Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Proceed order?

Export
  • 1
    facet.materialart.
    Unknown
    German Medical Science; Düsseldorf, Köln
    In:  Hypertonie 2004; 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga; 20041124-20041127; Hannover; DOC04hochP40 /20050810/
    Publication Date: 2005-08-11
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Keywords: RECEPTOR ; EXPRESSION ; Germany ; MODEL ; SUPPORT ; VOLUME ; TISSUE ; MICE ; INJURIES ; LIGAND ; NEPHRITIS ; RANTES ; kidney ; MACROPHAGES ; murine ; MARKER ; renal ; RAT ; CONTRAST ; INJECTION ; fibroblasts ; treatment ; IDENTIFICATION ; LESIONS ; immunohistochemistry ; MARKERS ; LIGANDS ; RECRUITMENT ; leukocyte ; STRATEGIES ; intravenous ; NEPHROPATHY ; chemokine ; INITIATION ; ANTAGONIST ; inflammation ; INJURY ; FOCAL SEGMENTAL GLOMERULOSCLEROSIS ; CHEMOKINE RECEPTOR ; fibrosis ; PERSISTENT ; INFILTRATION ; MURINE MODEL ; chemokines ; OBSTRUCTIVE NEPHROPATHY ; progressive nephropathy ; receptor blockade ; RENAL-DISEASE
    Abstract: Background. CC chemokines mediate leukocyte infiltration into inflamed tissue. We have recently shown that blockade of the CC chemokine receptor CCR1 reduces interstitial inflammation and fibrosis in murine obstructive nephropathy. However, it is not known whether CCR 1 blockade is protective in progressive renal injury associated with severe proteinuria. We therefore studied the effect of the small-molecule CCR1 antagonist BX471 in a murine model of adriamycin-induced focal segmental glomerulosclerosis (FSGS) with nephrotic syndrome and progressive interstitial inflammation and fibrosis. Methods. Adriamycin nephropathy with persistent proteinuria was induced in male BALB/c mice by two intravenous injections of adriamycin (13 mg/kg) at day 0 and 14. BX471 treatment was started at day 14 when proteinuria and interstitial inflammation had developed. At 6 weeks, renal histology was studied by morphometry and immunohistochemistry. Results. At week 6, adriamycin-treated mice showed FSGS, associated with tubulointerstitial injury consisting of tubular dilation and atrophy, interstitial leukocyte infiltration, and fibrosis. The mRNA expression of CCR1 and CC chemokines, including the CCR1 ligands CCL3 (MIP-1alpha) and CCL5 (RANTES), was up-regulated in diseased kidneys, with a prominent interstitial expression of CCL5. Compared to vehicle-treated controls BX471 significantly reduced the amount of macrophages and Tlymphocytes in interstitial lesions by 51% and 22%, respectively. Markers of renal fibrosis such as interstitial fibroblasts (48%) and interstitial volume (23%) were significantly reduced by BX471 treatment. In contrast, the extent of proteinuria and glomerular sclerosis was not affected by BX471 treatment. Conclusion. Blockade of CCR1 substantially reduced interstitial leukocyte accumulation and the subsequent renal fibrosis in a murine model of nephrotic syndrome and FSGS. These findings support a role for CCR1 in interstitial leukocyte recruitment and suggest that CCR1 blockade might be a new therapeutic strategy in progressive nephropathies such as FSGS
    Type of Publication: Journal article published
    PubMed ID: 15569315
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: albumin, apheresis, BIOPSIES, BIOPSY, BLOOD, cryoglobulinemia, CRYOGLOBULINEMIC GLOMERULONEPHRITIS,
    Abstract: A 38-year-old pregnant woman (19th week of pregnancy) complained of fatigue, cold inducible paresthesias, generalized edema and mild arterial hypertension. Her past medical history was notable for frequent episodes of polyarthralgia and positivity for rheumatoid factor. On admission, acanthocyturia and unselective glomerular-tubular proteinuria with 19 g/d were detected with a slight decrease in creatinine clearance. Rheumatoid factor was robustly elevated and a cryocrit of 1.5 vol%, caused by a so far unknown replicative hepatitis C, was detected. Renal biopsy yielded membrano-proliferative glomerulonephritis. During pregnancy, high-dose corticosteroid therapy was administered. Edema disappeared and blood pressure normalized under albumin substitution and low-dose furosemide application. However, Cesarian section became necessary due to placental insufficiency at 27 weeks of gestation. Thereafter, neither virus load, cryocrit nor proteinuria decreased significantly under a combined therapy with pegylated interferon-a and ribavirin. Thus, cryoprecipitate apheresis was initiated resulting in robust decreases of clinical complaints, viral load, cryocrit and proteinuria. Cryoglobulinemia with renal involvement caused by hepatitis C is difficult to treat due to limitations of immunosuppressive and anti-viral therapy. In our patient, cryoprecipitate apheresis was a safe and effective therapeutic addition to standard therapy
