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Niedmann, Peter D.
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Niedmann, Peter D.
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Niedmann, Peter D.
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Niedmann, P. D.
Niedmann, Peter
Niedmann, P.
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1998Journal Article [["dc.bibliographiccitation.firstpage","443"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Hepatology"],["dc.bibliographiccitation.lastpage","449"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Nolte, Wilhelm"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Schindler, Christian G."],["dc.contributor.author","Unterberg, Knut"],["dc.contributor.author","Finkenstaedt, Michael"],["dc.contributor.author","Niedmann, Peter D."],["dc.contributor.author","Hartmann, Heinz"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2017-09-07T11:44:25Z"],["dc.date.available","2017-09-07T11:44:25Z"],["dc.date.issued","1998"],["dc.description.abstract","Background/Aims: Deposition of paramagnetic substances in basal ganglia, resulting in increased signals in T1-weighted magnetic resonance images (bright basal ganglia), is frequently seen in liver cirhrosis. The present study describes the prevalence of bright basal ganglia and its clinical significance in patients with long-standing portal vein thrombosis in the absence of liver cirrhosis.Methods: Six patients with angiographically proven complete portal vein thrombosis and cavernomatous transformation without signs of acute or chronic liver disease were studied by magnetic resonance imaging of the brain, neuropsychiatric evaluation, psychometric tests, electroencephalography, and determination of arterial ammonia levels and of serum manganese concentrations from peripheral venous blood.Results: Five out of six patients demonstrated increased signal intensity in the basal ganglia. Overt portal-systemic encephalopathy was not noted prior to or at the time of evaluation. Normal EEG results were recorded in all patients. Only one of the six patients had pathological results in at least two out of four psychometric tests. This latter patient had had a large right-sided brain infarction. Arterial ammonia concentrations were normal in four of the six patients; one patient with increased ammonia levels had concomitant renal insufficiency with azotemia. The other four patients had no relevant concomitant diseases. Serum manganese levels were non-significantly increased compared with control group (p=0.06), but they were significantly correlated to basal ganglia signal intensity (R=0.88; p=0.02).Conclusions: Our results demonstrate that bright basal ganglia primarily represent shunt-induced alterations. They are not directly associated with disturbed liver function nor with portal-systemic encephalopathy."],["dc.identifier.doi","10.1016/s0168-8278(98)80063-9"],["dc.identifier.gro","3151659"],["dc.identifier.pmid","9764992"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8476"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0168-8278"],["dc.title","Bright basal ganglia in T1-weighted magnetic resonance images are frequent in patients with portal vein thrombosis without liver cirrhosis and not suggestive of hepatic encephalopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2003Conference Abstract [["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Therapeutic Drug Monitoring"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Binder, L."],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Niedmann, P. D."],["dc.contributor.author","Pouwels, Claudia"],["dc.contributor.author","Nacke, A."],["dc.contributor.author","Oellerich, M."],["dc.contributor.author","Binder, Claudia"],["dc.date.accessioned","2018-11-07T10:37:31Z"],["dc.date.available","2018-11-07T10:37:31Z"],["dc.date.issued","2003"],["dc.format.extent","496"],["dc.identifier.isi","000184445500054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45586"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","8th International Congress of Therapeutic Drug Monitoring and Clinical Toxicology"],["dc.relation.eventlocation","BASEL, SWITZERLAND"],["dc.relation.issn","0163-4356"],["dc.title","A simple and rapid HPLC method for the determination of meropenem - Preanalytical and analytical aspects"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2000Journal