G
Gregory J. Kato
Researcher at University of Pittsburgh
Publications - 285
Citations - 14873
Gregory J. Kato is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Sickle cell anemia & Pulmonary hypertension. The author has an hindex of 63, co-authored 278 publications receiving 13121 citations. Previous affiliations of Gregory J. Kato include CSL Behring & Johns Hopkins University.
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Journal ArticleDOI
Deconstructing sickle cell disease: Reappraisal of the role of hemolysis in the development of clinical subphenotypes
TL;DR: Hemolysis plays less of a role in the vaso-occlusive-viscosity complications of disease like the acute painful episode, osteonecrosis of bone and the acute chest syndrome, and agents that decrease hemolysis or restore NO bioavailability or responsiveness may have potential to reduce the incidence and severity of the hemolytic subphenotypes of sickle cell disease.
Journal ArticleDOI
Dysregulated arginine metabolism, hemolysis-associated pulmonary hypertension, and mortality in sickle cell disease.
Claudia R. Morris,Gregory J. Kato,Mirjana Poljakovic,Xunde Wang,William C. Blackwelder,Vandana Sachdev,Stanley L. Hazen,Elliott Vichinsky,Sidney M. Morris,Mark T. Gladwin +9 more
TL;DR: These data support a novel mechanism of disease in which hemolysis contributes to reduced nitric oxide bioavailability and endothelial dysfunction via release of erythrocyte arginase, which limits arginine bioavailability, and release of ______ hemoglobin, which scavengesNitric oxide.
Journal ArticleDOI
Sickle cell disease
Gregory J. Kato,Frédéric B. Piel,Clarice D. Reid,Marilyn H. Gaston,Kwaku Ohene-Frempong,Lakshmanan Krishnamurti,Wally R. Smith,Julie A. Panepinto,David J. Weatherall,Fernando Ferreira Costa,Elliott Vichinsky +10 more
TL;DR: SCD is characterized by a remarkable phenotypic complexity; common acute complications are acute pain events, acute chest syndrome and stroke; chronic complications (including chronic kidney disease) can damage all organs.
Journal ArticleDOI
Lactate dehydrogenase as a biomarker of hemolysis-associated nitric oxide resistance, priapism, leg ulceration, pulmonary hypertension, and death in patients with sickle cell disease
Gregory J. Kato,Gregory J. Kato,Gregory J. Kato,Vicki R. McGowan,Vicki R. McGowan,Vicki R. McGowan,Roberto F. Machado,Roberto F. Machado,Roberto F. Machado,Jane A. Little,Jane A. Little,Jane A. Little,James G. Taylor Vi,James G. Taylor Vi,James G. Taylor Vi,Claudia R Morris,Claudia R Morris,Claudia R Morris,James S. Nichols,James S. Nichols,James S. Nichols,Xunde Wang,Xunde Wang,Xunde Wang,Mirjana Poljakovic,Mirjana Poljakovic,Mirjana Poljakovic,Sidney M. Morris,Sidney M. Morris,Sidney M. Morris,Mark T. Gladwin,Mark T. Gladwin,Mark T. Gladwin +32 more
TL;DR: It is proposed that LDH elevation identifies patients with a syndrome of hemolysis-associated NO resistance, endothelial dysfunction, and end-organ vasculopathy, as well as a clinical subphenotype of pulmonary hypertension, leg ulceration, priapism, and risk of death in patients with sickle cell disease.
Journal ArticleDOI
Intravascular hemolysis and the pathophysiology of sickle cell disease
TL;DR: Intravascular hemolysis represents an intrinsic mechanism for human vascular disease that manifests clinical complications in sickle cell disease and other chronic hereditary or acquired hemolytic anemias.