    Type of Publication: Journal article published
    PubMed ID: 17474561
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Keywords: BLOOD ; Germany ; DENSITY ; HISTORY ; NEW-YORK ; PROTEIN ; PROTEINS ; HEART ; PATIENT ; kidney ; FAMILY ; antibodies ; antibody ; CLEAVAGE ; DELETION ; NO ; family history ; MUTATION ; PRESSURE ; BLOOD-PRESSURE ; ABNORMALITIES ; echocardiography ; FAILURE ; ultrasound ; SERUM ; DEFICIENCY ; FAMILIES ; LEVEL ; heparin ; FAMILY-HISTORY ; USA ; SYMPTOMS ; ARF ; FRAGMENT ; COMPLEMENT ; thrombotic thrombocytopenic purpura ; ACUTE-RENAL-FAILURE ; HUS
    Abstract: A 36-year-old patient complained of progressing fatigue, lack of appetite, and weakness for a few weeks, for which he had been using paracetamol (acetaminophen) intermittently. He was referred to our center from another hospital with hemolysis, thrombocytopenia, and acute renal failure (ARF). On admission, the patient did not complain of any specific additional symptoms. Besides paracetamol, he had not received any other medication. The patient reported flu-like symptoms 3 months before admission. The family history was unremarkable. Physical examination revealed a pale-looking patient (180 cm; 81 kg) with icteric sclerae. He was tachycardic (110 heart beats per min) and had elevated blood pressure (155/90mmHg). No other physical abnormalities were detectable. Laboratory investigations are depicted in Table 1. Specific analyses: von Willebrand factor cleavage protease activity 31% (40-120%), von Willebrand Factor Multimere negative, antibodies to von Willebrand Factor cleavage protease negative, factor H 614 mgl(-1) (345-590 mgl(-1)). Western blot analyses with patient's serum revealed the presence of complement factor H (CFH) and complement factor H-like protein 1 (CFHL1), but no detectable levels of complement factor H-related proteins 1 and 3 (CFHR1 and CFHR3) (Figure 1a). Antibodies to CFHR1 were negative. Genetic analyses 1 showed no CFH mutation, but revealed homozygous deletion of a 83 kb genomic fragment representing CFHR3 and CFHR1 (Figure 1b). Kidneys were of normal size with increased density by ultrasound examination. Electrocardiography revealed ischemic changes posteroseptally, and hypertrophy of the left ventricle was diagnosed by echocardiography
    Type of Publication: Journal article published
    PubMed ID: 18449173
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Keywords: brain ; Germany ; DIAGNOSIS ; imaging ; HISTORY ; SKIN ; MAGNETIC-RESONANCE ; magnetic resonance imaging ; LESIONS ; PLASMA ; ATHEROSCLEROSIS ; cholesterol ; ANGIOGRAPHY ; FAILURE ; proteinuria ; BIOPSY ; MEDICAL HISTORY ; INCREASE ; metabolic syndrome ; acute renal failure ; MEDICINE ; CARDIAC-CATHETERIZATION ; cholesterol crystal embolism ; EMBOLIZATION SYNDROME
    Abstract: Case Report: A 69-year-old man was admitted to the authors' hospital with an increase of plasma creatinine from 1.4 up to 4.9 mg/dl within 4 months and the clinical complaints of painful purple toes, recurrent epistaxis and disturbances of equilibrium. His past medical history was remarkable for three transient ischemic attacks and the diagnosis of a metabolic syndrome. Magnetic resonance imaging showed vasculitis-like lesions in the brain. Eosinophilia and tubular proteinuria were detected. Renal insufficiency was caused by cholesterol crystal embolism, as shown both by skin and renal biopsy. Aortic plaques were identified as the putative source of cholesterol embolization. Conclusion: In case of rapidly progressive renal failure, cholesterol crystal embolism must be considered even without preceding angiography
    Type of Publication: Journal article published
    PubMed ID: 18807234
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    facet.materialart.
    Unknown
    German Medical Science; Düsseldorf, Köln
    In:  Hypertonie 2005; 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga; 20051123-20051125; Berlin; DOC05hochP174 /20060808/
    Publication Date: 2006-08-09
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    facet.materialart.
