ArticleAmerican journal of physiology. Renal physiology2010
Early and prominent alterations in hemodynamics, signaling, and gene expression following renal ischemia in sickle cell disease.
Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Innovations in Drug Discovery for Sickle Cell Disease Targeting Oxidative Stress and NRF2 Activation-A Short Review.International journal of molecular sciences · 2025Review
- Hydroxyurea Mitigates Heme-Induced Inflammation and Kidney Injury in Humanized Sickle Cell Mice.International journal of molecular sciences · 2025Article
- New insights into the role of heme oxygenase-1 in acute kidney injury.Kidney research and clinical practice · 2020Review
- Heme oxygenase-2 protects against ischemic acute kidney injury: influence of age and sex.American journal of physiology. Renal physiology · 2019Article
- Effect of renin-angiotensin-aldosterone system blocking agents on progression of glomerulopathy in sickle cell disease.British journal of haematology · 2019Observational
- Sickle cell nephropathy: an update on pathophysiology, diagnosis, and treatment.International urology and nephrology · 2018Review
- RON kinase inhibition reduces renal endothelial injury in sickle cell disease mice.Haematologica · 2018Article
- Long-Term Endothelin-A Receptor Antagonism Provides Robust Renal Protection in Humanized Sickle Cell Disease Mice.Journal of the American Society of Nephrology : JASN · 2017Article
- Acute kidney injury during a pediatric sickle cell vaso-occlusive pain crisis.Pediatric nephrology (Berlin, Germany) · 2017Article
- Article
- Sickle cell disease: renal manifestations and mechanisms.Nature reviews. Nephrology · 2015Review
- The glomerulopathy of sickle cell disease.American journal of hematology · 2014Review
- Vasculature and kidney complications in sickle cell disease.Journal of the American Society of Nephrology : JASN · 2012Article
- Regional and systemic hemodynamic responses following the creation of a murine arteriovenous fistula.American journal of physiology. Renal physiology · 2011Article
- Genetic deficiency of Smad3 protects against murine ischemic acute kidney injury.American journal of physiology. Renal physiology · 2011Article
- Selective enhancement of contractions to α1-adrenergic receptor activation in the aorta of mice with sickle cell disease.Journal of cardiovascular pharmacology · 2011Article
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Authors and funding
7 authors at 4 institutions in 1 country.
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Abstract
Acute ischemic insults to the kidney are recognized complications of human sickle cell disease (SCD). The present study analyzed in a transgenic SCD murine model the early renal response to acute ischemia. Renal hemodynamics were profoundly impaired following ischemia in sickle mice compared with wild-type mice: glomerular filtration rate, along with renal plasma flow and blood flow rates, were markedly reduced, while renal vascular resistances were increased more than threefold in sickle mice following ischemia. In addition to these changes in renal hemodynamics, there were profound disturbances in renal signaling processes: phosphorylation of members of the MAPK and Akt signaling proteins occurred in the kidney in wild-type mice after ischemia, whereas such phosphorylation did not occur in the kidney in sickle mice after ischemia. ATP content in the postischemic kidney in sickle mice was less than half that observed in wild-type mice. Examination of the expression of candidate genes uncovered changes that may predispose to increased sensitivity of the kidney in sickle mice to ischemia: increased expression of inducible nitric oxide synthase and decreased expression of endothelial nitric oxide synthase, and increased expression of TNF-alpha. Inducibility of anti-inflammatory, cytoprotective genes, such as heme oxygenase-1 and IL-10, was not impaired in sickle mice after ischemia. We conclude that the kidney in SCD is remarkably vulnerable to acute ischemic insults. We speculate that such sensitivity of the kidney to ischemia in SCD may underlie the occurrence of acute kidney injury in patients with SCD and may set the stage for the emergence of chronic kidney disease in SCD.
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