Beyond the exome

DFG funded Research Group

People of Beyond the exome

Prof. Dr. med. Kai Schmidt-Ott

Testbeschreibung Medizinische Hochschule Hannover
Klinik für Nieren- und Hochdruckerkrankungen
Carl-Neuberg-Straße 1
D-30625 Hannover, Germany

Phone: +49 (0) 511-532 6319 or -2394
FAX: +49 (0) 511-552 366
Email: nephrologie@mh-hannover.de
Homepage: https://www.mhh.de/nephrologie/



Kai Schmidt-Ott, MD, is a tenured W3 Professor of Nephrology and Chief of the Department of Nephrology and Hypertension at Hannover Medical School (Medizinische Hochschule Hannover, MHH). Berlin. Kai Schmidt-Ott studied medicine in Berlin and New York. After receiving his doctorate (summa cum laude) at Prof. Martin Paul’s Department of Clinical Pharmacology (Freie Universität Berlin), he investigated the molecular basis of kidney development and regeneration from 2003 to 2007 as part of the DFG-funded Phase 1 Emmy Noether Program at Columbia University in New York, USA. From 2007, he led a research group on "Molecular and translational Kidney Research" at the Max Delbrück Center for Molecular Medicine in Berlin, first as part of the Emmy-Noether program (phase 2), then as a junior/W2 professor at Charité - Universitätsmedizin Berlin. His scientific work is funded by the German Research Foundation (DFG), the European Commission, the Federal Ministry of Education and Research, and the Urological Research Foundation. Currently, Professor Schmidt-Ott is a board member in two DFG-funded collaborative projects (Collaborative Research Unit 1365 "Renoprotection" and Research Group 2481 "Beyond the exome") and project leader in the Research Training Group 2318 "TJ-Train" and in the ERA PerMed network "OnAKI-ICI" of the European Commission. In parallel to his scientific activities, he completed his clinical training at Charité - Universitätsmedizin Berlin. In 2012, he became attending physician, in 2019 Section Chief of Nephrology Charité – Campus Benjamin Franklin. In 2022, Kai Schmidt-Ott accepted the call to take up his current position at MHH. Professor Schmidt-Ott published more than 100 scientific articles in high-ranking international journals. He also received several patents for diagnostics in the field of acute kidney injury. For his scientific activities, he received several awards, including the Franz Volhard Award of the German Society of Nephrology (2021), the Dr. Werner Jackstädt Award (2017), the Ernst Reuter Award for the best dissertation across faculties at Freie Universität Berlin in 2002, and the Young Investigator Award of the German Society of Hypertension (2001). Kai Schmidt-Ott has a major research interest in the molecular basis of kidney development and disease. One key research topic addresses the molecular, developmental and homeostatic functions of transcription factors in the kidney, focusing on kidney tubular epithelial differentiation, epithelial barrier characteristics of the renal collecting duct, renal osmoregulation, and the kidney’s response to acute injury.

Publications (selection)

Mansour F, Hinze C, Telugu NS, Kresoja J, Shaheed IB, Mosimann C, Diecke S, Schmidt-Ott KM. The centrosomal protein 83 (CEP83) regulates human pluripotent stem cell differentiation toward the kidney lineage. Elife, 2022;11:e80165.

Hinze C, Kocks C, Leiz J, Karaiskos N, Boltengagen A, Cao S, Skopnik CM, Klocke J, Hardenberg JH, Stockmann H, Gotthardt I, Obermayer B, Haghverdi L, Wyler E, Landthaler M, Bachmann S, Hocke AC, Corman V, Busch J, Schneider W, Himmerkus N, Bleich M, Eckardt KU, Enghard P, Rajewsky N, Schmidt-Ott KM. Single-cell transcriptomics reveals common epithelial response patterns in human acute kidney injury. Genome Medicine, 2022;14:103.

Hinze C, Karaiskos N, Boltengagen A, Walentin K, Redo K, Himmerkus N, Bleich M, Potter SS, Potter AS, Eckardt KU, Kocks C, Rajewsky N#, Schmidt-Ott KM#: Kidney Single-cell Transcriptomes Predict Spatial Corticomedullary Gene Expression and Tissue Osmolality Gradients. Journal of the American Society of Nephrology, 32:291-306, 2021.

Vukićević T*, Hinze C*, Baltzer S, Himmerkus N, Quintanova C, Zühlke K, Compton F, Ahlborn R, Dema A, Eichhorst J, Wiesner B, Bleich M, Schmidt-Ott KM#, Klussmann E#. Fluconazole Increases Osmotic Water Transport in Renal Collecting Duct through Effects on Aquaporin-2 Trafficking. Journal of the American Society of Nephrology, 30:795-810, 2019.

Vigolo E*, Marko L*, Hinze C, Müller DN#, Schmidt-Ullrich R#, Schmidt-Ott KM#. Canonical BMP signaling in tubular cells mediates recovery after acute kidney injury. Kidney International, 95:108-122, 2019.

Hinze C*, Ruffert J*, Walentin K*, Himmerkus N, Nikpey E, Tenstad O, Wiig H, Mutig K, Yurtdas ZY, Klein JD, Sands JM, Branchi F, Schumann M, Bachmann S, Bleich M, Schmidt-Ott KM. GRHL2 is required for collecting duct epithelial barrier function and renal osmoregulation. Journal of the American Society of Nephrology, 29:857-868, 2018.

Werth M*, Schmidt-Ott KM*, Leete T, Qiu A, Hinze C, Viltard M, Paragas N, Shawber CJ, Yu W, Lee P, Chen X, Sarkar A, Mu W, Rittenberg A, Lin CS, Kitajewski J, Al-Awqati Q, Barasch J. Transcription factor TFCP2L1 patterns cells in the mouse kidney collecting ducts. eLife, 6:e24265, 2017.

Marko L*, Vigolo E*, Hinze C, Park JK, Roel G, Balogh A, Choi M, Wuebken A, Cording J, Blasig IE, Luft FC, Scheidereit C, Schmidt-Ott KM#, Schmidt-Ullrich R#, Muller DN#: Tubular Epithelial NF-kB Activity Regulates Ischemic AKI. Journal of the American Society of Nephrology, 27:2658-2669, 2016.

Aue A*, Hinze C*, Walentin K, Ruffert, Yurtdas Y, Werth M, Chen W, Rabien A, Kilic E, Schulzke JD, Schumann M, Schmidt-Ott KM. A grainyhead-like 2/ovo-like 2 pathway regulates renal epithelial barrier function and lumen expansion. Journal of the American Society of Nephrology, 26:2704-15, 2015.

Walentin K, Hinze C, Werth M, Haase N, Varma S, Morell R, Aue A, Pötschke E, Warburton D, Qiu A, Barasch J, Purfürst B, Dieterich C, Popova E, Bader M, Dechend R, Staff AC, Yurtdas ZY, Kilic E, Schmidt-Ott KM. A Grhl2-dependent gene network controls trophoblast branching morphogenesis. Development, 142:1125-1136, 2015.

*equal contribution | #Corresponding authors