RESUMO
A 70-year-old man with polycystic kidney disease developed nephrotic syndrome, deteriorating to renal insufficiency. Histological examination revealed IgA nephropathy. With treatment of prednisolone, an angiotensin-converting enzyme inhibitor, and an angiotensin II receptor-blocker, his proteinuria markedly decreased and renal function was stabilized. This case supports the idea that renal biopsy is needed in patients with polycystic kidney disease with nephrotic-range proteinuria, for appropriate treatment and prevention of renal failure.
Assuntos
Glomerulonefrite por IGA/etiologia , Síndrome Nefrótica/etiologia , Rim Policístico Autossômico Dominante/complicações , Idoso , Biópsia , Dipiridamol/uso terapêutico , Glomerulonefrite por IGA/tratamento farmacológico , Humanos , Rim/patologia , Losartan/uso terapêutico , Masculino , Síndrome Nefrótica/tratamento farmacológico , Rim Policístico Autossômico Dominante/tratamento farmacológico , Rim Policístico Autossômico Dominante/patologia , Prednisolona/uso terapêutico , Tiazepinas/uso terapêuticoRESUMO
BACKGROUND/AIMS: Carrageenan is a high molecular weight polysaccharide and is widely used as a food additive for the solidification of plant oils and the thickening of many beverages. It is known that acute toxicity of carrageenan is possibly induced by the activation of phagocytic cells. We investigated other effects of carrageenan on lymphocytes in this study. METHODS: Carrageenan was intraperitoneally injected once into mice and phenotypic and functional characterizations were conducted in various immune organs. RESULTS: Natural killer (NK) cells were prominently activated in the liver, lungs, and spleen. A time-kinetic study showed sequential activation of NK and natural killer T (NKT) cells in the liver on days 3-10 after the injection. In parallel with the activation of NK and NKT cells in number, NK and NKT cytotoxicities were augmented. At this time, liver injury was induced, accompanied by massive hepatic necrosis and the elevation of transaminases. The in vivo elimination of NK cells reduced the liver injury induced by carrageenan. Direct binding of carrageenan onto NK cells was also demonstrated. Such a binding then induced a subsequent production of IFN gamma. Perforin molecules of NK cells were responsible for this liver injury. CONCLUSIONS: These results suggest that not only phagocytic cells but also primitive lymphocyte (mainly NK cells) subsets might be important targets for the acute toxicity of carrageenan.
Assuntos
Carragenina/farmacologia , Células Matadoras Naturais/imunologia , Hepatopatias/imunologia , Linfócitos T Citotóxicos/imunologia , Animais , Divisão Celular/imunologia , Interferon gama/biossíntese , Células Matadoras Naturais/citologia , Células Matadoras Naturais/efeitos dos fármacos , Cinética , Fígado/citologia , Fígado/imunologia , Pulmão/citologia , Pulmão/imunologia , Ativação Linfocitária/efeitos dos fármacos , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Camundongos Knockout , Baço/citologia , Baço/imunologia , Linfócitos T Citotóxicos/citologia , Linfócitos T Citotóxicos/efeitos dos fármacosRESUMO
A 40-year-old woman was referred to our hospital with severe hypovolemic shock and anasarca. The laboratory findings showed marked hemoconcentration and a decrease in total serum protein with the presence of monoclonal IgG-lambda. She had had a similar episode of generalized edema 2 years previously. We diagnosed the patient as having typical systemic capillary leak syndrome (SCLS) and she improved gradually after infusion of albumin-containing fluid. SCLS is a very rare condition caused by unexplained episodic capillary hyperpermeability. Its treatment has remained largely supportive and the prognosis is generally poor. Awareness of SCLS is necessary for improvement of the outcome.
