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2.
Praxis (Bern 1994) ; 97(15): 845-7, 2008 Jul 30.
Artigo em Alemão | MEDLINE | ID: mdl-18754338

RESUMO

We discuss the case of a young man presenting with "renal colic" whose flank pain however, turned out to be the result of renal infarction due to dissection of an accessory renal artery with fibromuscular dysplasia. The condition was diagnosed after exclusion of nephrolithiasis and work-up of new onset arterial hypertension developing in the later course. He was successfully treated by ethanol ablation (renal ethanol angioinfarction) and coiling of the accessory renal artery with resolution of hypertension in the absence of any antihypertensive medication.


Assuntos
Cólica/etiologia , Infarto/diagnóstico , Nefropatias/etiologia , Rim/irrigação sanguínea , Obstrução da Artéria Renal/diagnóstico , Adulto , Algoritmos , Dissecção Aórtica/diagnóstico , Dissecção Aórtica/terapia , Aortografia , Cólica/terapia , Diagnóstico Diferencial , Embolização Terapêutica , Displasia Fibromuscular/diagnóstico , Displasia Fibromuscular/terapia , Humanos , Infarto/terapia , Nefropatias/terapia , Masculino , Artéria Renal/anormalidades , Obstrução da Artéria Renal/terapia , Tomografia Computadorizada por Raios X
3.
Int J Artif Organs ; 30(1): 16-24, 2007 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-17295189

RESUMO

BACKGROUND: Intradialytic morbid events (IMEs, mostly hypotension) are frequent complications during hemodialysis (HD). This study investigated whether automatic feedback control via adjustment of the ultrafiltration rate reduces IME frequency. METHODS: In this multi-center cross-over study, 56 hypotension-prone patients were treated both with standard HD (sHD, applying a constant ultrafiltration rate) and HD applying a blood volume controlled ultrafiltration rate (cHD). The relative blood volume (RBV) was continuously monitored. The individual relative blood volume limit (RBVcrit ) was determined from the measured RBV during initial sHD. During cHD, the ultrafiltration rate was automatically adjusted to keep the actual RBV above RBVcrit. RESULTS: In 3,081 HD treatments, slightly fewer IMEs were observed during cHD than during sHD (0.785+/-0.613 versus 0.695+/-0.547 per treatment, P=0.144). Less symptomatic events were seen during cHD: -13% for symptomatic hypotension (0.594 versus 0.685 per treatment, P=0.120), and -32% for cramps (0.049 versus 0.072 per treatment, P=0.009). Thirty-one patients with the highest IME rate (IME in at least every second treatment) especially benefited from cHD: 1.185+/-0.554 versus 0.979+/-0.543 IME per treatment (P=0.004). The reduction in blood pressure (BP) and the increase in heart rate were lower during the treatments with cHD than with sHD: systolic BP: -18.8+/-26.7 versus -22.2+/-28.9 mmHg (P=0.007), diastolic BP: -7.8+/-14.8 versus -9.1+/-15.3 mmHg (P=0.064), heart rate: 1.8+/-10.4 versus 2.3+/-11.6 per minute (P=0.014). Neither treatment duration nor ultrafiltration volume was significantly different between cHD and sHD. CONCLUSION: For cHD, less intradialytic morbid events were observed than for sHD, and pre- to post-dialytic changes in blood pressure and heart rate were less pronounced.


