E Kuwertz-Bröking

Universitätsklinikum Münster, Muenster, North Rhine-Westphalia, Germany

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Publications (55)339.26 Total impact

  • R. Beetz, E. Kuwertz-Bröking
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    ABSTRACT: Verbesserte diagnostische Verfahren und die Verfügbarkeit neuer Medikamente haben zu einer Optimierung der Behandlung von Harnwegsinfektionen (HWI) geführt. Aktuell diskutierte Fragen betreffen u. a. Therapiestrategien bei Pyelonephritis im Säuglings- und Kleinkindalter, den Umgang mit der Resistenzentwicklung uropathogener Bakterien, konkurrierende Konzepte der bildgebenden Diagnostik und die Effizienz der antibakteriellen Rezidivprophylaxe. Die kalkulierte antibakterielle Therapie muss sich zunehmend an der jeweils regionalen Resistenzsituation uropathogener Bakterien orientieren. Jenseits des frühen Säuglingsalters ist die orale Applikation geeigneter Antibiotika bei unkomplizierten Pyelonephritiden angemessen. In aktuellen Leitlinien gehört die Sonographie im Säuglings- und Kleinkindalter zur Basisdiagnostik bei fieberhaften HWI. Die Refluxdiagnostik bleibt dagegen denjenigen Kindern vorbehalten, bei denen angesichts klinischer Kriterien oder dem Vorliegen wegweisender sonographischer Auffälligkeiten ein behandungsbedürftiger vesikorenaler Reflux wahrscheinlich ist. Aktuelle Studien belegen die Effizienz einer antibakteriellen Rezidivprophylaxe bei gefährdeten Patienten. Bei Mädchen mit rezidivierenden Zystitiden gewinnen die pathogenetische Rolle von Blasen- und Darmfunktionsstörungen und der Einsatz der Urotherapie praktische Relevanz. Abstract Improved diagnostic procedures as well as the availability of novel drugs have led to an optimization in the treatment of urinary tract infections in infancy and childhood. Current important issues under discussion are the therapeutic strategies for pyelonephritis in infancy and early childhood, how to deal with resistance development of uropathogenic bacteria, competing concepts of diagnostic imaging and the efficiency of antibacterial prophylaxis for recurrence. Increasingly, calculated antibacterial therapy must be oriented to the respective regional resistance situation of uropathogenic bacteria. Beyond early infancy, oral administration of suitable antibiotics is appropriate in uncomplicated cases of pyelonephritis. According to the current guidelines, sonography in infancy and early childhood is part of the basic diagnostic regimen for febrile urinary tract infections. Reflux diagnostics, however, remain reserved for children in whom a vesicorenal reflux is likely in view of clinical criteria or the existence of conclusive sonographic abnormalities. Recent studies have proven the efficiency of prophylaxis for antibacterial recurrence in patients at risk. In girls presenting with recurrent cystitis, the pathogenic role of functional bladder or bowel disorders as well as the use of urotherapy are gaining practical relevance.
    Monatsschrift Kinderheilkunde 04/2015; 163(4):323-330. DOI:10.1007/s00112-014-3225-3 · 0.28 Impact Factor
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    ABSTRACT: The treatment of children and adolescents with meningomyelocele has experienced a clear change in the last 30 years. The establishment of pharmacotherapy, clean intermittent catheterization (CIC) and infection prophylaxis have improved the prognosis for patients and have led to new therapeutic strategies. The interdisciplinary cooperation between neonatologists, neurosurgeons, pediatric neurologists, pediatric urologists, pediatric nephrologists, pediatric orthopedists and pediatric surgeons leads to optimization of individualized therapy. These guidelines present definitions and classifications, investigations and timing which are described in detail. The conservative and operative therapy options for neurogenic bladder function disorders are described and discussed with reference to the current literature. The brief overview provides in each case assistance for the treating physician in the care of this patient group and facilitates the interdisciplinary cooperation.