Article [["dc.bibliographiccitation.firstpage","22"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","HERZ KREISLAUF"],["dc.bibliographiccitation.lastpage","28"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Buchhorn, Reiner"],["dc.contributor.author","Kiessling, C."],["dc.contributor.author","Wessel, Alok D."],["dc.contributor.author","Grunewald, Rolf W."],["dc.contributor.author","Hufner, M."],["dc.contributor.author","Niedmann, P. D."],["dc.contributor.author","Bursch, J."],["dc.date.accessioned","2018-11-07T11:06:01Z"],["dc.date.available","2018-11-07T11:06:01Z"],["dc.date.issued","2000"],["dc.description.abstract","Background: The negative impact of persistant neurohormonal activation on morbidity and mortality due to congestive heart failure is well established in adults while little is known of its role in infants with congenital heart diseases. Methods. We retrospectively analysed 2043 neurohormonal datas from 436 pediatric patients treated in our institution from 1987-1997 (plasmareninactivity = PRA[ng/ml/h] aldosterone = ALDO[pg/ml], norepinephrine = NOR[ng/l], epinephrine = EPl[ng/l], angiotensin converting enzyme = ACE[nmol/min/ml]) Results. PRA, ALDO and NOR were considerably elevated in the first trimenon (PRA = 94 +/- 116. ALDO = 1970 +/- 2380) and in patients with left-to-right-shunts (PRA = 52 +/- 83 ALDO = 990 +/- 1090 NOR = 640 +/- 630). complex cardiac anomalies (PRA = 83 +/- 84, ALDO = 1720 +/- 1970, NOR = 1350 +/- 1700) aortic coarcrations (PRA = 100 +/- 195 ALDO = 2700 +/- 4150) and cardiomyopathies (PRA = 49 +/- 55 ALDO = 910 +/- 1070 NOR = 700 +/- 570). After complete repair and cavopulmonary connection these values are normal in the average in contrast to high values after palliative surgery like pulmonary trunk banding and aorto pulmonary shunt in 129 patients, who had cardiac catheterization, we found no significant correlations of NOR and hemodynamic data but highly significant correlations of PRA and mean atrial pressure (r = -0,57), systemic vascular resistance (r = -0.31). ratio of pulmonary to systemic flow (r = 0.38); pulmonary cardiac index (r = 0,31), pulmonary oxygen saturation (r = 0.39) and mean pulmonary artery pressure (r = 0,36). Patients with a significant neurohormonal activation had a significantly higher incidence of cardiac surgery and higher mortality. Conclusions: Significant neurohormonal stimulation was predominantly found in young infants with heart failure due to left-to-right shunts or aortic coarctation prior ro complete repair The hemodynamic trigger for renin release was arterial hypotension. Neurohormonal stimulation was an important risk factor for mortality and necessity og cardiac surgery."],["dc.identifier.isi","000084866600006"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52206"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pflaum Verlag Kg"],["dc.relation.issn","0046-7324"],["dc.title","Neurohormonal stimulation in patients with congenital heart diseases - Influence of age, cardiac defect and hemodynamic"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2001Journal Article Discussion [["dc.bibliographiccitation.firstpage","1485"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Clinical Chemistry"],["dc.bibliographiccitation.lastpage","1488"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Shipkova, Maria"],["dc.contributor.author","Armstrong, Victor William"],["dc.contributor.author","Kiehl, M. G."],["dc.contributor.author","Niedmann, P. D."],["dc.contributor.author","Schutz, Ekkehard"],["dc.contributor.author","Oellerich, M."],["dc.contributor.author","Wieland, Eberhard"],["dc.date.accessioned","2018-11-07T08:47:01Z"],["dc.date.available","2018-11-07T08:47:01Z"],["dc.date.issued","2001"],["dc.identifier.isi","000170077300029"],["dc.identifier.pmid","11468247"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20839"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Clinical Chemistry"],["dc.relation.issn","0009-9147"],["dc.title","Quantification of mycophenolic acid in plasma samples collected during and immediately after intravenous administration of mycophenolate mofetil"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]Details PMID PMC WOS2004Journal Article [["dc.bibliographiccitation.firstpage","683"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","689"],["dc.bibliographiccitation.volume","111"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Berger, C."],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Mayer, G."],["dc.contributor.author","Niedmann, P. D."