Assuntos
Diálise Renal/efeitos adversos , Diálise Renal/métodos , Idoso , Pressão Sanguínea , Volume Sanguíneo , Estudos Cross-Over , Hemodiafiltração , Humanos , Hipotensão/etiologia , Cãibra Muscular/etiologia , Ultrafiltração
4.
Praxis (Bern 1994) ; 95(23): 949-51, 2006 Jun 07.
Artigo em Alemão | MEDLINE | ID: mdl-16779906
8.
Ther Umsch ; 59(3): 117-21, 2002 Mar.
Artigo em Alemão | MEDLINE | ID: mdl-11975399

RESUMO

Progressive renal failure occurs in a large number of patients even in the absence of the original cause of injury. It is suggested that the initial reduction in nephron number progressively damages the remaining ones. Various mechanisms underlie the pathogenesis of progressive glomerular injury. Several studies have extensively shown that both dietary protein restriction and pharmacologic intervention with ACE-inhibitiors and angiotensin receptor antagonists effectively slow the progression of chronic renal diseases. This article will present treatment recommendations designed to delay the progression of chronic renal disease, to optimize its medical management and to reduce complications induced by renal insufficiency including hypertension, renal osteodystrophy and anemia. Ten steps in the management of patients with chronic renal failure recommended by an international panel of experts based on existing guidelines are presented.


Assuntos
Falência Renal Crônica/terapia , Anemia/tratamento farmacológico , Anemia/etiologia , Inibidores da Enzima Conversora de Angiotensina/administração & dosagem , Inibidores da Enzima Conversora de Angiotensina/uso terapêutico , Calcitriol/uso terapêutico , Agonistas dos Canais de Cálcio/uso terapêutico , Distúrbio Mineral e Ósseo na Doença Renal Crônica/tratamento farmacológico , Distúrbio Mineral e Ósseo na Doença Renal Crônica/etiologia , Diuréticos/uso terapêutico , Eritropoetina/administração & dosagem , Eritropoetina/uso terapêutico , Taxa de Filtração Glomerular , Humanos , Hipertensão Renal/tratamento farmacológico , Hipertensão Renal/etiologia , Falência Renal Crônica/complicações , Falência Renal Crônica/dietoterapia , Falência Renal Crônica/tratamento farmacológico , Testes de Função Renal , Proteinúria/diagnóstico , Proteinúria/etiologia , Terapia de Substituição Renal
11.
J Infect Dis ; 184(2): 206-10, 2001 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-11424020

RESUMO

Adult Macaca radiata (n=22) were infected intragastrically with 10(12) Escherichia coli O157:H7 strain 84-01, which produces Shiga toxins 1 and 2. Clinical symptoms and bacterial excretion were documented in each monkey for a specified time period before they were killed. At necropsy, samples were obtained for culture and histologic and ultrastructural examination. Seventeen monkeys had diarrhea: E. coli O157 was isolated from postinfection stool samples from all monkeys and from autopsy cultures for 14 of 22 monkeys. Histologic examination showed attaching-effacing lesions, which appeared at 12 h and persisted for 7 days, in 12 monkeys. Widening of the intercellular spaces, degeneration and vacuolization of the epithelial cells, epithelial tufting, extrusion of epithelial cells, and neutrophilic infiltration were characteristic features seen in 20 of the 22 infected monkeys but not in 4 control monkeys. This monkey model closely parallels the early stages of the disease produced by E. coli O157:H7 and would be useful in the further study of pathogenic mechanisms and prevention methods in enterohemorrhagic E. coli infections.


Assuntos
Diarreia/microbiologia , Infecções por Escherichia coli/complicações , Infecções por Escherichia coli/patologia , Hemorragia Gastrointestinal/microbiologia , Hemorragia Gastrointestinal/patologia , Mucosa Intestinal/patologia , Animais , Diarreia/patologia , Modelos Animais de Doenças , Macaca radiata , Microscopia Eletrônica
12.
Infect Immun ; 68(9): 5167-75, 2000 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-10948140

