Schmidt-Ott Lab

Schmidt-Ott Lab

Molecular and Translational Kidney Research


Kidney disease affects millions of people and causes substantial morbidity and mortality. Our research group studies the molecular and cellular mechanisms that govern kidney development in the embryo and kidney disease later in life.

We strive to discover novel diagnostic markers and therapeutic targets, and to better understand the molecular networks that control tissue differentiation, homeostasis, and regeneration.

We conduct clinical studies and utilize model organisms employing a wide spectrum of cell and molecular biology techniques, as well as systems biology approaches. Our central goal is to improve the diagnosis and therapy of kidney disease.


Head of the group

Prof. Dr. Kai Schmidt-Ott

Scientific background

since 2014 Professorship of Urogenital Research at Charité - Universitätsmedizin Berlin and Max Delbrueck Center for Molecular Medicine
since 2014 Project leader DFG research unit 1368: “Molecular physiology and epigenetics of NF-κB/BMP interactions in the post-ischemic kidney (with PD Dr. D. N. Müller and Dr. R. Schmidt-Ullrich)
since 2014 Project leader DFG research unit 1368: “Therapeutic implications and pathophysiological role of calprotectin in acute kidney injury" (with Prof. Dr. T. Westhoff)
since 2008 

Adjunct Assistant Professor, Columbia University College of Physicians and Surgeons, New York, NY, USA

2007-2013 Junior research group leader (Emmy Noether Program, Phase II) at the Max-Delbrück Center for Molecular Medicine, Berlin
2009-2014 Junior Professor of Molecular Medicine, Charité – Universitätsmedizin Berlin
2011-2013 Project leader DFG research unit 1368: " NF-κB and BMP signaling in acute kidney injury“ (with PD Dr. D. N. Müller und Dr. R. Schmidt-Ullrich)

Project leader, DFG research unit 667 “Epithelial mechanisms of renal volume regulation“

2003-2007 Stipend of the German Research Foundation (Emmy Noether Program, Phase I, DFG), Postdoctoral Research Associate, Department of Medicine, Division of Nephrology, PI: Prof. Dr. Jonathan Barasch, Columbia University College of Physicians and Surgeons, New York
1996-2002 Medical dissertation, Department of Clinical Pharmacology and Toxicology, Freie Universität Berlin, Prof. Dr. Martin Paul, Title: “Endothelin-dependent morphological transformation of hypoxic astrocytes“ (summa cum laude)
1998-1999  Visiting Scholar (Gottfried Daimler and Carl Benz Foundation), Department of Physiology, Prof. Dr. M. I. Phillips, University of Florida

Clinical Background

since 2012  Attending physician, Department of Nephrology, Charité – Universitätsmedizin Berlin, Campus Mitte
2010-2012  Board certified physician in Internal Medicine, Department of Nephrology, Charité – Universitätsmedizin Berlin, Campus Mitte
2001-2003, 2007-2009 Clinical resident/nephrology fellow, Department of Nephrology and Hypertensiology (Prof. Dr. F. C. Luft), Charité – Universitätsmedizin Berlin, Campus Buch

Stipends and Awards

2007 Emmy Noether stipend of the DFG (Phase II)
2003 Emmy Noether stipend of the DFG (Phase I)
2003  Ernst Reuter Award of the Free University of Berlin (Best doctoral thesis of the year 2002)
2001 Young Investigator Award of the German Society of Hypertension
1998 Research stipend of the Gottlieb Daimler and Carl Benz Foundation

Profile at Google Scholar

Team members


Dr. rer. nat. Katharina Walentin, postdoctoral scientist

Dr. med. Christian Hinze, postdoctoral scientist, physician

Dr. med. Eugenia Singer, postdoctoral scientist, physician

Dr. med. Eva Schrezenmeier, postdoctoral scientist, physician (Charité/BIH Junior Clinical Scientist program)

Janett Ruffert, PhD student (Urological Research Foundation, Transcard Research School)

Emilia Vigolo, PhD student (Transcard Research School)

Zeliha Yesim Yurtdas, PhD student (Urological Research Foundation, Transcard Research School)

Fatma A. A. Mansour, PhD student (Stipend from Cairo University)

Ricarda Merle Viol, medical doctoral student

Carolin Elfriede Markus, medical doctoral student

Jutta Swolinsky, medical doctoral student

Paula Halbeisen, medical doctoral student

Tatjana Luganskaja, technical assistant



The kidney is a central organ in cardiovascular diseases. It excretes toxins into the urine, regulates blood pressure and solute homeostasis, and produces hormones. High blood pressure (hypertension) and chronic kidney disease rank among the top risk factors for cardiovascular end organ damage

Embryonic kidney epithelia labeled by in situ hybridization for Sostdc1

The kidney is composed of structural units called nephrons, which consist of more than 20 different types of epithelial cells that facilitate transport between the urinary compartment and the interstitium. In the embryo, kidney development is initiated during mid-embryogenesis, when the ureteric bud, an epithelial tubule extending from the nephric duct, interacts with an adjacent cell population of committed stem cells in the metanephric mesenchyme. The ureteric bud undergoes branching morphogenesis to give rise to the ureter, renal pelvis and collecting duct system, while the metanephric mesenchyme progenitors generate many additional cell types of the nephron. 

The molecular and cellular events underlying kidney development are intricately linked to kidney disease. Exogenous or genetic perturbations of kidney development result in urogenital malformations, cystic kidney diseases and other types of congenital kidney disease. Furthermore, adult kidney epithelia preserve the ability to reactivate molecular pathways from earlier developmental stages in certain disease states, including acute kidney injury, kidney fibrosis, and kidney tumors.

Our group investigates the molecular mechanisms that govern kidney development and kidney disease. We focus on gene regulatory networks that determine aspects of epithelial differentiation, regeneration, and homeostasis. We employ a wide spectrum of cell and molecular biology techniques utilizing genetic model organisms and systems biology approaches.



Prof. Dr. Kai Schmidt-Ott
Prof. Dr. Kai Schmidt-Ott