B Satirapoj1, R Witoon2, P Ruangkanchanasetr2, P Wantanasiri3, M Charoenpitakchai4, P Choovichian2. 1. Division of Nephrology, Department of Medicine, Phramongkutklao Hospital and College of Medicine, Bangkok, Thailand. Electronic address: satirapoj@yahoo.com. 2. Division of Nephrology, Department of Medicine, Phramongkutklao Hospital and College of Medicine, Bangkok, Thailand. 3. Department of Pharmacy Practice, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand. 4. Department of Pathology, Phramongkutklao Hospital and College of Medicine, Bangkok, Thailand.
Abstract
BACKGROUND: Chronic allograft nephropathy (CAN) represents the main cause of renal allograft failure after transplantation. Noninvasive CAN testing is required. Periostin promotes the expression of a mesenchymal phenotype in renal tubules and is a promising urine biomarker for progressive renal injury. Information regarding periostin expression in the setting of CAN remains scarce. METHODS: Subjects were recruited from our outpatient transplantation clinic. Random urine samples were collected from CAN patients (n = 24) and renal transplant patients with normal renal function (transplant controls, n = 18). Control samples were collected from healthy volunteers (n = 18) who had normal renal function. Urine periostin was measured by enzyme-linked immunosorbent assay. RESULTS: The median urine periostin in CAN patients was significantly higher than in transplant and healthy controls (1.74 vs 0.00 vs 0.14 ng/mg creatinine, respectively; P < .001). Urine periostin enzyme-linked immunosorbent assay at a cutoff value of 0.152 ng/mg creatinine demonstrated the sensitivity, specificity, and accuracy for distinguishing CAN patients from transplant patients with normal renal function (91.7%, 77.8%, and 85.7%, respectively). In addition, urine periostin levels correlated directly with urine protein creatinine ratio (R = 0.566, P < .001) and serum creatinine (R = 0.522; P < .001), whereas inverse significant correlations were evidenced with estimated glomerular filtration rate (R = -0.431; P < .001). CONCLUSION: The appearance of urine periostin in CAN patients but not in healthy and transplant controls underscores its value as a potential biomarker for chronic progressive renal injury in transplant recipients. Crown
BACKGROUND:Chronic allograft nephropathy (CAN) represents the main cause of renal allograft failure after transplantation. Noninvasive CAN testing is required. Periostin promotes the expression of a mesenchymal phenotype in renal tubules and is a promising urine biomarker for progressive renal injury. Information regarding periostin expression in the setting of CAN remains scarce. METHODS: Subjects were recruited from our outpatient transplantation clinic. Random urine samples were collected from CAN patients (n = 24) and renal transplant patients with normal renal function (transplant controls, n = 18). Control samples were collected from healthy volunteers (n = 18) who had normal renal function. Urine periostin was measured by enzyme-linked immunosorbent assay. RESULTS: The median urine periostin in CAN patients was significantly higher than in transplant and healthy controls (1.74 vs 0.00 vs 0.14 ng/mg creatinine, respectively; P < .001). Urine periostin enzyme-linked immunosorbent assay at a cutoff value of 0.152 ng/mg creatinine demonstrated the sensitivity, specificity, and accuracy for distinguishing CAN patients from transplant patients with normal renal function (91.7%, 77.8%, and 85.7%, respectively). In addition, urine periostin levels correlated directly with urine protein creatinine ratio (R = 0.566, P < .001) and serum creatinine (R = 0.522; P < .001), whereas inverse significant correlations were evidenced with estimated glomerular filtration rate (R = -0.431; P < .001). CONCLUSION: The appearance of urine periostin in CAN patients but not in healthy and transplant controls underscores its value as a potential biomarker for chronic progressive renal injury in transplant recipients. Crown
Authors: C Alfieri; A Regalia; G Moroni; D Cresseri; F Zanoni; M Ikehata; P Simonini; M P Rastaldi; G Tripepi; C Zoccali; C Chatziantoniou; Piergiorgio Messa Journal: J Nephrol Date: 2019-01-10 Impact factor: 3.902
Authors: Michał Szyszka; Piotr Skrzypczyk; Anna Stelmaszczyk-Emmel; Małgorzata Pańczyk-Tomaszewska Journal: J Clin Med Date: 2021-05-15 Impact factor: 4.241