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Endothelial injury and altered hemodynamics in thalassemia
Punnee Butthep1, Issarang Nuchprayoon, Narisa Futrakul
1Hematology Division, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Bangkok, Thailand.
Increased activated circulating endothelial cells, enhanced von Willebrand factor (vWF:Ag) and adhesion molecules (sVCAM-1) are observed in patients with beta-thalassemia/hemoglobin E. Such evidences of endothelial cell injury are associated with altered intrarenal hemodynamics with a significant reduction in renal plasma flow. Altered renal functions (namely depleted creatinine clearance) and abnormal tubular function test, which is reflected by abnormally increased fractional excretion of magnesium (FE Mg), are also delineated. The increased FE Mg implies tubulointerstitial injury which may relate to the microvascular endothelial injury and chronic ischemia.
Increased activated circulating endothelial cells, enhanced von Willebrand factor (vWF:Ag) and adhesion molecules (sVCAM-1) are observed in patients with beta-thalassemia/hemoglobin E. Such evidences of endothelial cell injury are associated with altered intrarenal hemodynamics with a significant reduction in renal plasma flow. Altered renal functions (namely depleted creatinine clearance) and abnormal tubular function test, which is reflected by abnormally increased fractional excretion of magnesium (FE Mg), are also delineated. The increased FE Mg implies tubulointerstitial injury which may relate to the microvascular endothelial injury and chronic ischemia.
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