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Acute kidney injury (AKI) is a common complication in critically ill patients. Urinary excretion of liver-type fatty acid-binding protein (L-FABP), which is expressed in the proximal tubules, reflects the presence of tubular injury. Urinary excretion of podocalyxin (PCX), a glycoprotein prominently expressed on podocytes, is associated with podocyte injury. Our aims were to evaluate the utility of urinary L-FABP for the early detection of AKI and to examine whether podocyte injury is present in AKI patients using the biomarker of urinary PCX.
Patients admitted to the intensive care unit (ICU) were divided into the AKI group (n = 14) and non-AKI group (n = 11), according to the occurrence of AKI during hospitalization in the ICU. Changes in various biomarkers were evaluated.
In the AKI group, elevation of urinary L-FABP level [maximum value of L-FABP, 199.0 (92.5-433.6) μg/g creatinine, median (25-75% interquartile range)], which reflects tubular injury (area under the curve 0.95, cut-off value 44.1 μg/g Cr), occurred between -30 and 0 h before the occurrence of AKI (i.e., the time at which serum creatinine peaked), and elevation of urinary PCX level [maximum value of PCX, 389.5 (267.0-501.0) μg/g creatinine; upper limit of reference value, 160 μg/g creatinine] occurred during the time of recovery from AKI when serum creatinine levels were decreasing between 34.0 and 72.0 h after the occurrence of AKI. Furthermore, a parameter with the primary large AUC for predicting the onset of AKI was urinary L-FABP.
Our study suggests that L-FABP is a useful biomarker for early detection of AKI and that podocyte injury was induced during the recovery phase of AKI.
Department of Nephrology and Hypertension, Internal Medicine, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-Ku, Kawasaki, Kanagawa, 216-8511, Japan.
This article was published in the following journal.
Name: Clinical and experimental nephrology
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Abrupt reduction in kidney function defined as an absolute increase in serum CREATININE of more than or equal to 0.3. mg/dl, a percentage increase in serum creatinine of more than or equal to 50%, or a reduction in urine output. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.
Acute kidney failure resulting from destruction of EPITHELIAL CELLS of the KIDNEY TUBULES. It is commonly attributed to exposure to toxic agents or renal ISCHEMIA following severe TRAUMA.
A severe irreversible decline in the ability of kidneys to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal failure, either acute (KIDNEY FAILURE, ACUTE) or chronic (KIDNEY FAILURE, CHRONIC), requires HEMODIALYSIS.
A sex-linked recessive disorder affecting multiple systems including the EYE, the NERVOUS SYSTEM, and the KIDNEY. Clinical features include congenital CATARACT; MENTAL RETARDATION; and renal tubular dysfunction (FANCONI SYNDROME; RENAL TUBULAR ACIDOSIS; X-LINKED HYPOPHOSPHATEMIA or vitamin-D-resistant rickets) and SCOLIOSIS. This condition is due to a deficiency of phosphatidylinositol 4,5-bisphosphate-5-phosphatase leading to defects in PHOSPHATIDYLINOSITOL metabolism and INOSITOL signaling pathway. (from Menkes, Textbook of Child Neurology, 5th ed, p60; Am J Hum Genet 1997 Jun;60(6):1384-8)
A double-walled epithelial capsule that is the bulbous closed proximal end of the kidney tubular system. It surrounds the cluster of convoluted capillaries of KIDNEY GLOMERULUS and is continuous with the convoluted PROXIMAL KIDNEY TUBULE.
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