  • New England Journal of Medicine 12/2011; 365(24):2340-2. DOI:10.1056/NEJMc1107484 · 54.42 Impact Factor
  • Transplantation 11/2011; 92(10):e57-9. DOI:10.1097/TP.0b013e318234b337 · 3.78 Impact Factor
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    ABSTRACT: Vitamin D supplementation for the prevention of rickets is one of the oldest and most effective prophylactic measures in medicine, having virtually eradicated rickets in North America. Given the potentially toxic effects of vitamin D, the recommendations for the optimal dose are still debated, in part owing to the increased incidence of idiopathic infantile hypercalcemia in Britain in the 1950s during a period of high vitamin D supplementation in fortified milk products. We investigated the molecular basis of idiopathic infantile hypercalcemia, which is characterized by severe hypercalcemia, failure to thrive, vomiting, dehydration, and nephrocalcinosis. We used a candidate-gene approach in a cohort of familial cases of typical idiopathic infantile hypercalcemia with suspected autosomal recessive inheritance. Identified mutations in the vitamin D-metabolizing enzyme CYP24A1 were evaluated with the use of a mammalian expression system. Sequence analysis of CYP24A1, which encodes 25-hydroxyvitamin D 24-hydroxylase, the key enzyme of 1,25-dihydroxyvitamin D(3) degradation, revealed recessive mutations in six affected children. In addition, CYP24A1 mutations were identified in a second cohort of infants in whom severe hypercalcemia had developed after bolus prophylaxis with vitamin D. Functional characterization revealed a complete loss of function in all CYP24A1 mutations. The presence of CYP24A1 mutations explains the increased sensitivity to vitamin D in patients with idiopathic infantile hypercalcemia and is a genetic risk factor for the development of symptomatic hypercalcemia that may be triggered by vitamin D prophylaxis in otherwise apparently healthy infants.
    New England Journal of Medicine 06/2011; 365(5):410-21. DOI:10.1056/NEJMoa1103864 · 54.42 Impact Factor
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    ABSTRACT: Acute antibody-mediated rejections (aAMR) after renal transplantation are defined by rapidly deteriorating graft function, detection of donor-specific antibodies (DSA) and characteristic histological features. In adults, anti-rejection strategies comprise intravenous immunoglobulin (IVIG), steroid pulses, plasmapheresis and rituximab. Data of children with aAMR are scarce. We report four episodes of aAMR in three children (aged 10, 10 and 11 years respectively) occurring early after renal transplantation. Pre-transplant complement-dependent cytotoxicity crossmatches were negative; in the case of re-transplantation repeated antigens were excluded. Basic immunosuppression comprised cyclosporine A, MMF and steroids. All four rejection episodes were histologically proven and associated with acute renal failure. De novo DSAs were detected in two aAMRs; one patient was additionally tested positive for AT1-receptor antibodies. All aAMRs were treated with steroid pulses, tacrolimus, MMF, IVIG, plasmapheresis and one single dose of rituximab. Despite therapy one graft was lost; in the remaining three cases kidney function re-established within 1-8 weeks. At follow-up, 14, 15 and 22 months' post-rejection their GFRs were 65, 88 and 105 ml/min/1.73 m(2) respectively. A combined therapy of steroid pulses, IVIG, plasmapheresis and rituximab is potentially effective in the treatment of aAMR in children.
    Pediatric Nephrology 04/2011; 26(7):1149-56. DOI:10.1007/s00467-011-1864-3 · 2.88 Impact Factor
  • J König, M Konrad, B Kranz, E Kuwertz-Bröking
    Klinische Pädiatrie 03/2011; 223(S 01). DOI:10.1055/s-0031-1273889 · 1.90 Impact Factor
  • New England Journal of Medicine 01/2011; 365(5):410-21. · 54.42 Impact Factor
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    ABSTRACT: Mutations in podocyte genes are associated with steroid-resistant nephrotic syndrome (SRNS), mostly affecting younger age groups. To date, it is unclear whether these patients benefit from intensified immunosuppression with cyclosporine A (CsA). The aim of this study was to evaluate the influence of podocyte gene defects in congenital nephrotic syndrome (CNS) and pediatric SRNS on the efficacy of CsA therapy and preservation of renal function. Design, settings, participants, & measurements: Genotyping was performed in 91 CNS/SRNS patients, irrespective of age at manifestation or response to CsA. Mutations were identified in 52% of families (11 NPHS1, 17 NPHS2, 11 WT1, 1 LAMB2, 3 TRPC6). Sixty-eight percent of patients with nongenetic SRNS responded to CsA, most of them achieved complete remission. In contrast, none of the patients with genetic CNS/SRNS experienced a complete remission and only two (17%) achieved a partial response, both affected by a WT1 mutation. Preservation of renal function was significantly better in children with nongenetic disease after a mean follow-up time of 8.6 years (ESRD in 29% versus 71%). The mutation detection rate in our population was high (52%). Most patients with genetic CNS/SRNS did not benefit from CsA with significantly lower response rates compared with nongenetic patients and showed rapid progression to end-stage renal failure. These data strongly support the idea not to expose CNS/SRNS patients with inherited defects related to podocyte function to intensified immunosuppression with CsA.
