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Prof. Dr. med. habil. Kathrin Burgmaier

Professorin

LA 27-2.16

0991/3615-8338


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Zeitschriftenartikel

  • M. Stich
  • V. Di Cristanziano
  • B. Tönshoff
  • L. Weber
  • J. Dötsch
  • M. Rammer
  • S. Rieger
  • E. Heger
  • S. Garbade
  • Kathrin Burgmaier
  • L. Benning
  • Claudius Speer
  • Sandra Habbig
  • Sophie Haumann

Humoral immune response and live-virus neutralization of the SARS-CoV-2 omicron (BA.1) variant after COVID-19 mRNA vaccination in children and young adults with chronic kidney disease

In: Pediatric Nephrology (Berlin, Germany) pg. 1-14.

  • 21.11.2022 (2022)

DOI: 10.1007/s00467-022-05806-9

BACKGROUND Data on humoral immune response to standard COVID-19 vaccination are scarce in adolescent patients and lacking for children below 12 years of age with chronic kidney disease including kidney transplant recipients. METHODS We therefore investigated in this retrospective two-center study (DRKS00024668; registered 23.03.2021) the humoral immune response to a standard two-dose mRNA vaccine regimen in 123 CKD patients aged 5-30 years. A live-virus assay was used to assess the serum neutralizing activity against the SARS-CoV-2 omicron (BA.1) variant. RESULTS Children aged 5-11 years had a comparable rate and degree of immune response to adolescents despite lower vaccine doses (10 µg vs. 30 µg BNT162b2). Treatment with two (odds ratio 9.24) or three or more (odds ratio 17.07) immunosuppressants was an independent risk factor for nonresponse. The immune response differed significantly among three patient cohorts: 48 of 77 (62.3%) kidney transplant recipients, 21 of 26 (80.8%) patients on immunosuppressive therapy, and 19 of 20 (95.0%) patients with chronic kidney disease without immunosuppressive therapy responded. In the kidney transplant recipients, immunosuppressive regimens comprising mycophenolate mofetil, an eGFR of < 60 mL/min/1.73 m2, and female sex were independent risk factors for nonresponse. Two of 18 (11.1%) and 8 of 16 (50.0%) patients with an anti-S1-RBD IgG of 100-1411 and > 1411 BAU/mL, respectively, showed a neutralization activity against the omicron variant. CONCLUSION A standard mRNA vaccine regimen in immunosuppressed children and adolescents with kidney disease elicits an attenuated humoral immune response with effective live virus neutralization against the omicron variant in approximately 10% of the patients, underlying the need for omicron-adapted vaccination. A higher resolution version of the Graphical abstract is available as Supplementary information.
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Zeitschriftenartikel

  • P. Petsophonsakul
  • Mathias Burgmaier
  • B. Willems
  • S. Heeneman
  • N. Stadler
  • F. Gremse
  • S. Reith
  • Kathrin Burgmaier
  • Florian Kahles
  • Nikolaus Marx
  • Ehsan Natour
  • Elham Bidar
  • Michael Jacobs
  • Barend Mees
  • Chris Reutelingsperger
  • Malgorzata Furmanik
  • Leon Schurgers

Nicotine promotes vascular calcification via intracellular Ca2+-mediated, Nox5-induced oxidative stress, and extracellular vesicle release in vascular smooth muscle cells

In: Cardiovascular Research vol. 118 pg. 2196-2210.

  • (2022)

