RESUMO
During the course of heparin-induced extracorporeal lipoprotein apheresis, a patient with no prior known renal impairment or proteinuria demonstrated sustained improvement in estimated glomerular filtration rate, commensurate with reduction in serum lipids and creatine phosphokinase levels. Causes and implications of this observation, which was not a priori, are discussed.
Assuntos
Remoção de Componentes Sanguíneos/métodos , Heparina/farmacologia , Hiperlipoproteinemias/terapia , Rim/fisiopatologia , Creatina Quinase/sangue , Feminino , Taxa de Filtração Glomerular , Humanos , Hiperlipoproteinemias/fisiopatologia , Pessoa de Meia-IdadeAssuntos
Transplante de Rim , Rim , Doadores Vivos , Obtenção de Tecidos e Órgãos , Transplantes , Nível de Saúde , Humanos , Índia , Transplante de Rim/economia , Transplante de Rim/legislação & jurisprudência , Doadores Vivos/legislação & jurisprudência , Doadores Vivos/provisão & distribuição , Pobreza , Obtenção de Tecidos e Órgãos/economia , Obtenção de Tecidos e Órgãos/legislação & jurisprudência , Transplantes/economia , Transplantes/provisão & distribuiçãoRESUMO
The early neutropenia that occurs with cellulose-based dialysis membranes is believed to result from a cascade of immune events: complement activation, engagement of leukocyte adhesion molecules, cytokine release, and leukocyte sequestration. The beta2 integrin CR3 (CD11b/CD18) is upregulated during hemodialysis, binds complement factor iC3b, and mediates leukocyte adhesion to endothelium and leukoaggregation. Despite being invoked in dialysis-induced neutropenia, there is no direct evidence of a role for CD11b/CD18 in the neutropenia. A unique animal model of beta2-integrin deficiency was discovered in calves experiencing recurrent infections and a paucity of leukocytes in infected tissue. We hypothesized that beta2 integrins mediate the neutropenia of dialysis and directly tested this hypothesis using beta2-integrin-deficient calves. Two 3-month old beta2-integrin-deficient and two age-matched Holstein calves were dialyzed using cuprophane dialyzers. Beta2-integrin-deficient calves had less than 2% of normal neutrophil CD18 expression by flow cytometry. Normal calves had a marked decrease in circulating neutrophils (P < 0.05) to 15% of normal 15 minutes into dialysis (total, four treatments), as well as a decrease in monocytes to 39% (P < 0.05) and lymphocytes to 58% (P < 0.05). CD18-deficient calves had an attenuated decrease in neutrophils (65%; P = not significant), monocytes (78%; P = not significant), and lymphocytes (105%; P = not significant) at 15 minutes. These data, although obtained in a small sample, show that a bovine model can be used to study the early neutropenia of dialysis. These data also suggest that a direct role of beta2 integrins may be occurring in this process.
Assuntos
Antígenos CD11/fisiologia , Antígenos CD18/fisiologia , Neutropenia/etiologia , Neutropenia/imunologia , Diálise Renal/efeitos adversos , Análise de Variância , Animais , Antígenos CD11/análise , Antígenos CD18/análise , Bovinos , Citometria de Fluxo , Contagem de Leucócitos , Membranas Artificiais , Modelos Animais , Diálise Renal/instrumentação , Tamanho da AmostraRESUMO
To determine whether Diastat grafts can meet the challenges of daily needle punctures required for home hemodialysis (HD), a retrospective analysis was performed on the experience with 47 grafts placed in 44 patients receiving HD three times a week. The control group consisted of 17 patients who received 17 stretch polytetrafluoroethylene (s-PTFE) grafts. Apart from their ability to better contain bleeding after needle withdrawal, in all measures of longevity the Diastat grafts were outperformed by the s-PTFE grafts. No more direct data exist to address the original challenge.