Tenured Professor, Critical Care Medicine
Professor of Medicine, Bioengineering and Clinical & Translational Science
Vice Chair for Research
Director, Center for Critical Care Nephrology
Director, Center for Assistance in Research using eRecord (CARe)
Dr. Kellum is a clinician scientist whose research interests span various aspects of Critical Care Medicine, but center in critical care nephrology (including acid-base, and renal replacement therapy), sepsis and multi-organ failure (including blood purification), and clinical epidemiology. His research has received continuous funding from the National Institutes of Health since 2001 and he has active funding from multiple different NIH Institutes. Dr Kellum has authored more than 300 publications and has also edited several major textbooks including Critical Care Nephrology 2nd Edition (WB Saunders), and Stewart’s Textbook of Acid-Base, 2nd Edition (www.acidbase.org). He has won several awards for teaching; he lectures widely and has given more than 300 seminars and invited lectures related to his research. Dr. Kellum has been involved in the development of several clinical practice guidelines. He is a founding member and past president of the Acute Dialysis Quality Initiative (www.ADQI.net) and is co-chair of the Kidney Diseases Improving Global Outcomes (KDIGO) clinical practice guideline on acute kidney injury (www.kdigo.org). Finally Dr. Kellum is a leader in electronic research especially in critical illness and is the Director of CARe (Center for Assistance in Research using the eRecord) at the University of Pittsburgh (www.eresearch.pitt.edu).
Education & Training
|Medical College of Ohio
|University of Rochester, Strong Memorial Hosp & Affiliate Hospitals, Rochester, NY||Intern/
|University of Pittsburgh Medical Center, Pittsburgh, PA||Fellow||1994||Critical Care Medicine|
|University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA||Coursework toward MPH||1994||Biostatistics & Epidemiology|
Vice Chair for Research, Dept of Critical Care Medicine
Director, The Center for Critical Care Nephrology, CRISMA Center
Director, Center for Assistance in Research using eRecord (CARe)
|1998||Fellow, American College of Physicians|
|1999||MCCTP Faculty of the Year|
|1999||Fellow, American College of Critical Care Medicine (FCCM)|
|2002||Keynote Address: Intensive Care Society of Ireland, Londonderry, Ireland|
|2002||Thomas Iberti Memorial lecturer, Rochester, NY|
|2004||Keynote Address: Second International Symposium on Critical Care Nephrology Melbourne, Australia|
|2005-2011||Member, American Board of Internal Medicine, CCM Subspecialty Board|
|2007||International Vicenza Award in Critical Care Nephrology|
|2008||Conferral of Tenure, University of Pittsburgh School of Medicine|
|2009||Pitt Innovator Award|
|2009||SCCM Annual Scientific Award|
|2010||Kern Visiting Professor in Critical Care|
R01HL091757 (PI N Shapiro) Endothelial Cell signaling and Microcirculatory Flow in Sepsis
P50GM076659 (PI D Angus) Protocolized Care of Early Septic Shock (ProCESS)
R01A1070896 (PI F Silveira) Optimizing Dosing of Colistin for Infections Resistant to All Other Antibiotics
R01GM61992: (PI: D Angus) 5/1/01-4/30/05
Genetic and inflammatory markers of sepsis (GenIMS).
Sepsis, a diffuse inflammatory response to infection, occurs in over 450,000 cases per year in the US and frequently progresses to organ dysfunction and death. Although experimental studies using cells and animals have greatly improved our understanding of the pathophysiology of sepsis, there remains a remarkable paucity of biochemical and genetic data regarding the natural history of this important public health problem. In particular, there is a need for better markers of sepsis and outcome and a more rigorous evaluation of the complex relationships among the many genetic, inflammatory, and clinical factors that appear to influence the development and outcome of sepsis. Because pneumonia is the most common cause of sepsis, patients with this infection represent an excellent clinical model for studying sepsis in a relatively homogeneous population. This study is still generating new and valuable information regarding existing lines of inquiry and laboratory investigation; new hypotheses arising from the use of time-dependent modeling; and new clinical decision tools that have immediate and practical value for designing clinical trials and improving patient care.
V689P-3049 (PI P Palevsky) 01/15/04-12/31/07
VA Cooperative Study Program (CSP#530) Acute Renal Failure Trial Network (ATN)
This multicenter clinical trial compared Intensive vs. Conventional renal support for the treatment of acute renal failure. 1124 patients were randomized to receive either intensive treatment strategy of intermittent hemodialysis six times per week and continuous venovenous hemodiafiltration at 35 ml per kilogram of body weight per hour; or less-intensive treatment strategy with the corresponding treatments provided thrice weekly and at 20 ml per kilogram per hour. Intensive renal support in critically ill patients with acute kidney injury did not decrease mortality, improve recovery of kidney function, or reduce the rate of nonrenal organ failure as compared with less-intensive therapy involving a defined dose of intermittent hemodialysis three times per week and continuous renal-replacement therapy at 20 ml per kilogram per hour. (ClinicalTrials.gov number, NCT00076219.)
Hemoadsorption to Improve Donor Organ Recovery (HIDonOR)
While brain-dead organ donors represent the majority of the organ donor pool, it appears that graft survival is independently adversely affected by brain-death itself. In addition to disturbances in the hormonal, hemodynamic and metabolic homeostasis, immunological changes have recently been shown to occur after brain-death and these changes contribute both to vascular collapse and organ injury. Increased expression of proinflammatory cytokines and their receptors have been demonstrated consistently in the organs and in the circulation of brain-dead animals and humans. Furthermore, the increased inflammatory response seen during and immediately after brain death has also been associated with poor allograft function. Thus, we hypothesize that down- regulating this inflammatory response will lead to improved organ function in the donor and thereby increase organ recovery and subsequent allograft function. While drug therapy has not shown significant attenuation on the entire inflammatory response, we have shown in preliminary studies highly efficient removal of several inflammatory mediators from the blood of experimental animals using a novel hemoadsorption device. This device is safe in humans with chronic renal failure and increases survival time in animals exposed to lethal endotxemia. Therefore the purpose of this project was to determine whether short-term attenuation of the inflammatory response using CytoSorb can reduce pre-explantation organ dysfunction and thereby improve organ recovery. Our specific goals were: 1. to reduce circulating cytokine levels in potential organ donors (IL-6), 2. to improve organ function in those donors (reversal of shock) and, 3. to increase organ recovery per donor (number of organs recovered per donor).
A Hemoadsorption Device for the Treatment of SIRS
The overall objective of this project was to develop a hemoperfusion device for the clinical treatment of sepsis and other conditions related to the Systemic Inflammatory Response Syndrome (SIRS). We have completed promising in vitro and in vivo laboratory studies in several models of acute sepsis using a new polymer in a packed bead column device for hemoadsorption. These studies indicate that the polymer efficiently removes cytokines from whole blood, causes significant and beneficial modulation of the inflammatory response and improves survival time in a lethal animal model of sepsis. These data strongly suggest that this treatment may be beneficial to patients with sepsis and related SIRS conditions. However, before hemoadsorption can be used in clinical trials with critically ill patients, several important tasks must be achieved. The Phase I objectives of this project will determine optimal system characteristics for removal of several representative molecules from whole blood. The ultimate goal of Phase I will be to establish the optimal specifications for the adsorbent polymer, the device containing the polymer, the physical or chemical conditions and clinical parameters so that pilot human clinical trials in patients with SIRS can be designed.