RESUMO

The protozoan parasite Cryptosporidium parvum is a significant cause of diarrheal disease worldwide. Attachment to and invasion of host intestinal epithelial cells by C. parvum sporozoites are crucial steps in the pathogenesis of cryptosporidiosis. The molecular basis of these initial interactions is unknown. In order to identify putative C. parvum adhesion- and invasion-specific proteins, we raised monoclonal antibodies (MAbs) to sporozoites and evaluated them for inhibition of attachment and invasion in vitro. Using this approach, we identified two glycoproteins recognized by 4E9, a MAb which neutralized C. parvum infection and inhibited sporozoite attachment to intestinal epithelial cells in vitro. 4E9 recognized a 40-kDa glycoprotein named gp40 and a second, >220-kDa protein which was identified as GP900, a previously described mucin-like glycoprotein. Glycoproteins recognized by 4E9 are localized to the surface and apical region of invasive stages and are shed in trails from the parasite during gliding motility. The epitope recognized by 4E9 contains alpha-N-acetylgalactosamine residues, which are present in a mucin-type O-glycosidic linkage. Lectins specific for these glycans bind to the surface and apical region of sporozoites and block attachment to host cells. The surface and apical localization of these glycoproteins and the neutralizing effect of the MAb and alpha-N-acetylgalactosamine-specific lectins strongly implicate these proteins and their glycotopes as playing a role in C. parvum-host cell interactions.


Assuntos
Anticorpos Monoclonais/imunologia , Cryptosporidium parvum/fisiologia , Mucinas/fisiologia , Animais , Células CACO-2 , Epitopos , Glicosilação , Interações Hospedeiro-Parasita , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Peso Molecular , Mucinas/imunologia
13.
J Infect Dis ; 182 Suppl 1: S139-42, 2000 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-10944496

RESUMO

Nutrition is a central public health concern in the twenty-first century. Previous international research in nutrition was primarily descriptive epidemiology and included large-scale intervention trials. There has been insufficient attention to the mechanisms by which nutrient supplements appear to reduce mortality and little specificity in application and delineation of the forms of a specific nutrient to maximize benefits and minimize adverse affects and on the effect of nutrient combinations. After the dramatic success of the green revolution, agricultural research support was reduced despite an expanding world population and an increasing need for agricultural products. The potential of molecular genetics to improve food quality, specific nutrient content, and yield and disease resistance has just begun to be explored. In addition, the development of edible vaccines as a way to immunize a greater proportion of the world's children is a highly desirable goal and is achievable with sufficient resources.


Assuntos
Infecções/fisiopatologia , Cooperação Internacional , Micronutrientes , National Institutes of Health (U.S.) , Fenômenos Fisiológicos da Nutrição , Saúde Pública , Apoio à Pesquisa como Assunto/tendências , Humanos , Estados Unidos
16.
J Infect Dis ; 181(2): 664-70, 2000 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-10669353

RESUMO

Shiga toxin-producing Escherichia coli (STEC) cause significant disease; treatment is supportive and antibiotic use is controversial. Ciprofloxacin but not fosfomycin causes Shiga toxin-encoding bacteriophage induction and enhanced Shiga toxin (Stx) production from E. coli O157:H7 in vitro. The potential clinical relevance of this was examined in mice colonized with E. coli O157:H7 and given either ciprofloxacin or fosfomycin. Both antibiotics caused a reduction in fecal STEC. However, animals treated with ciprofloxacin had a marked increase in free fecal Stx, associated with death in two-thirds of the mice, whereas fosfomycin did not. Experiments that used a kanamycin-marked Stx2 prophage demonstrated that ciprofloxacin, but not fosfomycin, caused enhanced intraintestinal transfer of Stx2 prophage from one E. coli to another. These observations suggest that treatment of human STEC infection with bacteriophage-inducing antibiotics, such as fluoroquinolones, may have significant adverse clinical consequences and that fluoroquinolone antibiotics may enhance the movement of virulence factors in vivo.