DOI: 10.1093/cvr/cvab244

AIMS Smokers are at increased risk of cardiovascular events. However, the exact mechanisms through which smoking influences cardiovascular disease resulting in accelerated atherosclerosis and vascular calcification are unknown. The aim of this study was to investigate effects of nicotine on initiation of vascular smooth muscle cell (VSMC) calcification and to elucidate underlying mechanisms. METHODS AND RESULTS We assessed vascular calcification of 62 carotid lesions of both smoking and non-smoking patients using ex vivo micro-computed tomography (µCT) scanning. Calcification was present more often in carotid plaques of smokers (n = 22 of 30, 73.3%) compared to non-smokers (n = 11 of 32, 34.3%; P < 0.001), confirming higher atherosclerotic burden. The difference was particularly profound for microcalcifications, which was 17-fold higher in smokers compared to non-smokers. In vitro, nicotine-induced human primary VSMC calcification, and increased osteogenic gene expression (Runx2, Osx, BSP, and OPN) and extracellular vesicle (EV) secretion. The pro-calcifying effects of nicotine were mediated by Ca2+-dependent Nox5. SiRNA knock-down of Nox5 inhibited nicotine-induced EV release and calcification. Moreover, pre-treatment of hVSMCs with vitamin K2 ameliorated nicotine-induced intracellular oxidative stress, EV secretion, and calcification. Using nicotinic acetylcholine receptor (nAChR) blockers α-bungarotoxin and hexamethonium bromide, we found that the effects of nicotine on intracellular Ca2+ and oxidative stress were mediated by α7 and α3 nAChR. Finally, we showed that Nox5 expression was higher in carotid arteries of smokers and correlated with calcification levels in these vessels. CONCLUSION In this study, we provide evidence that nicotine induces Nox5-mediated pro-calcific processes as novel mechanism of increased atherosclerotic calcification. We identified that activation of α7 and α3 nAChR by nicotine increases intracellular Ca2+ and initiates calcification of hVSMCs through increased Nox5 activity, leading to oxidative stress-mediated EV release. Identifying the role of Nox5-induced oxidative stress opens novel avenues for diagnosis and treatment of smoking-induced cardiovascular disease.
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Vortrag

  • Kathrin Burgmaier

Risikofaktoren für das Nierenüberleben bei Patienten mit Autosomal rezessiver polyzystischer Nierenerkrankung (ARPKD) [ePoster-Vortrag]

In: Jahrestagung der Gesellschaft für Pädiatrische Nephrologie

Freiburg i. Breisgau

  • 17.05.2022 (2022)
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Vortrag

  • Kathrin Burgmaier

Hepatischer Phänotyp und Komplikationen bei Patienten mit Autosomal rezessiver polyzystischer Nierenerkrankung (ARPKD)

In: Jahrestagung der Gesellschaft für Pädiatrische Nephrologie

Freiburg i. Breisgau

  • 17.05.2022 (2022)
  • Angewandte Gesundheitswissenschaften
  • GESUND
Vortrag

  • Kathrin Burgmaier

Risk factors for kidney survival in patients with autosomal recessive polycystic kidney disease (ARPKD) [online presentation]

In: 54th Annual Meeting of European Society for Paediatric Nephrology

Ljubljana, Slovenia

  • 26.06.2022 (2022)
  • Angewandte Gesundheitswissenschaften
  • GESUND
Zeitschriftenartikel

  • A. Milzi
  • R. Dettori
  • R. Lubberich
  • Kathrin Burgmaier
  • N. Marx
  • S. Reith
  • Mathias Burgmaier

Coronary microvascular dysfunction as assessed by angiography-derived index of microvascular resistance co-localizes with and may explain the presence of ischemia in stress-cardiac magnetic resonance imaging in the absence of coronary artery disease

In: Frontiers in Cardiovascular Medicine vol. 9 pg. 1060764.

  • 24.11.2022 (2022)