    Clinical Journal of the American Society of Nephrology 11/2010; 5(11):2075-84. DOI:10.2215/CJN.01190210 · 5.25 Impact Factor
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    ABSTRACT: Mutations of LAMB2 typically cause autosomal recessive Pierson syndrome, a disorder characterized by congenital nephrotic syndrome, ocular and neurologic abnormalities, but may occasionally be associated with milder or oligosymptomatic disease variants. LAMB2 encodes the basement membrane protein laminin beta2, which is incorporated in specific heterotrimeric laminin isoforms and has an expression pattern corresponding to the pattern of organ manifestations in Pierson syndrome. Herein we review all previously reported and several novel LAMB2 mutations in relation to the associated phenotype in patients from 39 unrelated families. The majority of disease-causing LAMB2 mutations are truncating, consistent with the hypothesis that loss of laminin beta2 function is the molecular basis of Pierson syndrome. Although truncating mutations are distributed across the entire gene, missense mutations are clearly clustered in the N-terminal LN domain, which is important for intermolecular interactions. There is an association of missense mutations and small in frame deletions with a higher mean age at onset of renal disease and with absence of neurologic abnormalities, thus suggesting that at least some of these may represent hypomorphic alleles. Nevertheless, genotype alone does not appear to explain the full range of clinical variability, and therefore hitherto unidentified modifiers are likely to exist.
    Human Mutation 09/2010; 31(9):992-1002. DOI:10.1002/humu.21304 · 5.05 Impact Factor
  • Kranz B, Kuwertz-Bröking E, Fründ S, H. H. Wolters, Bulla M, Konrad M
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    ABSTRACT: Despite an improved conservative therapy of end stage renal failure, dialysis associated complications and diet restrictions are not compatible with the normal development of a child. Renal transplantation is the primary goal in the therapy of end stage renal disease in childhood. Due to the increasing number of patients on the waiting list and the lack of organs for transplantation each transplant centre has to optimize and to extend the renal transplant program.This study evaluated the local pediatric renal transplant program in Muenster/Germany between 1981 and 2009 with special regard to the differences between kidney transplantation before and after 1995.The data were taken from the local registry documented in the Eurotransplant ENIS program.Since 1981, 138 kidney transplantations were performed in 127 children younger than 18 years (mean age: 11.6 ± 4.5 years). Since 1995 an increase was documented in the number of kidney transplantations per year (3.6 to 6.2), the number of living related (31 versus 1) and pre-emptive transplantations (7 versus 2). The mean recipient age and the time on dialysis remained stable. Before 1995 the transplant survival after 1 and 5 years was 80.3% and 60.2%, respectively. Thereafter the transplant survival improved to 96.8% (p=0.025) and 80.4% (p=0.015).In summary an increase of pediatric kidney transplantations was documented. Living related and pre-emptive renal transplantation has been established without decreasing the time on dialysis. The 1 and 5 year transplant survival have clearly improved.