Assuntos
Anti-Infecciosos/toxicidade , Toxinas Bacterianas/biossíntese , Ciprofloxacina/toxicidade , Colífagos/efeitos dos fármacos , Infecções por Escherichia coli/microbiologia , Escherichia coli O157/efeitos dos fármacos , Animais , Antibacterianos/farmacologia , Anti-Infecciosos/farmacologia , Toxinas Bacterianas/genética , Ciprofloxacina/farmacologia , Colífagos/genética , Colífagos/fisiologia , Modelos Animais de Doenças , Infecções por Escherichia coli/tratamento farmacológico , Infecções por Escherichia coli/mortalidade , Escherichia coli O157/metabolismo , Escherichia coli O157/virologia , Fosfomicina/farmacologia , Humanos , Intestinos/virologia , Masculino , Camundongos , Toxinas Shiga
17.
Infect Immun ; 67(12): 6670-7, 1999 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-10569789

RESUMO

Shiga toxin-producing Escherichia coli (STEC) is an important food-borne pathogen that causes hemolytic-uremic syndrome. Following ingestion, STEC cells colonize the intestine and produce Shiga toxins (Stx), which appear to translocate across the intestinal epithelium and subsequently reach sensitive endothelial cell beds. STEC cells produce one or both of two major toxins, Stx1 and Stx2. Stx2-producing STEC is more often associated with disease for reasons as yet undetermined. In this study, we used polarized intestinal epithelial cells grown on permeable filters as a model to compare Stx1 and Stx2 movement across the intestinal epithelium. We have previously shown that biologically active Stx1 is able to translocate across cell monolayers in an energy-dependent, saturable manner. This study demonstrates that biologically active Stx2 is also capable of movement across the epithelium without affecting barrier function, but significantly less Stx2 crossed monolayers than Stx1. Chilling the monolayers to 4 degrees C reduced the amount of Stx1 and Stx2 movement by 200-fold and 20-fold respectively. Stx1 movement was clearly directional, favoring an apical-to-basolateral translocation, whereas Stx2 movement was not. Colchicine reduced Stx1, but not Stx2, translocation. Monensin reduced the translocation of both toxins, but the effect was more pronounced with Stx1. Brefeldin A had no effect on either toxin. Excess unlabeled Stx1 blocks the movement of (125)I-Stx1. Excess Stx2 failed to have any effect on Stx1 movement. Our data suggests that, despite the many common physical and biochemical properties of the two toxins, they appear to be crossing the epithelial cell barrier by different pathways.


Assuntos
Toxinas Bacterianas/metabolismo , Mucosa Intestinal/citologia , Mucosa Intestinal/metabolismo , Animais , Transporte Biológico , Brefeldina A/farmacologia , Linhagem Celular , Polaridade Celular , Chlorocebus aethiops , Colchicina/farmacologia , Células Epiteliais/citologia , Células Epiteliais/metabolismo , Humanos , Monensin/farmacologia , Toxinas Shiga , Células Vero
18.
Infect Immun ; 67(11): 5985-93, 1999 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-10531258

RESUMO

In the 1980s, Shiga toxin (Stx)-producing Escherichia coli O157:H7 (STEC) was identified as a cause of hemorrhagic colitis in the United States and was found to be associated with hemolytic uremic syndrome (HUS), a microangiopathic hemolytic anemia characterized by thrombocytopenia and renal failure. The precise way that Stxs cause hemorrhagic colitis and HUS is unclear. Stxs have been thought to cause disease by killing or irreversibly harming sensitive cells through a nonspecific blockade of mRNA translation, eventually resulting in cytotoxicity by preventing synthesis of critical molecules needed to maintain cell integrity. Because STEC is noninvasive, we have been exploring the host-toxin response at the level of the gastrointestinal mucosa, where STEC infection begins. We have found that Stx is capable of interleukin-8 (IL-8) superinduction in a human colonic epithelial cell line. Despite a general blockade of mRNA translation, Stx treatment results in increased IL-8 mRNA as well as increased synthesis and secretion of IL-8 protein. Our data suggest that an active Stx A subunit is required for this activity. Ricin, which has the same enzymatic activity and trafficking pathway as Stx, has similar effects. Exploration of the effects of other protein synthesis inhibitors (cycloheximide, anisomycin) suggests a mechanism of gene regulation that is distinct from a general translational blockade. Use of the specific p38/RK inhibitor SB202190 showed that blocking of this pathway results in decreased Stx-mediated IL-8 secretion. Furthermore, Stxs induced mRNA of the primary response gene c-jun, which was subsequently partially blocked by SB202190. These data suggest a novel model of how Stxs contribute to disease, namely that Stxs may alter regulation of host cell processes in sensitive cells via activation of at least one member of the mitogen-activated protein kinase family in the p38/RK cascade and induction of c-jun mRNA. Stx-induced increases in chemokine synthesis from intestinal epithelial cells could be important in augmenting the host mucosal inflammatory response to STEC infection.