DOI: 10.3389/fcvm.2022.1060764

INTRODUCTION Ischemia with no obstructive coronary disease (INOCA) is a frequent phenomenon in the cath lab. A possible cause is coronary microvascular dysfunction (CMD), which may be assessed by invasive testing with possible complications; therefore, less invasive approaches have emerged, such as the angiography-derived index of microvascular resistance (aIMR). The aim of our study was to investigate the association of single-vessel aIMR as a measure of CMD with areas of INOCA in stress testing. METHODS We measured aIMR in 286 vessels from 102 patients undergoing both stress cMRI and coronary angiography. Groups were (a) INOCA group (93 vessels, 32 patients); (b) coronary artery disease (CAD) control group (116 vessels, 42 patients) with ischemia due to relevant stenosis; and (c) control group (77 vessels, 28 patients) without ischemia or relevant stenosis. RESULTS INOCA patients presented higher mean aIMR (28.3 ± 5.7) compared to both CAD patients (17.4 ± 5.7, p < 0.001) and controls (22.1 ± 5.9, p < 0.001). Furthermore, in INOCA patients aIMR was significantly increased (33.0 ± 8.1 vs. 25.8 ± 6.3, p = 0.021) in vessels with vs. without ischemia. Single vessel aIMR presented a very good diagnostic efficiency in detecting INOCA [AUC 0.865 (0.804-0.925), optimal cut-off 27.1, p < 0.001]. CONCLUSION CMD, as assessed by 3-vessel aIMR, co-localizes with and may explain the presence of ischemia in stress-cMRI in INOCA.
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Zeitschriftenartikel

  • M. Verploegen
  • R. Vargas-Poussou
  • S. Walsh
  • H. Alpay
  • A. Amouzegar
  • G. Ariceta
  • B. Atmis
  • J. Bacchetta
  • P. Bárány
  • S. Baron
  • U. Bayrakci
  • H. Belge
  • M. Besouw
  • A. Blanchard
  • A. Bökenkamp
  • O. Boyer
  • Kathrin Burgmaier
  • et al.

Parathyroid hormone and phosphate homeostasis in patients with Bartter and Gitelman syndrome: an international cross-sectional study

In: Nephrology, Dialysis, Transplantation : Official publication of the European Dialysis and Transplant Association - European Renal Association vol. 37 pg. 2474-2486.

  • (2022)

DOI: 10.1093/ndt/gfac029

BACKGROUND Small cohort studies have reported high parathyroid hormone (PTH) levels in patients with Bartter syndrome and lower serum phosphate levels have anecdotally been reported in patients with Gitelman syndrome. In this cross-sectional study, we assessed PTH and phosphate homeostasis in a large cohort of patients with salt-losing tubulopathies. METHODS Clinical and laboratory data of 589 patients with Bartter and Gitelman syndrome were provided by members of the European Rare Kidney Diseases Reference Network (ERKNet) and the European Society for Paediatric Nephrology (ESPN). RESULTS A total of 285 patients with Bartter syndrome and 304 patients with Gitelman syndrome were included for analysis. Patients with Bartter syndrome type I and II had the highest median PTH level (7.5 pmol/L) and 56% had hyperparathyroidism (PTH >7.0 pmol/L). Serum calcium was slightly lower in Bartter syndrome type I and II patients with hyperparathyroidism (2.42 versus 2.49 mmol/L; P = .038) compared to those with normal PTH levels and correlated inversely with PTH (rs -0.253; P = .009). Serum phosphate and urinary phosphate excretion did not correlate with PTH. Overall, 22% of patients had low serum phosphate levels (phosphate-standard deviation score < -2), with the highest prevalence in patients with Bartter syndrome type III (32%). Serum phosphate correlated with tubular maximum reabsorption of phosphate/glomerular filtration rate (TmP/GFR) (rs 0.699; P < .001), suggesting renal phosphate wasting. CONCLUSIONS Hyperparathyroidism is frequent in patients with Bartter syndrome type I and II. Low serum phosphate is observed in a significant number of patients with Bartter and Gitelman syndrome and appears associated with renal phosphate wasting.
  • Angewandte Gesundheitswissenschaften
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Zeitschriftenartikel

  • A. Milzi
  • R. Dettori
  • R. Lubberich
  • Kathrin Burgmaier
  • N. Marx
  • S. Reith
  • Mathias Burgmaier

Quantitative Flow Ratio Is Related to Anatomic Left Main Stem Lesion Parameters as Assessed by Intravascular Imaging

In: Journal of Clinical Medicine vol. 11

  • 12.10.2022 (2022)

