Biomarkers of Acute Kidney Injury

Edelstein, Charles L.

doi:10.1053/j.ackd.2008.04.003

Cited by 194 publications

(159 citation statements)

References 98 publications

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“…Pro-inflammatory cytokine found in urine after acute ischemic damage to proximal tubules [73] ; associated with AKI-related mortality, although not organspecific [70] ; might be involved in myocardial cell damage in the setting of ACS [74] Sensitive and specific to detect ischemic AKI with an area under the ROC curve of 0.78 [71] ; levels rise 48 h before those of creatinine [69] Detection in urine Inhibitors expressed in stem cells are protective in models of myocyte injury [74] L-FABP Selectively binds free unsaturated fatty acids and products of lipid oxidation in cells in the setting of hypoxic tissue injury; detected in the urine in the setting of AKI [7] Might predict dialysis-free survival in patients with AKI [76] Detection in urine -…”

Section: Il-18mentioning

confidence: 99%

Cardiorenal syndromes

McCullough

Ahmad²

2011

WJC

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Cardiorenal syndromes (CRS) have been subclassified as five defined entities which represent clinical circumstances in which both the heart and the kidney are involved in a bidirectional injury and dysfunction via a final common pathway of cell-to-cell death and accelerated apoptosis mediated by oxidative stress. Types 1 and 2 involve acute and chronic cardiovascular disease (CVD) scenarios leading to acute kidney injury or accelerated chronic kidney disease. Types 2 and 3 describe acute and chronic kidney disease leading primarily to heart failure, although it is possible that acute coronary syndromes, stroke, and arrhythmias could be CVD outcomes in these forms of CRS. Finally, CRS type 5 describes a simultaneous insult to both heart and kidneys, such as sepsis, where both organs are injured simultaneously. Both blood and urine biomarkers are reviewed in this paper and offer a considerable opportunity to enhance the understanding of the pathophysiology and known epidemiology of these recently defined syndromes.

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Section: Il-18mentioning

confidence: 99%

Cardiorenal syndromes

McCullough

Ahmad²

2011

WJC

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“…Lines of evidence showed that urinary NGAL, IL-18, Cys-C, KIM-1 and some other candidate molecules were believed as potential markers to the diagnosis of AKI (Adiyanti and Loho, 2012;Edelstein, 2008) [8] [9]. But until now, none of them are currently established well enough to replace serum creatinine as a marker of renal function.…”

Section: Introductionmentioning

confidence: 99%

Urinary Kidney Injury Molocule-1 Level in Preterm Neonates with Respiratory Distress Syndrome

Youssef¹,

Abdel-Salam²,

Saeed³

et al. 2016

OJPed

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Background: Despite recent advances in perinatal and neonatal care in respiratory distress syndrome (RDS) prevention and treatment, a considerable number of these neonates suffer from acute kidney injury (AKI), and it is associated with poor outcome as an independent risk factor. KIM-1 mRNA and protein are expressed at a low level in normal kidney but are increased in post ischemic kidney. Aim: The aim is to detect the value of urinary KIM-1 measurement as an early predictor marker of acute kidney injury in preterm neonates with respiratory distress syndrome. Patients and methods: The study included 30 preterm newborn with (RDS) ≤36 weeks during the period from October 2014 to March 2015. Also the study included 30 apparently healthy newborn ≤36 weeks as controls. They were selected from NICU of Manshiate Elbakry hospital Cairo, Egypt. uKIM-1 along with serum creatinine levels and eGFR were assessed in days 1 of life for both groups and in day 3 for cases. Results: In day one of life, we found a significant increase in uKIM-1 levels in preterm newborn with RDS compared to their controls (2.88 ± 1.01 ng/ml and 0.95 ± 0.52 ng/ml respectively (p = 0.001)). There is no significant difference between both groups regarding serum creatinine and eGFR. In day 3 of life, preterm with RDS had significant decrease in uKIM-1 levels compared to day 1 of life with significant increase in non-survivor compared to survivor group ( 2.30 ± 1.56 ng/ml and 1.30 ± 0.90 ng/ml respectively (p = 0.03)). The sensitivity and specificity of uKIM-1 and serum creatinine was calculated (100.00%, 86.67% and 33.33%; 95.00%) respectively. Conclusion: Preterm neonate with RDS is at high risk of developing AKI. Early and serial uKIM-1 measurements can be used as a non-invasive indicator of kidney injury in premature newborn with RDS.

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“…ACCEPTED MANUSCRIPT 12 Generally, in response to low oxygen tension, cells target to stabilize and activate hypoxic inducible factors (HIFs), a heterodimer (HIF-α and HIF-β subunits) which regulate transcriptional activity to coordinate the adaptive response to hypoxia [47]. In renal artery clamp models HIF1-α protein was induced within an hour post-insult in whole kidneys of pigs, and collecting ducts, papillary tubular cells and interstitial cells of rats [47,48].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…Traditionally, the clinical standards for diagnosis of AKI have been serum creatinine and blood urea nitrogen (BUN), however this has progressed to more sophisticated scoring systems that take into account urine output [11,12]. AKI has also been referred to as acute renal failure and has been difficult to quantify because of the multiple definitions of AKI found in the literature.…”

Section: Aki and Traumamentioning

confidence: 99%

Molecular mechanisms of trauma-induced acute kidney injury: Inflammatory and metabolic insights from animal models

Burmeister

Gómez

Dubick

2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Trauma-induced acute kidney injury (AKI), such as after hemorrhagic shock (HS) or burn, remains a significant problem in the intensive care unit and is associated with increased mortality. The pathophysiology that drives AKI post-trauma is multi-factorial, and includes both inflammatory and metabolic alterations. Identifying the systemic profile that contributes to AKI is crucial not only for early diagnosis, but also for identifying treatments that improve kidney function and maintaining long-term patient health. In an effort to elucidate this molecular pathophysiology researchers have utilized a variety of animal models including chemically-induced (i.e., cisplatin), blocking renal perfusion (i.e., arterial clamping) and inducing burn or HS. As the latter burn and HS models are unequivocally applicable to studying AKI in the context of traumatic injury, this review will summarize the inflammatory and metabolic insights associated with AKI gained with these animal models. Moreover, novel therapeutic strategies brought forth with these models will be discussed.

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Biomarkers of Acute Kidney Injury

Cited by 194 publications

References 98 publications

Cardiorenal syndromes

Cardiorenal syndromes

Urinary Kidney Injury Molocule-1 Level in Preterm Neonates with Respiratory Distress Syndrome

Molecular mechanisms of trauma-induced acute kidney injury: Inflammatory and metabolic insights from animal models

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