Assuntos
Toxinas Bacterianas/toxicidade , Interleucina-8/metabolismo , Mucosa Intestinal/efeitos dos fármacos , Anisomicina/farmacologia , Cicloeximida/farmacologia , Genes jun , Humanos , Imidazóis/farmacologia , Interleucina-8/genética , Mucosa Intestinal/metabolismo , Proteínas Quinases JNK Ativadas por Mitógeno , Proteínas Quinases Ativadas por Mitógeno/fisiologia , Piridinas/farmacologia , RNA Mensageiro/análise , Toxinas Shiga , Células Tumorais Cultivadas , Fator de Necrose Tumoral alfa/farmacologia
19.
Scand J Gastroenterol ; 34(8): 777-83, 1999 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-10499478

RESUMO

BACKGROUND: Shiga toxin causes net fluid secretion in rabbit jejunum by selectively targeting, and inhibiting protein synthesis in, absorptive villous cells. The effect of Shiga toxin on the colon, where it is presumably produced, is not known. This study was undertaken to investigate the effect of Shiga toxin on the rat distal colon. METHODS: Net absorption of water and Na was determined by in vivo perfusion of closed loops of rat colon pre-exposed to Shiga toxin or saline. Unidirectional and net fluxes of 22Na and 36Cl were measured in vitro under voltage-clamp conditions across rat distal colon mucosa pre-exposed to Shiga toxin. Shiga toxin binding to sections of rat distal colon was localized by immunohistochemistry. Protein synthesis was measured in surface and crypt colonocytes with 3H-leucine incorporation. RESULTS: In the in vivo perfusion studies net absorption of Na and water was increased in Shiga toxin-treated colon compared with controls (P < 0.01). In the studies carried out in vitro, J(net)Na and J9net)Cl across Shiga toxin-treated mucosa were found to be significantly higher than in control tissue (P < 0.001 and P < 0.01, respectively). Net absorption of Na or Cl did not increase further in the presence of 25 mM butyrate, indicating the absence of short-chain fatty acids (SCFA)-linked NaCl absorption in Shiga toxin-treated colon. Moreover, Shiga toxin-treated colon failed to respond to theophylline, which induced secretion in the normal colon. Immunohistochemistry showed Shiga toxin binding to crypt cells but not to surface cells in the distal colon. Shiga toxin inhibited protein synthesis (by 27.3%) in crypt cells but not in surface cells (P < 0.05). CONCLUSIONS: An unexpected increase in water and NaCl absorption was noted in Shiga toxin-treated rat distal colon, which appears to result from selective effects of the toxin on secretory crypt cells.


Assuntos
Toxinas Bacterianas/farmacologia , Colo/efeitos dos fármacos , Exotoxinas/farmacologia , Transporte de Íons/efeitos dos fármacos , Cloreto de Sódio/metabolismo , Animais , Toxinas Bacterianas/metabolismo , Colo/metabolismo , Exotoxinas/metabolismo , Feminino , Imuno-Histoquímica , Técnicas In Vitro , Absorção Intestinal , Masculino , Ligação Proteica , Radioisótopos , Ratos , Ratos Wistar , Toxinas Shiga , Shigella dysenteriae , Estatísticas não Paramétricas
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