Abstract
BackgroundSemaphorin 3A is a secreted protein that regulates cell motility and attachment in axon guidance, vascular growth, immune cell regulation and tumor progression. However, nothing is known about its role in kidney pathophysiology. Here, we determined whether semaphorin3A is induced after acute kidney injury (AKI) and whether urinary semaphorin 3A can predict AKI in humans undergoing cardiopulmonary bypass (CPB).Methods and Principal FindingsIn animals, semaphorin 3A is localized in distal tubules of the kidney and excretion increased within 3 hr after reperfusion of the kidney whereas serum creatinine was significantly raised at 24 hr. In humans, using serum creatinine, AKI was detected on average only 48 hours after CPB. In contrast, urine semaphorin increased at 2 hours after CPB, peaked at 6 hours (2596±591 pg/mg creatinine), and was no longer significantly elevated 12 hours after CPB. The predictive power of semaphorin 3A as demonstrated by area under the receiver-operating characteristic curve for diagnosis of AKI at 2, 6, and 12 hours after CPB was 0.88, 0.81, and 0.74, respectively. The 2-hour urine semaphorin measurement strongly correlated with duration and severity of AKI, as well as length of hospital stay. Adjusting for CPB time and gender, the 2-hour semaphorin remained an independent predictor of AKI, with an odds ratio of 2.19.ConclusionOur results suggest that semaphorin 3A is an early, predictive biomarker in experimental and pediatric AKI, and may allow for the reliable early diagnosis and prognosis of AKI after CPB, much before the rise in serum creatinine.
Highlights
Acute kidney injury (AKI) due to ischemia is a frequent and serious complication in the hospital setting
Our results suggest that semaphorin 3A is an early, predictive biomarker in experimental and pediatric AKI, and may allow for the reliable early diagnosis and prognosis of AKI after cardiopulmonary bypass (CPB), much before the rise in serum creatinine
Immunolocalization of Semaphorin 3A kidney from Normal Animals and Animal which were Subjected to Acute and Chronic Kidney Injury
Summary
Acute kidney injury (AKI) due to ischemia is a frequent and serious complication in the hospital setting. The diagnosis currently depends on detection of reduced kidney function by the rise in serum creatinine concentration, which is a delayed and unreliable measure in the acute setting [5]. Experimental studies have identified interventions that may prevent or treat AKI if instituted early in the disease process, well before the serum creatinine rises [6]. The lack of early predictive biomarkers has impaired our ability to translate these promising findings to human AKI. We determined whether semaphorin3A is induced after acute kidney injury (AKI) and whether urinary semaphorin 3A can predict AKI in humans undergoing cardiopulmonary bypass (CPB)
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