    Unknown
    German Medical Science; Düsseldorf, Köln
    In:  Hypertonie 2003; 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga; 20031126-20031129; Bonn; DOC03hochP61 /20041111/
    Publication Date: 2004-11-12
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; IN-VITRO ; CELL ; Germany ; IN-VIVO ; VITRO ; VIVO ; DISEASE ; MICE ; ACTIVATION ; DNA ; INFECTION ; kidney ; MECHANISM ; murine ; SERA ; renal ; CONTRAST ; DENDRITIC CELLS ; mechanisms ; INJECTION ; antibodies ; PROGRESSION ; ESCHERICHIA-COLI ; EPITHELIAL-CELLS ; VIRAL-INFECTION ; AUTOIMMUNITY ; BACTERIAL CPG-DNA ; CHEMOKINE RECEPTOR ; chemokines,autoimmune diseases,kidney,lupus,immunity ; IMMUNE-COMPLEX GLOMERULONEPHRITIS ; IMMUNIZATION ; NZB/NZW MICE ; SYSTEMIC-LUPUS-ERYTHEMATOSUS
    Abstract: How bacterial or viral infections trigger flares of autoimmunity is poorly understood. As toll-like receptor (TLR)-9 activation by exogenous or endogenous CpG-DNA may contribute to disease activity of systemic lupus erythematosus, we examined the effects of CpG-oligodeoxynucleotides (ODN) or DNA derived from Escherichia coli (E. coli) on the course of nephritis in MRL1pr/1pr mice. In kidneys of these mice, TLR9 localized to glomerular, tubulointerstitial, and perivascular infiltrates. After intraperitoneal injection labeled CpG-ODN localized to glomerular and interstitial macrophages and dendritic cells in nephritic kidneys of MRL1pr/1pr mice but not in healthy MRL controls. Furthermore, murine J774 macrophages and splenocytes from MRL1pr/1pr mice, but not tubular epithelial cells, renal fibroblasts, or mesangial cells, expressed TLR9 and up-regulated CCL5/RANTES mRNA upon stimulation with CpG-ODN in vitro. In vivo both E. coli DNA and CpG-ODN increased serum DNA autoantibodies of the IgG(2a) isotype in MRL1pr/1pr mice. This was associated with progression of mild to crescentic glomerulonephritis, interstitial fibrosis, and heavy proteinuria. CpG-ODN increased renal CCL2/MCP-1 and CCL5/RANTES expression associated with increased glomerular and interstitial leukocyte recruitment. In contrast control GpC-ODN had no effect. We conclude that TLR9 activation triggers disease activity of systemic autoimmunity, for example, lupus nephritis, and that adaptive and innate immune mechanisms contribute to the CpG-DNA-induced progression of lupus nephritis
    Type of Publication: Journal article published
    PubMed ID: 14734643
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    ISSN: 1432-1041
    Keywords: Torasemide ; metabolites ; end-stage renal disease ; pharmacokinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract The pharmacokinetics of torasemide, a new loop diuretic, as well as its active metabolites M1 and M3, and its inactive main metabolite, M5, were studied in 12 patients with end-stage renal failure during single i.v. (n=6) or single oral (n=6) dosing of 200 mg torasemide, and during chronic oral treatment for 9 days (n=12). The elimination half-life (t1/2) of torasemide was unchanged in renal failure, whereas t1/2 of the torasemide metabolites M1, M3, and M5 were markedly prolonged. However t1/2 as well as the area under the plasma level time curve of torasemide and its metabolites were unchanged during chronic compared to acute administration. The results of this study suggest that despite the increased half-life of torasemide metabolites M1, M3 and M5 in end-stage renal failure patients, no accumulation of the parent drug torasemide and its metabolites during chronic dosing is demonstrable.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    ISSN: 1432-0584
    Keywords: Key words Fludarabine ; Autoimmune side effects ; Lymphoma ; T cell ; Pemphigus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  A 40-year-old patient with low-grade B-NHL developed a generalized macular-papular rash following the first cycle of fludarabine treatment which progressed to a complete epidermal necrolysis following the second cycle. Clinical symptoms and the results of the direct and indirect immunofluorescence were consistent with a mucocutaneous autoimmune syndrome (pemphigus). Immunohistochemical analysis demonstrated a dense epidermal infiltration of CD8+ lymphocytes associated with the histological features of single-cell necrosis of keratinocytes. Early and aggressive immunosuppressive treatment with steroids, cyclophosphamide, and high-dose immunoglobulins resulted in regression of symptoms and complete reconstitution of epidermal integrity. The malignant lymphoma has completely regressed. The findings suggest a fludarabine-induced defect in immunosurveillance – resulting in the uncontrolled activation of autoaggressive T-cell clones – as a pathogenetic mechanism of this life-threatening dermatological complication.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...