Our clinical research programs are active and growing rapidly. Our transplant nephrologists are actively involved in clinical transplantation research, particularly in the area of tolerance, in collaboration with faculty members in the departments of Surgery and Microbiology-Immunology.
Let by Daniel Batlle, MD, the Batlle Lab focuses on the renin angiotensin system as it relates to the understanding of this system in rodent kidney physiology. Of particular focus are the pathways and mechanisms that determine the enzymatic cleavage and degradation of Angiotensin II and other peptides within the system by ACE2-dependent and independent pathways. The lab uses a holistic approach involving ex vivo, in vitro and in vivo studies using various rodent models of diabetic and hypertensive kidney disease.
The lab is also involved in the search for biomarkers of kidney disease progression as part of the NIDDK Consortium on CKD. Other areas of research interest include nocturnal hypertension and the physiology and pathophysiology of electrolyte disorders such as distal renal tubular acidosis.
For more information, see Batlle's faculty profile.
Publications
View Batlle's publications via PubMed.
Contact
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We study the biophysics, pharmacology and physiology of ion channels. Currently, we are focused on two divergent groups: voltage gated sodium channels (Nav) and Polycystin channels (also called Polycystic Kidney Disease Proteins, PKDs). Aside from these foci, we actively explore novel ion channels found in prokaryotic and eukaryotic cells with the goal of understanding their function in cell physiology.
For more information, view the DeCaen Lab's Website.
The David Lab — led by Nicolae Valentin David, PhD — uses a basic science and translational research approach to characterize molecular events that are involved in the expression, post-translational modifications and secretion of the bone hormone FGF23 that is highly elevated in patients with chronic kidney disease (CKD). A major area of our research focuses on investigating a novel mechanism by which inflammatory signals and iron deficiency, common consequences of CKD, regulate FGF23. Our data show that acute inflammation stimulates FGF23 production, but simultaneous increases in FGF23 cleavage maintain normal levels of biologically active protein. However, chronic inflammation and sustained iron deficiency also increase biologically active FGF23, and show that these factors may contribute to elevated FGF23 levels in CKD.
This laboratory is funded by the National Institute of Health, National Institute of Diabetes and the National institute of Digestive and Kidney Diseases (NIDDK). To learn more, view David's faculty profile.
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Tamara Isakova, MD, MMSc, is leading an ancillary study within a multi-center pilot study that is funded by the U01 Consortium of Pilot Studies in chronic kidney disease (CKD). The parent study is designed to test the biochemical efficacy and safety of phosphate and FGF23-lowering interventions in patients with stage 3 to 4 CKD. The ancillary study supports baseline and follow up measurements of intermediate cardiovascular and renal end points. In addition to circulating biomarkers, Isakova is obtaining longitudinal measures of left ventricular mass using cardiac MRI and of renal oxygenation and fibrosis using BOLD MRI. To accomplish her aims, Isakova is working closely with investigators in the MRI imaging departments at Northwestern and NorthShore. Additional studies include ongoing investigations within large prospective cohort studies, including the CRIC Study.
View Isakova's faculty profile to learn more.The Jin Lab is interested in understanding the molecular mechanisms of kidney and vasculature diseases. Cell junction and matrix proteins play a major role in the disease etiology and progression. We study how vascular and glomerular basement membrane (GBM) matrix proteins are interwoven and the mechanisms for physiological and pathological GBM remodeling during repair. Specifically, we use mass spectrometry to map the patterns of post-translational modifications such as hydroxylation and glycosylation on the GBM collagen and study how these affect the meshwork topology. Ultimately, we hope such knowledge may help to devise targeted therapies for a broad range of kidney and vascular diseases
The lab is generally interested in the pathological mechanisms of kidney and vascular diseases. We take a proteomic approach to study molecules that serve structural or functional roles in kidney filtration. Particularly, we are trying to understand how the kidney podocytes maintain and regulate their slit diaphragm, as well as their interactions with the glomerular basement membrane.
For more information, see the faculty profile of Jing Jin, MD, PhD.
The focus of our lab, led by Pinelopi Kapitsinou, MD, is to understand how endogenous pathways governed by oxygen sensing mechanisms affect kidney disease development. In the kidney, low tissue pO2 levels arise because of limited oxygen supply by a specialized vascular network and high oxygen demands of tubular epithelium. Being particularly susceptible and responsive to hypoxia, the kidney serves as an ideal organ system to study adaptive and maladaptive effects of hypoxia signaling. The central mediators of systemic and cellular adaptation to O2 deprivation are hypoxia-inducible transcription factors HIF-1 and HIF-2, whose activity is negatively regulated by prolyl hydroxylase domain–containing enzymes (PHDs). The high complexity of the oxygen sensing machinery is illustrated by both canonical and non-canonical regulation, exhibiting distinct expression patterns within kidney tissue and evoking cell type- and context-specific responses.