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T10:48:34Z"],["dc.date.available","2018-11-07T10:48:34Z"],["dc.date.issued","2004"],["dc.description.abstract","Assessment of serum total homocysteine (tHcy) in patients with obstructive sleep apnea (OSA) syndrome is highly relevant since both are strongly associated with stroke and cognitive dysfunction. Seven of 16 untreated OSA patients showed tHcy levels exceeding 11.7 mumol/l. The circadian pattern of serum tHcy in untreated and treated patients (p < 0.001) implied a diagnostic impact of blood sampling time. Treatment with continuous positive airway pressure (CPAP) effectively lowered tHcy levels in patients by about 30% (p < 0.005) and thus probably the (hyper)homocysteinemia-related cognitive dysfunction and the risk for cardio-/cerebrovascular diseases."],["dc.identifier.doi","10.1007/s00702-004-0130-2"],["dc.identifier.isi","000221692600003"],["dc.identifier.pmid","15168215"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48229"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","CPAP-therapy effectively lowers serum homocysteine in obstructive sleep apnea syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2000Journal Article [["dc.bibliographiccitation.firstpage","365"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Clinical Chemistry"],["dc.bibliographiccitation.lastpage","372"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Shipkova, Maria"],["dc.contributor.author","Schutz, Ekkehard"],["dc.contributor.author","Armstrong, Victor William"],["dc.contributor.author","Niedmann, P. D."],["dc.contributor.author","Oellerich, M."],["dc.contributor.author","Wieland, Eberhard"],["dc.date.accessioned","2018-11-07T09:04:14Z"],["dc.date.available","2018-11-07T09:04:14Z"],["dc.date.issued","2000"],["dc.description.abstract","Background: The acyl glucuronide (AcMPAG) of mycophenolic acid (MPA) has been found to possess pharmacologic and potentially proinflammatory activity in vitro. To establish its pharmacologic and toxicologic relevance in vivo, a reversed-phase HPLC method was modified to simultaneously determine MPA, the phenolic MPA-glucuronide (7-O-MPAG), and AcMPAG. In addition, cross-reactivity of AcMPAG in the Emit assay for MPA was investigated. Methods: The procedure used simple sample preparation, separation with a Zorbax Eclipse-XDB-C8 column, and gradient elution. AcMPAG was quantified as 7-O-MPAG-equivalents. Results: The assay was linear up to 50 mg/L for MPA, 250 mg/L for 7-O-MPAG, and 10 mg/L for AcMPAG (r >0.999). Detection limits were 0.01, 0.03, and 0.04 mg/L for MPA, 7-O-MPAG, and AcMPAG, respectively. The recoveries were 99-103% for MPA, 95-103% for 7-O-MPAG, and 104-107% for AcMPAG. The within-day imprecision was <5.0% for MPA (0.2-25 mg/L), <4.4% for 7-O-MPAG (10-250 mg/L), and less than or equal to 14% for AcMPAG (0.1-5 mg/L). The between-day imprecision was <6.2%, <4.5%, and less than or equal to 14% for MPA, 7-O-MPAG, and AcMPAG, respectively. When isolated from microsomes, purified AcMPAG (1-10 mg/L) revealed a concentration-dependent cross-reactivity in an Emit assay for the determination of MPA ranging from 135% to 185%. This is in accordance with the bias between HPLC and Emit calculated in 270 samples from kidney transplant recipients receiving mycophenolate mofetil therapy, which was greater (median, 151.2%) than the respective AcMPAG concentrations determined by HPLC. AcMPAG was found to undergo hydrolysis when samples were stored up to 24 h at room temperature or up to 30 days at 4 degrees C or -20 degrees C. Acidified samples (pH 2.5) were stable up to 30 days at -20 OC. Conclusions: The HPLC and Emit methods for AcMPAG described here may allow investigation of its relevance for the immunosuppression and side effects associated with mycophenolate mofetil therapy. (C) 2000 American Association for Clinical Chemistry."],["dc.identifier.isi","000085848400008"],["dc.identifier.pmid","10702523"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25069"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Clinical Chemistry"],["dc.relation.issn","0009-9147"],["dc.title","Determination of the acyl glucuronide metabolite of mycophenolic acid in human plasma by HPLC and Emit"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details