terapia , Anciano , Bronquios/lesiones , Fístula Bronquial/fisiopatología , Nutrición Enteral , Alimentos Formulados/efectos adversos , Humanos , Masculino , Paracentesis , Pleura/lesiones , Derrame Pleural/fisiopatología , Síndrome de Dificultad Respiratoria/etiología , Síndrome de Dificultad Respiratoria/fisiopatología , Índice de Severidad de la Enfermedad , Resultado del TratamientoRESUMEN
OBJECTIVE AND DESIGN: The role of nitric oxide (NO) on leucocyte migration has been investigated in rat carrageenin-induced pleurisy. MATERIAL: Male Wistar rats. TREATMENT: L-arginine, NOC-18 and aminoguanidine were administered subcutaneously 1 h prior to carrageenin injection. METHODS: Leucocyte accumulation into the pleural cavity was measured 4 h after carrageenin challenge. Statistical significance was calculated by Bonferroni test. RESULTS: L-arginine (10 mg/kg) or the NO donor NOC-18 (10 mg/kg), significantly inhibited leucocyte infiltration by 31% and 20% respectively (P<0.01). On the contrary, when these compounds were given at high doses (L-arginine 300 mg/kg; NOC-18 30 mg/kg), leucocyte accumulation was increased by 22% and 33% respectively (P<0.01). Aminoguanidine, a relatively selective inhibitor of the inducible NO synthase, depending on the dose, showed a biphasic effect on cell migration. Thus, at low doses (30 and 100 mg/kg), aminoguanidine increased (by 40% and 74% respectively, P< 0.01) leucocyte infiltration which was inhibited by 41% (P < 0.01) when the drug was given at high dose (300 mg/kg). CONCLUSIONS: These results suggest that in rat carrageenin-induced pleurisy NO primarily inhibits leucocyte migration.
Asunto(s)
Carragenina , Movimiento Celular/efectos de los fármacos , Leucocitos/fisiología , Óxido Nítrico/farmacología , Pleuresia/patología , Animales , Arginina/administración & dosificación , Arginina/farmacología , Presión Sanguínea , Inhibidores Enzimáticos/farmacología , Guanidinas/administración & dosificación , Guanidinas/farmacología , Masculino , Donantes de Óxido Nítrico/administración & dosificación , Donantes de Óxido Nítrico/farmacología , Óxido Nítrico Sintasa/antagonistas & inhibidores , Óxido Nítrico Sintasa de Tipo II , Compuestos Nitrosos/administración & dosificación , Compuestos Nitrosos/farmacología , Pleura/patología , Derrame Pleural/patología , Derrame Pleural/fisiopatología , Pleuresia/inducido químicamente , Ratas , Ratas WistarRESUMEN
This article describes the immunologic and pulmonary abnormalities and the chemical composition of pleural effusion fluid in a patient with intestinal lymphangiectasia as they are effected by therapeutic measures during a 7-year period. Lymphedema was first noticed in the patient at 3 years of age, and pleural effusions developed 7 years later. Thoracentesis demonstrated that the right pleural fluid was yellow, clear, and had the composition of lymph. The left pleural fluid was milky and had a higher triglyceride and lymphocyte content than the right pleural fluid. Complete removal of pleural fluid transiently increased total lung capacity to a maximum of 52% predicted. Strict dietary management with a low-fat and high-protein diet resulted in a transient partial reversal of circulating lymphopenia and low T cell concentration. This was accompanied by a decrease in lymphocyte and T cell concentration in the pleural fluid. Unstimulated mononuclear cells from pleural fluid synthesized increased amounts of DNA, and added mitogens or antigens further increased DNA synthesis. Dietary therapy had a minimal effect on this DNA synthesis. Despite circulating hypogammaglobulinemia, normal antibody activity was detected. The proportion of B cells in pleural fluid was greater than that in the circulation, and dietary therapy did not alter this difference. Pulmonary physiology improved during the initial 9-month period of diet therapy, but then the rate of fluid accumulation increased, causing respiratory compromise. Stability was achieved by a right-sided pleurodesis, followed 18 months later by a left pleurodesis with the addition of a shunt to provide internal lymph drainage.