HCKH - PI Ulrich Wenzel - Hamburg Center for Kidney Health

Laboratory for arterial hypertension and hypertensive end-organ damage

Ulrich Wenzel
.
- TEAM MEMBERS
- RESEARCH
- CV
- PUBLICATIONS
- FUNDING

Ulrich Wenzel

Mission Statement

“Understanding the underlying mechanisms for better prevention and treatment of arterial hypertension and hypertension induced end-organ damage”

— Ulrich Wenzel, MD

Team Members

MD student

Nicolas Ehnert

Technician

Stefan Gatzemeier

This email address is being protected from spambots. You need JavaScript enabled to view it.

Clinician Scientist

Leonie Dreher, MD

This email address is being protected from spambots. You need JavaScript enabled to view it.

Research

Increasing evidence indicates that hypertension and hypertensive end-organ damage are not only mediated by hemodynamic injury. Inflammation plays also an important role in the pathophysiology and contributes to the deleterious consequences of arterial hypertension. Sodium intake is indispensable for normal body function but can be detrimental when taken in excess of dietary requirements. Recent data show that sodium levels also modulate the function of monocyte/macrophages, dendritic cells, and different T cell subsets. Some of these effects are mediated by changes in the microbiome and metabolome that can be found after high salt intake.

The purpose of our work is to discover the mechanisms underlying arterial hypertension to better understand arterial hypertension and the resulting end-organ damage. We focus on three points:

Role of the complement system in hypertension.
Role of aldosterone and the mineralocorticoid receptor in inflammatory cells.
Pathogenesis of so-called malignant hypertension and malignant nephrosclerosis in humans.

Figure 1: Our current concept explaining arterial hypertension (from Hengel et al. 2022). We call it a modified mosaic theory putting inflammation and salt in the center.

Figure 2: Proinflamamtory effects of the mineralocorticoid receptor in innate and adapive immune cells (from Hengel et al 2022). Recent data suggest that the mineralocorticoid receptor is expressed in inflammatory cells and has proinflammatory effects.

Figure 3: The pathogensis of renal injury in so called malignannt nephrosclerosis is not understood. It is a form of thrombotic microangiopathy defined by progressive narrowing of interlobular arterial branches and afferent arterioles with intima fibrosis and onion-like appearance of intimal scarring as shown below (histology provided by T. Wiech).

©Ulrich Wenzel

Ulrich Wenzel, MD

Senior Physician

III. Department of Medicine, University Medical Center Hamburg-Eppendorf (UKE)
Martinistr. 52
20246 Hamburg, Germany

This email address is being protected from spambots. You need JavaScript enabled to view it.

CV

Current Position

Senior Physician

University Training

1983 - 1989

Medical School, Freie Universität Berlin, Germany

Academic qualifications

2002 - 2020	Habilitation and Venia legendi Internal Medicine, University Medical Center Hamburg Eppendorf, UKE
1992	Medical Thesis, Freie Universität Berlin

Previous professional career

Clinical postgraduate education:

2005	Hypertensiologe DHL^®
2004	Board Certification Nephrology
2000	Board Certification Internal Medicine

Scientific postgraduate education:

1993 - 1995

Post-Doc, University of Texas, Health Science Center at San Antonio, Department of Medicine, Division of Nephrology (H. Abboud, M. D., Professor of Medicine), San Antonio, Texas, USA

Selected awards and honors

2020 - 2023 - 2020	President German Society of Hypertension
2016	Franz Gross Award, Germany Society of Hypertension
2003	Dr. Martini-Award, Hamburg, Germany
2001	Adalbert Buding Award, Germany Society of Hypertension
1988 - 1989	Fellow Studienstiftung des Deutschen Volkes

Selected publications

1.	Deficiency of Complement C3a and C5a receptors Does Not Prevent Angiotensin II-Induced Hypertension and Hypertensive End-Organ Damage. Bode M, Herrnstadt GR, Dreher L, Ehnert N, Kirkerup P, Lindenmeyer MT, Meyer-Schwesinger CF, Ehmke H, Köhl J, Huber TB, Krebs CF, Steinmetz OM, Wiech T, Wenzel UO. Hypertension. 2024 Jan;81(1):138-150.
2.	Complement component C3 as a new target to lower albuminuria in hypertensive kidney disease. Bode M, Diemer JN, Luu TV, Ehnert N, Teigeler T, Wiech T, Lindenmeyer MT, Herrnstadt GR, Bülow J, Huber TB, Tomas NM, Wenzel UO. Br J Pharmacol. 2023, 180:2412-2435.
3.	The role of the mineralocorticoid receptor in immune cells in cardiovascular disease. van der Heijden CDCC, Bode M, Riksen NP, Wenzel UO. Br J Pharmacol. 179:3135-3151, 2022.
4.	Mosaic theory revisited: inflammation and salt play a central role in arterial hypertension. Hengel F, Benitah JP, Wenzel UO. Cell Mol Immunol. 19:561-576, 2022.
5.	The role of complement in arterial hypertension and hypertensive end organ damage.. Wenzel UO, Kemper C, Bode M. Br J Pharmacol. 178:2849-2862, 2021.
6.	The chemokine receptor CX3CR1 reduces renal injury in mice with angiotensin II-induced hypertension. Ahadzadeh E, Rosendahl A, Czesla D, Steffens P, Prüßner L, Meyer-Schwesinger C, Wanner N, Paust HJ, Huber TB, Stahl RAK, Wiech T, Kurts C, Seniuk A, Ehmke H, Wenzel UO. Am J Physiol Renal Physiol. 315:F1526-F1535, 2018.
7.	Adaptive immunity and IL-17A in chronic kidney disease in mice. Rosendahl A, Kabiri R, Bode M, Klinge S, Ehmke H, Mittrücker HW, Wenzel UO. Brit J Pharmacol. 176:2002-2014, 2019.
8.	Salt, inflammation, IL-17 and hypertension. Wenzel UO, Bode M, Kurts C, Ehmke H. Br J Pharmacol. 176:1853-1863, 2019.
9.	The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension. Weiss S, Rosendahl A, Czesla D, Meyer-Schwesinger C, Stahl R, Ehmke H, Kurts C, Zipfel P, Köhl J, Wenzel UO. Am J Physiol Renal Physiol. 310:F1356-65, 2016.
10.	Immune Mechanisms in Arterial Hypertension. Wenzel UO, Turner JE, Krebs C, Kurts C, Harrison DG, Ehmke H. J Am Soc Nephrol. 27:677-86, 2016.