PMID PMC WOS2001Conference Paper [["dc.bibliographiccitation.firstpage","1080"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Transplantation Proceedings"],["dc.bibliographiccitation.lastpage","1081"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Shipkova, Maria"],["dc.contributor.author","Wieland, Eberhard"],["dc.contributor.author","Schutz, Ekkehard"],["dc.contributor.author","Wiese, Christoph Hermann"],["dc.contributor.author","Niedmann, P. D."],["dc.contributor.author","Oellerich, M."],["dc.contributor.author","Armstrong, Victor William"],["dc.date.accessioned","2018-11-07T09:26:31Z"],["dc.date.available","2018-11-07T09:26:31Z"],["dc.date.issued","2001"],["dc.identifier.doi","10.1016/S0041-1345(00)02424-6"],["dc.identifier.isi","000167629900506"],["dc.identifier.pmid","11267199"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30321"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.publisher.place","New york"],["dc.relation.conference","18th World Congress of the Transplantation-Society"],["dc.relation.eventlocation","ROME, ITALY"],["dc.relation.issn","0041-1345"],["dc.title","The acyl glucuronide metabolite of mycophenolic acid inhibits the proliferation of human mononuclear leukocytes"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2002Journal Article [["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","DEUTSCHE ZEITSCHRIFT FUR SPORTMEDIZIN"],["dc.bibliographiccitation.lastpage","78"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Saur, P."],["dc.contributor.author","Joneleit, M."],["dc.contributor.author","Tolke, H."],["dc.contributor.author","Pudel, Volker"],["dc.contributor.author","Niedmann, P. D."],["dc.contributor.author","Kettler, Dietrich"],["dc.date.accessioned","2018-11-07T10:31:18Z"],["dc.date.available","2018-11-07T10:31:18Z"],["dc.date.issued","2002"],["dc.description.abstract","The purpose of this study was to examine the magnesium balance in endurance athletes. Clarification was to be obtained whether the athletes are more frequently magnesium-deficient than non-athletic persons. In addition, a check was made whether dietary factors are responsible for the onset of magnesium deficiency. 50 volunteers with a mean age of 25 years were enrolled in this randomized, prospective study. Based on a cycle ergometry test women with an aerobic-anaerobic threshold above 2.4 W/kg (n=7) and men above 2.6 W/kg (n=18) were assigned to the group of endurance athletes, the remaining 25 subjects formed the control group (8 women and 17 men), The athletes reported training at least 9 hours per week, the subjects in the control group less than 9 hours per week. Since earlier studies had shown that a serum magnesium concentration within the normal range does not necessarily exclude a magnesium deficiency, and magnesium retention can provide more precise information on the magnesium status using a magnesium loading test, the magnesium retention, plasma magnesium concentration, ionized fraction of plasma magnesium, erythrocytic magnesium concentration, renal magnesium excretion and oral magnesium intake were measured. The mean magnesium retention values in the control group measured using the intravenous magnesium loading test were lower than those in the endurance athletes. No differenees were found in the mean values of plasma magnesium concentration ionized fractions of plasma magnesium and erythrocytic magnesium concentration in the two groups, while the endurance trained subjects excreted significantly more magnesium via the kidneys and had a higher oral magnesium intake than the controt group. The study thus confirms that endurance athletes are more frequently magnesium-deficient than persons who do not engage in endurance sports. This deficiency was caused by elevated renal magnesium excretion. Although the athletes' magnesium intake with food was higher, the magnesium quantity consumed did not suffice to maintain a balanced magnesium status."],["dc.identifier.isi","000177152300003"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44076"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W W F Verlagsgesellschaft Mbh"],["dc.relation.issn","0344-5925"],["dc.title","Evaluation of the magnesium status in athletics"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2004Journal Article Discussion [["dc.bibliographiccitation.firstpage","438"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Clinical