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    ABSTRACT: Autosomal recessive polycystic kidney disease (ARPKD) [MIM 263200] belongs to a group of congenital hepatorenal fibrocystic syndromes and is caused by mutations in the PKHD1 gene encoding the multidomain protein fibrocystin/polyductin (FPC). The serine-threonine kinase mammalian target of rapamycin (mTOR) is one of the most important gate-keepers integrating numerous signals related to cell proliferation and growth. Whereas the direct activation of mTOR has been shown recently in autosomal-dominant PKD, no data are available on the role of mTOR signalling in proliferation and progression of ARPKD. Formalin-fixed and paraffin-embedded kidney specimens obtained during nephrectomy from children with ARPKD (n = 12) were used for immunohistochemical investigation of FPC expression (monoclonal antibody (mAb) 18, mAb 5a), proliferative activity (Ki-67) and activation of the mTOR pathway. Kidney specimens from children (n = 4) who died from causes not associated with kidney disease served as controls. For the detection of AKT, mTOR and S6K antibodies specifically recognizing the activated (phosphorylated) isoforms of these proteins were used. In all patients mutation analysis of the PKHD1 gene was performed. In 10 out of 12 patients, we could confirm the diagnosis by the identification of PKHD1 mutations. The tubular cyst epithelium of all kidney specimens stained strongly positive with the FPC-specific monoclonal antibody (mAb) 18 but only very faint signals were obtained with mAb 5a. In contrast, healthy kidneys showed rather weak signals with both FPC-specific mAbs, indicating dysregulated expression of FPC in our patients. Phosphorylated AKT as well as activated mTOR and its down-stream effector S6K were strongly expressed in cystic epithelia of all kidney specimens but not in control tissues. No association between the activation of this pathway and the proliferative activity (Ki-67 expression) was observed. Our results point to a central role of AKT/mTOR signalling in ARPKD and justify further investigations to evaluate the therapeutic potential of mTOR inhibitors in ARPKD patients.
    Nephrology Dialysis Transplantation 02/2009; 24(6):1819-27. DOI:10.1093/ndt/gfn744 · 3.49 Impact Factor
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    Journal of the American Society of Nephrology 02/2008; 19(1):171-81. DOI:10.1681/ASN.2007060709 · 9.47 Impact Factor
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    ABSTRACT: Acute focal bacterial nephritis (AFBN), formerly known as lobar nephronia, is a rare form of interstitial bacterial nephritis. Most often described in adults with diabetes, there is only limited knowledge of AFBN in children. Ultrasound shows circular hypoechogenic, hypoperfused parenchyma lesions, which may be misdiagnosed as a renal abscess or tumor. From 1984 to 2005, AFBN was diagnosed in 30 children at the University Hospital Münster and the General Hospital Celle, Germany. Data of 25 cases (14 girls, 11 boys) were available for retrospective evaluation. Twenty-five children with AFBN, mean age 4.5 years (range: 0.25-17.5 years), were followed up on average 4.2 years (range: 0.5-11 years). All children were admitted to hospital due to fever and rapid deterioration of clinical condition, initially suspected of having meningitis (four patients), urinary tract infections (five patients), renal tumor (three patients), pneumonia (two patients), appendicitis (one patient), or with only unspecific symptoms (ten patients). AFBN was diagnosed by ultrasound on average 3 days (range: 1-10 days) after onset of symptoms. Pyuria was found in 18/25 children, bacteriuria in 20/25 children, and hematuria in one patient. Blood cultures were negative in all but one patient. Urinary tract abnormalities were found in 12 children, including vesicoureteral reflux (8), megaureter (1), urethral valves (1), unilateral renal hypoplasia (1), and one patient with megacystis, megaureter, caudal dystopic left kidney combined with hypoplasia and dysplasia of the right kidney. High-resolution ultrasound showed AFBN lesions to have resolved completely within 12 weeks after onset of intravenous antibiotic therapy in 20/25 children. Renal parenchymal cysts remained in three cases and focal scarring in two. Blood pressure and renal function was normal in 24/25 cases. AFBN should be suspected in children with fever and rapid deterioration of clinical condition. Residual lesions such as cysts or scarring of renal parenchyma could remain.
    Pediatric Nephrology 12/2007; 22(11):1897-901. DOI:10.1007/s00467-007-0589-9 · 2.88 Impact Factor
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    ABSTRACT: Urinary tract infections (UTI) are among the most common bacterial infections in infants and children. The early diagnosis of a pyelonephritis and its rapid, calculated antibacterial therapy are decisive for the prognosis. Urogenital anomalies, renal damage and bladder dysfunction may influence the risk of recurrences of UTI and pyelonephritic scarring. Diagnostic strategies therefore should focus on their early recognition. Pediatricians, urologists and infectiologists are cooperating in diagnostic, therapy and prophylaxis of UTI. The aim of the interdisciplinary consensus presented was to work out a concept which may help to manage childhood UTI in daily practice.