We have explored these molecular principles in acute kidney injury and during transition to chronic kidney disease. We have shown a critical role for endothelial PHD/HIF axis in post-ischemic kidney injury and fibrosis. Furthermore, we are particularly interested in investigating metabolic pathways that operate under the control of oxygen sensing. For example, we recently demonstrated a novel role for hypoxia in promoting tryptophan degradation, leading to enhanced generation of kynurenic acid and NAD+. By employing state-of-the art mouse genetics, single-cell transcriptomic and metabolomic approaches in both in vivo and in vitro systems, our research program aims to generate novel insights in kidney disease leading to discovery of novel therapeutic targets.
For more information, see Kapitsinou's faculty profile.
Publications
View Kapitsinou's publications on PubMed.
Contact
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Our research program focuses on the contribution of the skeleton to the mineral balance in the body. Bone produces a hormone, Fibroblast Growth Factor (FGF)-23, that participates in this balance. However, in mineral metabolism disorders, such as in chronic kidney disease, the massive production of FGF23 is associated with negative outcomes and mortality. By understanding the mechanisms that control the production of FGF23, our goal is to develop new therapeutic strategies and improve outcomes in mineral metabolism disorders. To this goal, we perform basic and translational research using a combination of genetics, molecular biology, proteomics, histology and advanced imaging techniques.
A major focus of the lab is to investigate the transcriptional and post-translational regulation of FGF23 within the bone cells. In particular, we study the specific role of a known regulator of FGF23, Dentin Matrix Protein 1 (DMP1), on these regulations and on osteocyte biology in the context of diseases associated with FGF23 excess (e.g., chronic kidney disease, hypophosphatemic rickets). A second focus is to investigate the mechanisms involved in negative outcomes associated with FGF23 excess, including bone mineralization defects, cardiac hypertrophy and cognitive defects. Our team works in collaboration with the Center for Translational Metabolism & Health, the Division of Cardiology and additional collaborators and partnerships around the world.
The Martin Lab, led by Aline Martin, PhD, is sponsored by the National Institute of Health, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and by the Northwestern Women’s Health Research Institute.
Publications
For more information, see Martin's faculty profile or view lab publications via PubMed.
Contact Us
Contact the lab at aline.martin@northwestern.edu or 312-503-4805.
Rupal Mehta, MD, is an assistant professor in the Department of Medicine's Division of Nephrology & Hypertension and a core faculty member in the Center of Metabolism & Health within the Institute of Public Health & Medicine. Under the mentorship of Drs. Myles Wolf and Tamara Isakova, Mehta is studying microvascular disease in the retina in chronic kidney disease (CKD) to more broadly understand the pathogenesis of microvascular disease and its impact on cardiovascular burden in CKD. She is conducting ongoing investigations in multiple large cohort studies, including the Chronic Renal Insufficiency Cohort Study, Multi-Ethnic Study of Atherosclerosis and the Beaver Dam Eye Study. As a member of the Center of Metabolism & Health, Mehta aims to advance her training in epidemiologic and patient-oriented research with the goal of building an academic career centered on research that informs improvements in care of patients with CKD.
See Mehta's faculty profile for more information.
The Oliver Lab investigates how organs and cell types develop their unique characteristics during embryogenesis to understand diseases resulting from developmental defects. Focusing on the forebrain, visual system and lymphatic vasculature, we use animal models, 3D organ cultures, stem cells and iPSCs.
We identified key markers in lymphatic endothelial cells and discovered that defective lymphatics can cause obesity in mice — a finding we're exploring in humans. By growing eyes from stem cells in vitro, we study the genes and mechanisms behind the formation of complex structures like the eye and forebrain.
For more information, visit the Guillermo Oliver Lab site.
Joo-Seop Park, PhD, and the Park Lab study how stem/progenitor cells differentiate into specific cell types using the mouse kidney as a model system. The nephron, the functional unit of the kidney, is composed of at least 15 distinct cell types. Since all of the cell types found in the nephron originate from the common nephron progenitor cells, the mouse kidney serves as an excellent system to study cell fate decisions of stem/progenitor cells. We aim to:
- Determine the roles of developmental signaling pathways in nephron formation.
- Identify transcription factors that define cell identities for each cell type found in the nephron.
- Elucidate how these transcription factors coordinate with signaling pathways in gene regulatory networks.
For lab information and more, see Park's faculty profile or view our publication on PubMed.
Contact
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Our lab, led by Susan Quaggin, MD, focuses on the basic biology of vascular tyrosine kinase signaling in development and diseases of the blood and lymphatic vasculature. Our projects include uncovering the molecular mechanisms of diabetic vascular complications, thrombotic microangiopathy, glomerular diseases and glaucoma. Utilizing a combination of mouse genetic, cell biologic and proteomic approaches, we have identified key roles for Angiopoietin-Tie2 and VEGF signaling in these diseases Members of the lab are developing novel therapeutic agents that target these pathways.
For more information, see Quaggin's faculty profile.
Publications
View our publications in PubMed.
Contact
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