Chemistry"],["dc.bibliographiccitation.lastpage","441"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Shipkova, Maria"],["dc.contributor.author","Niedmann, P. D."],["dc.contributor.author","Armstrong, Victor William"],["dc.contributor.author","Oellerich, M."],["dc.contributor.author","Wieland, Eberhard"],["dc.date.accessioned","2018-11-07T10:51:18Z"],["dc.date.available","2018-11-07T10:51:18Z"],["dc.date.issued","2004"],["dc.identifier.doi","10.1373/clinchem.2003.026096"],["dc.identifier.isi","000188663700023"],["dc.identifier.pmid","14752016"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48861"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Clinical Chemistry"],["dc.relation.issn","0009-9147"],["dc.title","Determination of thiopurine methyltransferase activity in isolated human erythrocytes does not reflect putative in vivo enzyme inhibition by sulfasalazine"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2002Journal Article [["dc.bibliographiccitation.firstpage","390"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Therapeutic Drug Monitoring"],["dc.bibliographiccitation.lastpage","399"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Shipkova, Maria"],["dc.contributor.author","Armstrong, Victor William"],["dc.contributor.author","Weber, Lutz T."],["dc.contributor.author","Niedmann, P. D."],["dc.contributor.author","Wieland, Eberhard"],["dc.contributor.author","Haley, J."],["dc.contributor.author","Tonshoff, B."],["dc.contributor.author","Oellerich, M."],["dc.date.accessioned","2018-11-07T10:29:47Z"],["dc.date.available","2018-11-07T10:29:47Z"],["dc.date.issued","2002"],["dc.description.abstract","The acyl glucuronide metabolite (AcMPAG) of mycophenolic acid (MPA) has been found to possess both immunosuppressive and pro-inflammatory activity in vitro. In this study its pharmacokinetics were determined in pediatric renal transplant recipients receiving cyclosporine, steroids, and mycophenolate mofetil. Twelve-hour concentration-time profiles for AcMPAG, MPA, and the phenolic glucuronide (MPAG) were determined by high-performance liquid chromatography (HPLC) in the initial (1-3 wk; n=16) and stable (3-12 mo; n=22) phase,, after transplantation. In addition, the formation of covalent adducts between AcMPAG and plasma albumin (AcMPAG-Alb) was investigated using Western Blot analysis. AcMPAG-AUC(12h) showed significant (p<0.05) correlations with MPA-AUC(12h) (r=0.78) and MPAG-AUC(12h) (r=0.78). In molar equivalents the median AcMPAG-AUC(12h) was 10.3% (range, 4.6%-45.5%) of MPA-AUC(12h). Values (median [range]) of AcMPAG-AUC(12h) (10.1 [3.30-30.1] mg.h/L), AcMPAG-C-0 (0.48 [0.08-1.43] mg/L), and AcMPAG-C-max (1.95 [0.88-5.35] mg/L) were significantly (p<0.05) higher in the stable phase than in the initial phase: 3.54 [2.07-20.0] mg.h/L for AUC(12h); 0.25 [<0.04-0.97] mg/L for C-0, and 1.12 [0.32-2.44] mg/L for C-max. The increases in the AcMPAG pharmacokinetic variables were paralleled by significant increases in the corresponding MPA variables. In addition, a strong negative correlation (r=-0.69; p<0.05) was found between AcMPAG concentrations and the creatinine clearance. AcMPAG-Alb adducts were detected in all patient samples. They showed considerable interindividual variation and increased significantly with time from the initial phase to the stable phase. AcMPAG-Alb correlated significantly (p<0.05) with AcMPAG-AUC(12h) (r=0.70) and plasma albumin (r=0.40). AcMPAG plasma concentrations are dependent on renal function, MPA disposition, and glucuronidation. The pharmacokinetics of AcMPAG is characterized by broad interindividual variation. In some patients AcMPAG may significantly contribute to the immunosuppression during mycophenolate mofetil therapy. AcMPAG-Alb adduct formation may serve as a marker for extended AcMPAG exposure. The association of AcMPAG with adverse effects must be further investigated."],["dc.identifier.doi","10.1097/00007691-200206000-00011"],["dc.identifier.isi","000175866900011"],["dc.identifier.pmid","12021631"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43714"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0163-4356"],["dc.title","Pharmacokinetics and protein adduct formation of the pharmacologically active acyl glucuronide metabolite of mycophenolic acid in pediatric renal transplant recipients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS