366 results on '"Andreas Kribben"'
Search Results
352. Contents Vol. 26, 2003
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K. Fehsel, Katrin Ivens, Samar M. Hammad, Heimo Ehmke, Jan Gossmann, Wolfgang Niebel, Kerstin Amann, Debra J. Hazen-Martin, Uwe Heemann, Bolesław Rutkowski, Gerd Luippold, Marcus Baumann, Dan Yang Huang, Frantisek Sefrna, Soo Hyun Park, Lyn Powell-Braxton, Pavlína Zemanová, Walter H. Hörl, Sylvie Opatrná, Tomas Lenz, Christos Bantis, K.-P. Richter, V. Kolb-Bachhofen, Helmut Geiger, C. Birk, Ji Yeong Park, Eberhard Ritz, Hermann Josef Gröne, Mimi Sohn, Joanna Malek, Thomas Philipp, Peter Heering, Yun Jung Lee, Leslie Eldridge, Ladislav Vít, Tobias Saam, Jaroslav Racek, Timothy J. Lyons, Thomas Haak, Volker Vallon, Christian S. Haas, Wesley Won, Ho Jae Han, Karel Opatrný, Y. Luther, C. Piesch, Leszek Tylicki, and Andreas Kribben
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Nephrology ,General Medicine ,Cardiology and Cardiovascular Medicine - Published
- 2003
353. Subject Index Vol. 26, 2003
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Bolesław Rutkowski, V. Kolb-Bachhofen, Tomas Lenz, Eberhard Ritz, Yun Jung Lee, Leslie Eldridge, Ho Jae Han, Christos Bantis, Sylvie Opatrná, K. Fehsel, Pavlína Zemanová, C. Birk, Andreas Kribben, Wesley Won, Thomas Haak, Y. Luther, Katrin Ivens, Jan Gossmann, Walter H. Hörl, Samar M. Hammad, Jaroslav Racek, Christian S. Haas, Lyn Powell-Braxton, Thomas Philipp, Karel Opatrný, Kerstin Amann, Ladislav Vít, Debra J. Hazen-Martin, Tobias Saam, Timothy J. Lyons, Wolfgang Niebel, Helmut Geiger, Leszek Tylicki, Marcus Baumann, Soo Hyun Park, K.-P. Richter, Volker Vallon, Mimi Sohn, C. Piesch, Ji Yeong Park, Hermann Josef Gröne, Dan Yang Huang, Uwe Heemann, Heimo Ehmke, Gerd Luippold, Peter Heering, Joanna Malek, and Frantisek Sefrna
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Index (economics) ,Nephrology ,Chemistry ,Statistics ,Subject (documents) ,General Medicine ,Cardiology and Cardiovascular Medicine - Published
- 2003
354. Das hepatorenale Syndrom.
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Guido Gerken, Andreas Kribben, and Thomas Philipp
- Abstract
Copyright of Medizinische Klinik (Urban & Vogel) is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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- 2007
355. Inhibition of Aggregation and Calcium Influx of Human Platelets by Nitrendipine
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Armin Distler, E Fritschka, Thomas Philipp, and Andreas Kribben
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Pharmacology ,Nitrendipine ,Chemistry ,medicine ,Platelet ,Cardiology and Cardiovascular Medicine ,Calcium influx ,medicine.drug - Published
- 1987
356. Effects of nitrendipine and tiapamil on 45Ca2+ influx and on platelet aggregation
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Andreas Kribben, Emanuel Fritschka, Daniela Senger, Michael Sibold, Armin Distler, and Thomas Philipp
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Pharmacology ,Adult ,Blood Platelets ,Male ,Platelet Aggregation ,Propylamines ,Nitrendipine ,Tiapamil Hydrochloride ,Thrombin ,In Vitro Techniques ,Calcium Channel Blockers ,Humans ,Calcium ,Cardiology and Cardiovascular Medicine - Abstract
The effects of the dihydropyridine derivative nitrendipine and of the phenylalkylamine derivative tiapamil on 45Ca2+ influx was determined in platelets in vitro and on platelet aggregation ex vivo. Thrombin-stimulated 45Ca2+ influx was inhibited by 10 mumol/l nitrendipine and 100 mumol/l tiapamil. ADP- and adrenaline-induced platelet aggregation were inhibited in normotensive volunteers following short-term administration of nitrendipine (20 mg b.i.d.) but not after tiapamil (225 mg t.i.d.). Therefore, mechanisms other than the inhibition of Ca2+ influx should be considered to be responsible for inhibition of platelet aggregation by nitrendipine ex vivo.