    Der Urologe 03/2007; 46(2):112, 114-8, 120-3. DOI:10.1007/s00120-006-1254-9 · 0.44 Impact Factor
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    ABSTRACT: Im Säuglings- und Kindesalter gehören Harnwegsinfektionen (HWI) zu den häufigsten bakteriellen Infektionskrankheiten. Die frühzeitige Diagnose einer Pyelonephritis und die rasche, kalkulierte antibakterielle Therapie sind entscheidend für die Prognose. Die weiterführende Diagnostik dient der Früherkennung von Nieren- und Harnwegsfehlbildungen sowie Blasenfunktionsstörungen als Risikofaktoren rezidivierender HWI.In der Diagnostik, Therapie und Prophylaxe kindlicher HWI begegnen sich Kinderärzte, Urologen und Infektiologen. Ziel der vorliegenden Empfehlung ist es, ein gemeinsames Konzept zu erstellen, das dem behandelnden Arzt eine Hilfe für sein Handeln gibt und die interdisziplinäre Zusammenarbeit erleichtert.
    Der Urologe 01/2007; 46(2). · 0.44 Impact Factor
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    ABSTRACT: Dent disease is an X-linked tubulopathy frequently caused by mutations affecting the voltage-gated chloride channel and chloride/proton antiporter ClC-5. A recent study showed that defects in OCRL1, encoding a phosphatidylinositol 4,5-bisphosphate 5-phosphatase (Ocrl) and usually found mutated in patients with Lowe syndrome, also can provoke a Dent-like phenotype (Dent 2 disease). We investigated 20 CLCN5-negative males from 17 families with a phenotype resembling Dent disease for defects in OCRL1. In our complete series of 35 families with a phenotype of Dent disease, a mutation in the OCRL1 gene was detected in 6 kindreds. All were novel frameshift (Q70RfsX88 and T121NfsX122, detected twice) or missense mutations (I257T and R476W). None of our patients had cognitive or behavioral impairment or cataracts, 2 classic hallmarks of Lowe syndrome. All patients had mild increases in lactate dehydrogenase and/or creatine kinase levels, which rarely is observed in CLCN5-positive patients, but frequently found in patients with Lowe syndrome. To explain the phenotypic heterogeneity caused by OCRL1 mutations, we performed extensive data-bank mining and extended reverse-transcriptase polymerase chain reaction analysis, which provided no evidence for yet unknown (tissue-specific) alternative OCRL1 transcripts. Mutations in the OCRL1 gene are found in approximately 23% of kindreds with a Dent phenotype. Defective protein sorting/targeting of Ocrl might be the reason for mildly elevated creatine kinase and lactate dehydrogenase serum concentrations in these patients and a clue to suspect Dent disease unrelated to CLCN5 mutations. It remains to be elucidated why the various OCRL1 mutations found in patients with Dent 2 disease do not cause cataracts.
    American Journal of Kidney Diseases 01/2007; 48(6):942.e1-14. DOI:10.1053/j.ajkd.2006.08.018 · 5.76 Impact Factor
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    ABSTRACT: Adult data suggest that urinary tract infections occur frequently after renal transplantation (RTx) and contribute to mortality and graft loss; data in children are limited. Therefore, we evaluated prevalence, short and long-term morbidity and confounding factors of febrile UTI (fUTI) after paediatric RTx. In a retrospective cross-sectional study of three centres, we analysed data on 110 children followed for 4.9+/-3.4 years after successful transplantation. 40/110 (36%) patients had at least one fUTI at a median time of 0.98 years (range 0.02-8.96) after RTx; 11 patients (28%) had recurrent fUTI. Serum creatinine (SCr) rose significantly from 1.15+/-1.13 to 1.83+/-1.69 mg/dl, (P<0.001) during the fUTI, declining to baseline values after treatment. At the last followed-up calculated mean, GFR was comparable between fUTI and non-fUTI groups (75+/-26 vs 71+/-22 ml/min/1.73 m2). During fUTI mean, C-reactive protein (CRP) increased to 123+/-75 mg/l. Febrile UTI were significantly more frequent in girls compared to boys (22/44 vs 18/66, P<0.05) but occurred significantly earlier in boys than in girls [median 0.63 (range 0.02-4.15) vs 1.07 (0.04-8.96) years after RTx; P<0.02]. Also, patients with urinary tract malformations (UTMs) and neurogenic bladder as underlying diagnosis and those with urological surgery prior to transplantation had an increased risk for fUTI. fUTI is a frequent complication with significant short-term morbidity especially in girls and children with UTMs, neurogenic bladder and those with urological surgery. Long-term follow-up and prospective studies confirming specific risk factors, preventive measures and impact on graft survival are necessary.
