Objective: To investigate the efficacy of true fast imaging with steady state precession (true-FISP) compared with T2-weighted fast spin echo (T2W-FSE) in monitoring changes in cyst volume and renal expansion in an ischemia reperfusion (IR) injured PKD1 knockout (IKO) mouse model.
Materials And Methods: The animal study was approved by the local institutional authority. A total of 24 mice (14 PKD1 IKO mice and 10 control mice) were sequentially scanned on a 4.7-T scanner from 4 to 12 weeks after IR injury and the cysts and kidney volumes were measured from true-FISP and T2W-FSE MR images. Signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR) were calculated for the images generated from both methods.
Results: Cyst SNR and CNR in true-FISP images were significantly higher than in images employing the T2W-FSE sequence (P < 0.05). Both methods demonstrated kidney volume increase as well as cyst growth after IR injury in the mouse model. The kidney and cysts volume at different time points were strongly correlated between true-FISP and T2W-FSE measurements (r(kidney) = 0.99, r(cysts) = 0.97).
Conclusion: The true-FISP method offers shorter scan times and higher cyst SNR and cyst to kidney tissue contrast than T2W-FSE. Both sequences have identical accuracy in measuring the cysts and kidney volume changes in mice with PKD.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1097/RLI.0b013e3181be3501 | DOI Listing |
Kidney360
June 2021
Department of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama.
Ly6c infiltrating macrophage numbers are increased in injured, conditional mice, compared with controls. Loss of Ly6c infiltrating macrophages slows injury-accelerated cystic disease. Ly6c infiltrating macrophages drive cystic disease in non-–deficient cystic models.
View Article and Find Full Text PDFHum Mol Genet
November 2011
Renal Division, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA 02115, USA.
Autosomal dominant polycystic kidney disease (ADPKD) is a commonly inherited disorder mostly caused by mutations in PKD1, encoding polycystin-1 (PC1). The disease is characterized by development and growth of epithelium-lined cyst in both kidneys, often leading to renal failure. There is no specific treatment for this disease.
View Article and Find Full Text PDFInvest Radiol
January 2010
Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Objective: To investigate the efficacy of true fast imaging with steady state precession (true-FISP) compared with T2-weighted fast spin echo (T2W-FSE) in monitoring changes in cyst volume and renal expansion in an ischemia reperfusion (IR) injured PKD1 knockout (IKO) mouse model.
Materials And Methods: The animal study was approved by the local institutional authority. A total of 24 mice (14 PKD1 IKO mice and 10 control mice) were sequentially scanned on a 4.
Am J Pathol
October 2009
Kidney Genetics Group, Academic Unit of Nephrology, Sheffield Kidney Institute, The Henry Wellcome Laboratories for Medical Research, University of Sheffield Medical School, Sheffield S10 2RX, UK.
Autosomal dominant polycystic kidney disease (ADPKD) results from mutations in either PKD1 or PKD2 and accounts for 10% of all patients on renal replacement therapy. The kidney disease phenotype is primarily characterized by cyst formation, but there are also prominent interstitial changes (inflammation, apoptosis, proliferation, and fibrosis). Using a model of unilateral ischemia-reperfusion injury, we tested the hypothesis that Pkd2 heterozygous kidneys are more sensitive to injury and that this could lead to interstitial inflammation and fibrosis.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!