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- 1987
357. Calcium uptake into acini from rat pancreas: evidence for intracellular ATP-dependent calcium sequestration
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Hideyuki Wakasugi, Winfried Haase, Irene Schulz, R. Kaufmann, Toshinari Kimura, and Andreas Kribben
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Oligomycin ,GTP' ,Physiology ,Biophysics ,chemistry.chemical_element ,Biological Transport, Active ,Calcium ,chemistry.chemical_compound ,Adenosine Triphosphate ,Animals ,Pancreas ,Calcimycin ,Chemistry ,Endoplasmic reticulum ,Rats, Inbred Strains ,Cell Biology ,Mersalyl ,Rats ,Adenosine Diphosphate ,Kinetics ,Digitonin ,Biochemistry ,Secretagogue ,Intracellular - Abstract
Intracellular ATP-dependent Ca2+-sequestration mechanisms were studied in isolated dispersed rat pancreatic acini following treatment with saponin or digitonin to disrupt their plasma membranes. In the presence of 45Ca2+ concentrations less than 10(-6) mol/liter, addition of 5 mmol/liter ATP caused a rapid increase in 45Ca2+ uptake exceeding the control by fivefold. ADP mimicked the ATP effect by 50 to 60%, whereas other nucleotides such as AMP-PNP, AMP-PCP, CTP, UTP, ITP, GTP, cAMP and cGMP did not. Maximal ATP-promoted Ca2+ uptake was obtained at 10(-5) mol/liter Ca2+. Inhibition of Ca2+ uptake by mitochondrial inhibitors was dependent on the Ca2+ concentration, indicating the presence of different Ca2+ storage systems. Whereas the apparent half-saturation constant found for mitochondrial Ca2+ uptake was approximately 4.5 X 10(-7) mol/liter, in the presence of antimycin and oligomycin (nonmitochondrial uptake) it was approximately 1.4 X 10(-8) mol/liter. In the absence of Mg2+ both ATP- and ADP-promoted Ca2+ uptake was nearly abolished. The Ca2+ ionophore and mersalyl blocked Ca2+ uptake, Electron microscopy showed electron-dense precipitates in the rough endoplasmic reticulum of saponin-treated cells in the presence of Ca2+, oxalate and ATP, which were absent in intact cells and in saponin-cells without ATP or pretreated with A23187. The data suggest the presence of mitochondrial and nonmitochondrial ATP-dependent C2+ storage systems in pancreatic acini. The latter is likely to be located in the rough endoplasmic reticulum.