    Nephrology Dialysis Transplantation 12/2006; 21(11):3269-74. DOI:10.1093/ndt/gfl464 · 3.49 Impact Factor
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    ABSTRACT: Hypercalciuria is regarded as a characteristic symptom of Dent disease, an X-linked recessive tubulopathy characterized by low molecular weight (LMW) proteinuria, nephrocalcinosis/nephrolithiasis, and progressive renal failure due to mutations in the CLCN5 gene. As the presence of hypercalciuria may affect the decision to consider a CLCN5 mutation in the differential diagnosis, the phenotypic spectrum and the relative frequency of hypercalciuria in patients with CLCN5 mutations was determined. We assessed renal calcium excretion in 34 male patients with proven CLCN5 mutations, who had been referred because of LMW proteinuria and at least one additional symptom of Dent disease. Hypercalciuria was defined as renal calcium excretion exceeding 0.1 mmol/kg per day. Data obtained were compared with all series of CLCN5-positive patients identified by a systematic literature survey. In 7 of our 19 families, at least 1 affected male had normal calcium excretion. Hypercalciuria was observed in 22 of 31 patients tested (71%) compared to 85 of 90 (94.4%) in series from Europe and North America and 74.4% from Japan. LMW proteinuria was present in all CLCN5-positive patients; 25% of the patients in European and North American series, 45% of the Japanese, and 41% in the present series had only two of the four principal symptoms of Dent disease. Therefore, a CLCN5 mutation should be considered irrespective of the presence of hypercalciuria in a patient with LMW proteinuria and one additional symptom of Dent disease.
    Pediatric Nephrology 10/2006; 21(9):1241-50. DOI:10.1007/s00467-006-0172-9 · 2.88 Impact Factor
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    ABSTRACT: Congenital nephrotic syndrome is clinically and genetically heterogeneous. The majority of cases can be attributed to mutations in the genes NPHS1, NPHS2, and WT1. By homozygosity mapping in a consanguineous family with isolated congenital nephrotic syndrome, we identified a potential candidate region on chromosome 3p. The LAMB2 gene, which was recently reported as mutated in Pierson syndrome (microcoria-congenital nephrosis syndrome; OMIM #609049), was located in the linkage interval. Sequencing of all coding exons of LAMB2 revealed a novel homozygous missense mutation (R246Q) in both affected children. A different mutation at this codon (R246W), which is highly conserved through evolution, has recently been reported as causing Pierson syndrome. Subsequent LAMB2 mutational screening in six additional families with congenital nephrotic syndrome revealed compound heterozygosity for two novel missense mutations in one family with additional nonspecific ocular anomalies. These findings demonstrate that the spectrum of LAMB2-associated disorders is broader than previously anticipated and includes congenital nephrotic syndrome without eye anomalies or with minor ocular changes different from those observed in Pierson syndrome. This phenotypic variability likely reflects specific genotypes. We conclude that mutational analysis in LAMB2 should be considered in congenital nephrotic syndrome, if no mutations are found in NPHS1, NPHS2, or WT1.
    Kidney International 10/2006; 70(6):1008-12. DOI:10.1038/sj.ki.5001679 · 8.52 Impact Factor

Publication Stats

950 Citations
339.26 Total Impact Points


  • 2000–2011
    • Universitätsklinikum Münster
      • Institut für Transfusionsmedizin und Transplantationsimmunologie
      Muenster, North Rhine-Westphalia, Germany
    • Universität Basel
      Bâle, Basel-City, Switzerland
  • 2010
    • University of Iowa Children's Hospital
      Iowa City, Iowa, United States
    • Howard Hughes Medical Institute
      Ashburn, Virginia, United States
  • 2004
    • University Children's Hospital Basel
      Bâle, Basel-City, Switzerland
  • 1988–2004
    • University of Münster
      Muenster, North Rhine-Westphalia, Germany
  • 2003
    • Gesellschaft für Pädiatrische Nephrologie
      Muenster, North Rhine-Westphalia, Germany
  • 1995
    • University of Hamburg
      Hamburg, Hamburg, Germany