How is urine a precious indicator of one’s health?
Under certain circumstances the process of kidney repair can be impeded, which can eventually lead to chronic kidney disease. Some of the most frequently reported risk factors for non-recovery following kidney injury include age, severity of disease, hypertension, diabetes mellitus and cardiac disease. Based on my research expertise in kidney injury and identification of the role of fibrinogen in kidney injury (see this post) I followed up on my initial findings by documenting evidence for urinary fibrinogen to serve as a translational, noninvasive, and sensitive biomarker for early detection of acute kidney injury in patients. My research findings provide a novel insight into the role of fibrinogen as a diagnostic biomarker and as a therapeutic candidate in kidney disease.
Related publication:
Abstract
Fibrinogen (Fg) is significantly up-regulated in the kidney after acute kidney injury (AKI). We evaluated the performance of Fg as a biomarker for early detection of AKI. In rats and mice with kidney tubular damage induced by ischemia/reperfusion (I/R) or cisplatin administration, respectively; kidney tissue and urinary Fg increased significantly and correlated with histopathological injury, urinary kidney injury molecule-1 (KIM-1) and N-acetyl glucosaminidase (NAG) corresponding to the progression and regression of injury temporally. In a longitudinal follow-up of 31 patients who underwent surgical repair of abdominal aortic aneurysm, urinary Fg increased earlier than SCr in patients who developed postoperative AKI (AUC-ROC = 0.72). Furthermore, in a cohort of patients with biopsy-proven AKI (n = 53), Fg immunoreactivity in the tubules and interstitium increased remarkably and was able to distinguish patients with AKI from those without AKI (n = 59). These results suggest that immunoreactivity of Fg in the kidney, as well as urinary excretion of Fg, serves as a sensitive and early diagnostic translational biomarker for detection of AKI.