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- 1982
358. Analysis of Ca2+ fluxes and Ca2+ pools in pancreatic acini
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Winfried Haase, Hideyuki Wakasugi, Andreas Kribben, Irene Schulz, and Toshinari Kimura
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Atropine ,Chemistry ,Cell Membrane ,Biological Transport, Active ,Intracellular Membranes ,Endoplasmic Reticulum ,Intracellular ca ,Cell Compartmentation ,Mitochondria ,Rats ,Crystallography ,Ca2 flux ,Adenosine Triphosphate ,Biochemistry ,Rat Pancreas ,Animals ,Calcium ,Carbachol ,Cholecystokinin ,Pancreas - Abstract
45 Ca 2+ movements have been analysed in dispersed acini prepared from rat pancreas in a quasi-steady state for 45 Ca 2+ . Carbamyl choline (carbachol; Cch) caused a quick 45 Ca 2+ release that was followed by a slower 45 Ca 2+ ‘reuptake’. Subsequent addition of atropine resulted in a further transient increase in cellular 45 Ca 2+ . The data suggest the presence of a Cch-sensitive ‘trigger’ pool, which could be refilled by the antagonist, and one or more intracellular ‘storage’ pools. Intracellular Ca 2+ sequestration was studied in isolated acini pretreated with saponin to disrupt their plasma membranes. In the presence of 45 Ca 2+ (1 µM), addition of ATP at 5 mM caused a rapid increase in 45 Ca 2+ uptake exceeding the control by fivefold. Maximal ATP-promoted Ca 2+ uptake was obtained at 10 µM Ca 2+ (half-maximal at 0.32 µM Ca 2+ ). In the presence of mitochondrial inhibitors it was 0.1 µM (half-maximal at 0.014 µM). 45 Ca 2+ release could still be induced by Cch but the subsequent reuptake was missing. The latter was restored by ATP and atropine caused further 45 Ca 2+ uptake. Electron microscopy showed electron-dense precipitates in the rough endoplasmic reticulum of saponin-treated cells in the presence of Ca 2+ , oxalate and ATP which were absent in intact cells or cells pretreated with A23187. The data suggest the presence of a plasma membrane-bound Cch-sensitive ‘trigger’ Ca 2+ pool and ATP-dependent Ca 2+ storage systems in mitochondria and rough endoplasmic reticulum of pancreatic acini. It is assumed that Ca 2+ is taken up into these pools after secretagogue-induced Ca 2+ release.
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- 1981
359. Mg2+-DEPENDENT Ca2+TRANSPORT IN CELL MEMBRANES FROM THE EXOCRINE PANCREAS
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Irene Schulz and Andreas Kribben
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Chemistry ,General Neuroscience ,Ca2 transport ,Cell Membrane ,Biological Transport, Active ,Calcium-Transporting ATPases ,General Biochemistry, Genetics and Molecular Biology ,Cell biology ,Kinetics ,Membrane ,History and Philosophy of Science ,Microsomes ,Exocrine pancreas ,Cats ,Animals ,Calcium ,Ca(2+) Mg(2+)-ATPase ,Pancreas - Published
- 1982
360. Alpha2-and beta2-adrenoceptor downregulation in marathon runners
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H M Thiede, Markus Rothschild, Klaus-Detlev Schultz, Andreas Kribben, Armin Distler, E Fritschka, and Thomas Philipp
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medicine.medical_specialty ,Sympathetic nervous system ,Mean arterial pressure ,Physiology ,business.industry ,Alpha (ethology) ,Adrenergic ,Endocrinology ,medicine.anatomical_structure ,Internal medicine ,Heart rate ,Internal Medicine ,Catecholamine ,medicine ,Alpha-2 adrenergic receptor ,Cardiology and Cardiovascular Medicine ,Beta (finance) ,business ,medicine.drug - Abstract
The regulation of platelet alpha 2- and lymphocyte beta 2-adrenoceptor densities by alterations in endogenous catecholamines was examined. In order to activate the sympathetic nervous system eight trained male normotensive subjects carried out a marathon run. Adrenoceptor densities and plasma catecholamine concentrations were measured before and immediately after the run. Platelet alpha 2-adrenoceptor density and lymphocyte beta-adrenoceptor density decreased after the run (P less than 0.05), whereas both plasma noradrenaline and adrenaline concentrations increased (P less than 0.01). Mean arterial pressure decreased (P less than 0.05), and the heart rate increased (P less than 0.001). The data suggest that increases in endogenous catecholamine concentrations cause downregulation of both alpha- and beta-adrenoceptor densities on human blood cells.
- Published
- 1989
361. Erythropoietin overrides the triggering effect of DNA platination products in a mouse model of Cisplatin-induced neuropathy
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Juergen Thomale, Hans-Christoph Diener, Bernd Liedert, M.-S. Yoon, Andreas Kribben, M. Schäfers, Rupert Egensperger, Volker Limmroth, Zaza Katsarava, Mark Obermann, and Anna Dzagnidze
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Male ,DNA damage ,Medizin ,Neural Conduction ,Antineoplastic Agents ,Pharmacology ,Biology ,Mitochondrion ,lcsh:RC321-571 ,law.invention ,Mice ,Polyneuropathies ,Cellular and Molecular Neuroscience ,Microscopy, Electron, Transmission ,Dorsal root ganglion ,law ,Ganglia, Spinal ,medicine ,Animals ,lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry ,Erythropoietin ,Myelin Sheath ,Pain Measurement ,Cisplatin ,General Neuroscience ,lcsh:QP351-495 ,Immunohistochemistry ,Sciatic Nerve ,Recombinant Proteins ,Mitochondria ,Mice, Inbred C57BL ,lcsh:Neurophysiology and neuropsychology ,Neuroprotective Agents ,medicine.anatomical_structure ,Peripheral nervous system ,Immunology ,Recombinant DNA ,Sciatic nerve ,DNA Damage ,Research Article ,medicine.drug - Abstract
Background Cisplatin mediates its antineoplastic activity by formation of distinct DNA intrastrand cross links. The clinical efficacy and desirable dose escalations of cisplatin are restricted by the accumulation of DNA lesions in dorsal root ganglion (DRG) cells leading to sensory polyneuropathy (PNP). We investigated in a mouse model by which mechanism recombinant erythropoietin (rhEPO) protects the peripheral nervous system from structural and functional damage caused by cisplatin treatment with special emphasis on DNA damage burden. Results A cumulative dose of 16 mg cisplatin/kg resulted in clear electrophysiological signs of neuropathy, which were significantly attenuated by concomitant erythropoietin (cisplatin 32,48 m/s ± 1,68 m/s; cisplatin + rhEPO 49,66 m/s ± 1,26 m/s; control 55,01 m/s ± 1,88 m/s; p < 0,001). The co-application of rhEPO, however, did not alter the level of unrepaired cisplatin-DNA lesions accumulating in DRG target cells. Micro-morphological analyses of the sciatic nerve from cisplatin-exposed mice showed damaged myelin sheaths and mitochondria. Co-administered rhEPO inhibited myelin sheaths from structural injuries and resulted in an increased number of intact mitochondria. Conclusion The protective effect of recombinant erythropoietin is not mediated by reducing the burden of DNA platination in the target cells, but it is likely to be due to a higher resistance of the target cells to the adverse effect of DNA damage. The increased frequency of intact mitochondria might also contribute to this protective role.
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362. Serum cystatin C in mouse models: a reliable and precise marker for renal function and superior to serum creatinine.
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Su Song, Marko Meyer, Tobias R. Türk, Benjamin Wilde, Thorsten Feldkamp, Roland Assert, Kun Wu, Andreas Kribben, and Oliver Witzke
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CYSTATINS ,BIOMARKERS ,CREATININE ,BLOOD proteins ,LABORATORY mice ,GLOMERULAR filtration rate ,ACUTE kidney failure ,REPERFUSION injury - Abstract
Background. Serum creatinine (SCR) and blood urea nitrogen (BUN) determine the glomerular filtration rate (GFR) improperly in acute renal failure. Serum cystatin C (CYS) has the potential to be a more precise marker for GFR. The aim of this study was to compare the sensitivity of SCR, BUN and CYS with respect to the detection of acute renal failure in mice. Methods. In an ischaemia reperfusion (I/R) injury model, mice suffered 60-min left kidney ischaemia and right nephrectomy. In a nephrectomy model, mice were nephrectomized to a different extent: from unilateral (3/6Nx) to bilateral nephrectomy (BiNx). Blood samples were collected 2, 12 or 24 h post-op. Results. SCR, BUN and CYS increased significantly in the I/R-model in comparison to sham mice and 3/6Nx mice at 12 and 24 h post-op (SCR P = 0.009; BUN P P P P P = 0.13, 5/6Nx 1.00 ± 0.29, P P Conclusions. CYS can be used as a reliable and precise marker for renal function in mouse models. CYS is more sensitive than SCR, and it shows renal damage earlier than SCR and BUN. [ABSTRACT FROM AUTHOR]
- Published
- 2009
363. Evidence for involvement of nonesterified fatty acid-induced protonophoric uncoupling during mitochondrial dysfunction caused by hypoxia and reoxygenation.
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Thorsten Feldkamp, Joel M. Weinberg, Markus Hörbelt, Christina Von Kropff, Oliver Witzke, Jens Nürnberger, and Andreas Kribben
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MITOCHONDRIAL membrane abnormalities ,HYPOXEMIA ,FATTY acids ,HYPERBARIC oxygenation ,ISCHEMIA ,ANTIBIOTICS - Abstract
Background. Proximal tubules subjected to hypoxia in vitro under conditions relevant to ischaemia in vivo develop an energetic deficit that is not corrected even after full reoxygenation. We have provided evidence that accumulation of nonesterified fatty acids (NEFA) is the primary reason for this energetic deficit. In this study, we have further investigated the mechanism for the NEFA-induced energetic deficit. Methods. Mitochondrial membrane potential (Δψ) was measured in digitonin-permeabilized, freshly isolated proximal tubules by safranin O uptake. Addition of the potassium/proton exchanger nigericin enables the determination of the mitochondrial proton motive force (Δp) and the proton gradient (ΔpH). ATP was measured luminometrically and NEFA colorimetrically. Results. Tubule ATP content was depleted after hypoxia and recovered incompletely, even after full reoxygenation. Mitochondrial safranin O uptake was decreased in proximal tubules after hypoxia and reoxygenation (H/R). This decrease was attenuated by delipidated bovine serum albumin (dBSA) or citrate. Addition of nigericin increased safranin O uptake of mitochondria in normoxic proximal tubules, but not in proximal tubules after H/R. Addition of dBSA restored the effect of nigericin to increase mitochondrial safranin O uptake. Addition of the NEFA oleate had the same impact on mitochondrial safranin O uptake as subjecting proximal tubules to H/R. Conclusion. The mechanism of the NEFA-induced energetic deficit in freshly isolated rat proximal tubules induced by H/R is characterized by impaired ATP production after full reoxygenation, impaired recovery of Δψ and Δp, abrogation of ΔpH and sensitivity to citrate, consistent with involvement of the tricarboxylate carrier. The data support the concept that protonophoric uncoupling by NEFA movement on anion carriers plays a critical role in proximal tubule mitochochondrial dysfunction after H/R. [ABSTRACT FROM AUTHOR]
- Published
- 2009
364. CD4+CD25+ T-cell populations expressing CD134 and GITR are associated with disease activity in patients with Wegeners granulomatosis.
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Benjamin Wilde, Sebastian Dolff, Xin Cai, Christof Specker, Jan Becker, Martin Tötsch, Ulrich Costabel, Jan Dürig, Andreas Kribben, Jan Willem Cohen Tervaert, Kurt Werner Schmid, and Oliver Witzke
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GRANULOMATOSIS with polyangiitis ,GLUCOCORTICOID receptors ,TUMOR necrosis factors ,T cells ,CELL populations ,KIDNEY diseases ,VASCULITIS ,PATIENTS - Abstract
Background. An increased CD4+ CD25+ T-cell population is observed in Wegeners granulomatosis (WG). This T-cell population is not well characterized yet and their contribution to the disease pathogenesis remains obscure. Methods. Thirty patients with WG and 18 healthy controls (HC) were included in this study. The disease activity and extension were measured by the Birmingham Vasculitis Activity Score (BVAS) and the Disease Extent Index (DEI). Lymphocytes from peripheral blood were analysed by FACS for the expression of CD4, CD25, CD134 and GITR. Cytokine expression in these subsets was assessed too. Nasal, lung and renal tissues from WG patients were immunohistochemically stained for CD3 and CD134. Results. The percentage of CD134+ as well as GITR+ expressing CD4+CD25+ lymphocytes was increased in patients as compared to HC (37 ± 12% versus 27 ± 8%, P = 0.005; 18 ± 9% versus 11 ± 6%, P = 0.003). The expression of CD134 and GITR showed a significant correlation with disease activity (r = 0.5, P = 0.009; r = 0.55, P = 0.001). Most of these displayed the phenotype of effector memory T-cells (94 ± 4% and 91 ± 6%). CD134 T-cells were found in tissues affected by WG. Conclusions. CD4+CD25+ effector memory T-cells expressing CD134 and GITR seem to play a role in disease mechanisms, as suggested by their close association with disease activity and their participation in inflammatory process. [ABSTRACT FROM AUTHOR]
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- 2009
365. Coronary artery bypass surgery and acute kidney injury--impact of the off-pump technique.
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Parwis Massoudy, Soeren Wagner, Matthias Thielmann, Ulf Herold, Eva Kottenberg-Assenmacher, Günther Marggraf, Andreas Kribben, Thomas Philipp, Heinz Jakob, and Stefan Herget-Rosenthal
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ACUTE kidney failure ,CORONARY artery bypass ,MYOCARDIAL revascularization ,HEART disease risk factors - Abstract
Background. Acute kidney injury (AKI) is a serious and frequent complication after coronary artery bypass grafting (CABG). Cardiopulmonary bypass (CPB) was identified as a major AKI risk factor after CABG. Our aim was to assess the impact of the off-pump coronary artery bypass (OPCAB) compared to the on-pump coronary artery bypass (ONCAB) technique on the rate and severity of AKI, while taking other risk factors for AKI into account. Methods. An observational study of 201 consecutive adult patients was conducted; 100 were operated by the OPCAB and 101 by the ONCAB technique. All patients in each group were operated by a single, experienced surgeon. Fifteen pre-, intra- and postoperative variables that were repeatedly identified in previous studies as independent AKI risk factors were included in this analysis. AKI was defined as an increase of serum creatinine ≥50% or ≥0.3 mg/dL within 48 h and AKI severity was classified, according to current AKIN definitions. Results. Significantly fewer OPCAB patients developed AKI compared to ONCAB (14.0 versus 27.7%; P = 0.03). OPCAB was associated with milder stages of AKI, whereas ONCAB patients had more severe AKI. Congestive heart failure and chronic kidney disease were independent risk factors for AKI. The OPCAB technique for CABG was identified as the only independent factor associated with lower incidence of AKI. Conclusions. Using current AKI definitions and classifications, the OPCAB technique for CABG, which avoids CPB; was associated with a significantly lower rate and less severe AKI compared to ONCAB. The OPCAB technique was identified as the only modifiable and potentially protective factor against postoperative AKI. [ABSTRACT FROM AUTHOR]
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- 2008
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366. Ezetimibe treatment in hypercholesterolemic kidney transplant patients is safe and effective and reduces the decline of renal allograft function: a pilot study.
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Tobias R. Türk, Eva Voropaeva, Matthias Kohnle, Jens Nürnberger, Thomas Philipp, Andreas Kribben, Uwe Heemann, and Oliver Witzke
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ANTICHOLESTEREMIC agents ,DRUG efficacy ,KIDNEY transplantation ,CHOLESTEROL - Abstract
Background. Ezetimibe has shown efficacy in the therapy of hypercholesterolemia in renal transplant patients. This is the first study investigating the effect of ezetimibe on renal function in kidney transplant recipients. Methods. Fifty-six patients with statin-resistant hypercholesterolemia (total cholesterol >200 mg/dl) after renal transplantation received additional ezetimibe therapy (10 mg/day) for 12 months. A group receiving statin therapy (n = 28) served as controls in this prospective study. Results. Total cholesterol and LDL cholesterol concentrations decreased significantly in the ezetimibe-treated patients but remained stable in the control group (delta total cholesterol: â24 ± 49 mg/dl vs 19 ± 49 mg/dl, P vs â 3 ± 31 mg/dl, P vs â 4.8 ± 12.8 ml/min, P = 0.025; delta Modification of Diet in Renal Disease: â0.4 ± 6.2 ml/min/1.73 m2 vs 4.7 ± 8.8 ml/min/1.73 m2, P = 0.033). Conclusions. The data of our prospective caseâcontrol study suggest that ezetimibe appears to ameliorate the decline of renal function after renal transplantation. [ABSTRACT FROM AUTHOR]
- Published
- 2008
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