Urinary fatty acid-binding protein 1: an early predictive biomarker of kidney injury

Noiri, Eisei; Doi, Kent; Negishi, Kousuke; Tanaka, Tamami; Hamasaki, Yoshifumi; Fujita, Toshiro; Portilla, Didier; Sugaya, Takeshi

doi:10.1152/ajprenal.90513.2008

Cited by 142 publications

(124 citation statements)

References 53 publications

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“…Extensive effort has been devoted to search for early biomarker for kidney diseases focusing mostly on acute kidney disease 82 and less on CKD. 83 Proteins such as adiponectin, 84 ␥-glutamyltransferase, 85 cystatin C, 16 N-acetyl-␤-D-glucosaminidase, 86 fatty acid-binding protein 1, 87 and endothelin-1 88 were proposed as biomarkers. We documented that patients with early stage CKD (stage 1 and 2) already have significantly lower urinary Klotho, and urinary Klotho is progressively lowered with declining eGFR.…”

Section: Potential Clinical Utilitymentioning

confidence: 99%

Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease

Hu¹,

Shi²,

Zhang³

et al. 2011

Journal of the American Society of Nephrology

793

877

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Soft-tissue calcification is a prominent feature in both chronic kidney disease (CKD) and experimental Klotho deficiency, but whether Klotho deficiency is responsible for the calcification in CKD is unknown. Here, wild-type mice with CKD had very low renal, plasma, and urinary levels of Klotho. In humans, we observed a graded reduction in urinary Klotho starting at an early stage of CKD and progressing with loss of renal function. Despite induction of CKD, transgenic mice that overexpressed Klotho had preserved levels of Klotho, enhanced phosphaturia, better renal function, and much less calcification compared with wild-type mice with CKD. Conversely, Klotho-haploinsufficient mice with CKD had undetectable levels of Klotho, worse renal function, and severe calcification. The beneficial effect of Klotho on vascular calcification was a result of more than its effect on renal function and phosphatemia, suggesting a direct effect of Klotho on the vasculature. In vitro, Klotho suppressed Na ϩ -dependent uptake of phosphate and mineralization induced by high phosphate and preserved differentiation in vascular smooth muscle cells. In summary, Klotho is an early biomarker for CKD, and Klotho deficiency contributes to soft-tissue calcification in CKD. Klotho ameliorates vascular calcification by enhancing phosphaturia, preserving glomerular filtration, and directly inhibiting phosphate uptake by vascular smooth muscle. Replacement of Klotho may have therapeutic potential for CKD.

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Section: Potential Clinical Utilitymentioning

confidence: 99%

Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease

Hu¹,

Shi²,

Zhang³

et al. 2011

Journal of the American Society of Nephrology

793

877

View full text Add to dashboard Cite

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“…In the kidney, L-FABP is located in the proximal tubule and is excreted into the tubular lumen along with bound toxic peroxisomal products [109,110]. Increased L-FABP expression and urinary excretion prior to the increase in SCr have been described in several animal models of AKI, including ischemia-reperfusion and cisplatin AKI models [111,112].…”

Section: Kidney Injury Moleculementioning

confidence: 99%

Biomarkers of acute kidney injury: the pathway from discovery to clinical adoption

Kashani

Cheungpasitporn

Ronco

2017

Clinical Chemistry and Laboratory Medicine (CCLM)

228

197

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Acute kidney injury (AKI) is a common complication of critical illnesses and has a significant impact on outcomes, including mortality and morbidities. Unfortunately, apart from prophylactic measures, no effective treatment for this syndrome is known. Therefore, early recognition of AKI not only can provide better opportunities for preventive interventions, but also opens many gates for research and development of effective therapeutic options. Over the last few years, several new AKI biomarkers have been discovered and validated to improve early detection, differential diagnosis, and differentiation of patients into risk groups for progressive renal failure, need for renal replacement therapy (RRT), or death. These novel AKI biomarkers complement serum creatinine (SCr) and urine output, which are the standard diagnostic tools for AKI detection. In this article, we review the available literature on characteristics of promising AKI biomarkers that are currently the focus of preclinical and clinical investigations. These biomarkers include neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), liver-type fatty acid-binding protein, interleukin 18 (lL-18), insulin-like growth factor-binding protein 7, tissue inhibitor of metalloproteinase 2 (TIMP-2), calprotectin, urine angiotensinogen (AGT), and urine microRNA. We then describe the clinical performance of these biomarkers for diagnosis and prognostication. We also appraise each AKI biomarker's advantages and limitations as a tool for early AKI recognition and prediction of clinical outcomes after AKI. Finally, we review the current and future states of implementation of biomarkers in the clinical practice.

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“…The human L-FABP gene contains a hypoxia-inducible factor 1a response element, and consequently, L-FABP gene expression is induced by hypoxia (48,49). In renal transplant recipients, immediate post-transplant urinary L-FABP excretion is strongly correlated with ischemic time (49).…”

Section: L-fabpmentioning

confidence: 99%

Biomarkers of AKI

Alge

Arthur

2015

Clinical Journal of the American Society of Nephrology

255

188

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AKI is a common clinical condition associated with a number of adverse outcomes. More timely diagnosis would allow for earlier intervention and could improve patient outcomes. The goal of early identification of AKI has been the primary impetus for AKI biomarker research, and has led to the discovery of numerous novel biomarkers. However, in addition to facilitating more timely intervention, AKI biomarkers can provide valuable insight into the molecular mechanisms of this complex and heterogeneous disease. Furthermore, AKI biomarkers could also function as molecular phenotyping tools that could be used to direct clinical intervention. This review highlights the major studies that have characterized the diagnostic and prognostic predictive power of these biomarkers. The mechanistic relevance of neutrophil gelatinase-associated lipocalin, kidney injury molecule 1, IL-18, livertype fatty acid-binding protein, angiotensinogen, tissue inhibitor of metalloproteinase-2, and IGF-binding protein 7 to the pathogenesis and pathobiology of AKI is discussed, putting these biomarkers in the context of the progressive phases of AKI. A biomarker-integrated model of AKI is proposed, which summarizes the current state of knowledge regarding the roles of these biomarkers and the molecular and cellular biology of AKI.

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Urinary fatty acid-binding protein 1: an early predictive biomarker of kidney injury

Cited by 142 publications

References 53 publications

Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease

Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease

Biomarkers of acute kidney injury: the pathway from discovery to clinical adoption

Biomarkers of AKI

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