DOI: 10.3390/jcm11206024

INTRODUCTION Previously, an association between anatomic left main stem (LMS) lesion parameters, as described by intravascular ultrasound (IVUS) and fractional flow reserve (FFR), was shown. Quantitative flow ratio (QFR) is a novel, promising technique which can assess functional stenosis relevance based only on angiography. However, as little is known about the relationship between anatomic LMS parameters and QFR, it was thus investigated in this study. METHODS In 53 patients with LMS disease, we tested the association between anatomic assessment using OCT (n = 28) or IVUS (n = 25) on the one hand and functional assessment as determined by QFR on the other hand. LMS-QFR was measured using a dedicated approach, averaging QFR over left anterior descending (LAD) and circumflex (LCX) and manually limiting segment of interest to LMS. RESULTS The minimal luminal area of the LMS (LMS-MLA) as measured by intravascular imaging showed a consistent correlation with QFR (R = 0.61, p < 0.001). QFR could predict a LMS-MLA < 6 mm2 with very good diagnostic accuracy (AUC 0.919) and a LMS-MLA < 4.5 mm2 with good accuracy (AUC 0.798). Similar results were obtained for other stenosis parameters. CONCLUSIONS QFR might be a valuable tool to assess LMS disease. Further studies focusing on patient outcomes are needed to further validate the effectiveness of this approach.
  • Angewandte Gesundheitswissenschaften
  • GESUND
Zeitschriftenartikel

  • R. Ajiri
  • Kathrin Burgmaier
  • N. Akinci
  • I. Broekaert
  • A. Büscher
  • I. Dursun
  • A. Duzova
  • L. Eid
  • M. Fila
  • M. Gessner
  • I. Gokce
  • L. Massella
  • A. Mastrangelo
  • M. Miklaszewska
  • L. Prikhodina
  • B. Ranchin
  • N. Ranguelov
  • R. Rus
  • L. Sever
  • J. Thumfart
  • et al.

Phenotypic Variability in Siblings With Autosomal Recessive Polycystic Kidney Disease

In: Kidney International Reports vol. 7 pg. 1643-1652.

  • 04.05.2022 (2022)

DOI: 10.1016/j.ekir.2022.04.095

INTRODUCTION Autosomal recessive polycystic kidney disease (ARPKD) is a rare monogenic disorder characterized by early onset fibrocystic hepatorenal changes. Previous reports have documented pronounced phenotypic variability even among siblings in terms of patient survival. The underlying causes for this clinical variability are incompletely understood. METHODS We present the longitudinal clinical courses of 35 sibling pairs included in the ARPKD registry study ARegPKD, encompassing data on primary manifestation, prenatal and perinatal findings, genetic testing, and family history, including kidney function, liver involvement, and radiological findings. RESULTS We identified 70 siblings from 35 families with a median age of 0.7 (interquartile range 0.1-6.0) years at initial diagnosis and a median follow-up time of 3.5 (0.2-6.2) years. Data on PKHD1 variants were available for 37 patients from 21 families. There were 8 patients from 7 families who required kidney replacement therapy (KRT) during follow-up. For 44 patients from 26 families, antihypertensive therapy was documented. Furthermore, 37 patients from 24 families had signs of portal hypertension with 9 patients from 6 families having substantial hepatic complications. Interestingly, pronounced variability in the clinical course of functional kidney disease was documented in only 3 sibling pairs. In 17 of 20 families of our cohort of neonatal survivors, siblings had only minor differences of kidney function at a comparable age. CONCLUSION In patients surviving the neonatal period, our longitudinal follow-up of 70 ARPKD siblings from 35 families revealed comparable clinical courses of kidney and liver diseases in most families. The data suggest a strong impact of the underlying genotype.
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Kernkompetenzen

  • Fachärztin für Kinder- und Jugendmedizin
  • Schwerpunktbezeichnung Kinder-Nephrologie
  • Zusatzqualifikation Psychosomatische Grundversorgung
  • Zertifikat Medizindidaktik NRW
  • Klinische Forschung im Bereich Autosomal Rezessive Polyzystische Nierenerkrankung mit Organisation der internationalen Registerstudie ARegPKD als stellvertretende Registerleitung
  • Klinische Forschung im Bereich Akutes Nierenversagen bei Früh- und Neugeborenen