Increased Urinary Liver-Type Fatty Acid–Binding Protein Level Predicts Worsening Renal Function in Patients With Acute Heart Failure

Okubo, Yousaku; Sairaku, Akinori; Morishima, Nobuyuki; Ogi, Hiroshi; Matsumoto, Takeshi; Kinoshita, Hiroki; Kihara, Yasuki

doi:10.1016/j.cardfail.2018.07.003

Cited by 6 publications

(4 citation statements)

References 17 publications

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“…reported that elevated urinary L‐FABP levels are an independent predictor of increased creatinine and showed a non‐significant tendency to be associated with subsequent heart failure rehospitalization in 138 patients. 14 However, this study included small population and short follow‐up period of 1 year, which may have affected the results and conclusion. Moreover, the lack of the association between urinary L‐FABP and mortality may be attributed to reduced statistical power because of the relatively small patient sample.…”

Section: Discussionmentioning

confidence: 93%

“… 11 , 12 , 13 However, because AHF is also associated with reduced renal blood flow and hypoxia, L‐FABP may be a tubular marker that is more specific to the dysfunction exacerbated by heart failure. One study focused on urinary L‐FABP in 138 patients with AHF and found an association between higher levels of L‐FABP and worsening renal function during hospitalization 14 ; however, its clinical and prognostic implications remain unclear. Therefore, we examined the clinical implication and prognostic role of urinary L‐FABP in patients with AHF.…”

Section: Introductionmentioning

confidence: 99%

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Urinary liver‐type fatty acid‐binding protein as a prognostic marker in patients with acute heart failure

et al. 2021

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Aims Urinary liver-type fatty acid-binding protein (L-FABP) is expressed in proximal tubular epithelial cells and excreted into the urine during tubular injury. We hypothesized that high urinary L-FABP is associated with poor prognosis in patients with acute heart failure (AHF). Methods and resultsWe analysed 623 patients (74 ± 13 years old; 60.0% male patients) with AHF. Urinary L-FABP levels were measured at the time of admission and adjusted for the urinary creatinine concentration. The primary endpoint was all-cause mortality. The median value and interquartile range of urinary L-FABP levels were 6.66 and 3.37-21.1 μg/gCr, respectively. Urinary L-FABP levels were significantly correlated with both beta-2 microglobulin and cystatin C levels; the correlation with the former was higher than that with the latter. During the follow-up of 631 (interquartile range: 387-875) days, 142 deaths occurred. A high tertile of urinary L-FABP level was associated with high mortality; this association was retained after adjusting for other covariates (second tertile hazard ratio 1.40, P = 0.152 vs. first tertile; third tertile hazard ratio 1.94, P = 0.005 vs. first tertile). Conclusions Urinary L-FABP is more closely associated with tubular dysfunction than with glomerular dysfunction. Tubular dysfunction, which was evaluated based on urinary L-FABP levels, in patients with AHF is associated with all-cause mortality and is independent of pre-existing risk factors. L-FABP should be considered for use in the prognosis of AHF.

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Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Urinary liver‐type fatty acid‐binding protein as a prognostic marker in patients with acute heart failure

et al. 2021

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“…Urinary L-FABP has been proposed as an emerging acute proximal tubules injury biomarker for WRF in CRS-1 despites few related studies ( 77 , 78 ). Yousaku Okubo et al revealed that urinary L-FABP can predict WRF in patients with AHF and patients with higher L-FABP levels were more likely to have rehospitalization ( 55 ).…”

Section: Markers For Wrfmentioning

confidence: 99%

Insights of Worsening Renal Function in Type 1 Cardiorenal Syndrome: From the Pathogenesis, Biomarkers to Treatment

Hui

et al. 2021

Front. Cardiovasc. Med.

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Type-1 cardiorenal syndrome refers to acute kidney injury induced by acute worsening cardiac function. Worsening renal function is a strong and independent predictive factor for poor prognosis. Currently, several problems of the type-1 cardiorenal syndrome have not been fully elucidated. The pathogenesis mechanism of renal dysfunction is unclear. Besides, the diagnostic efficiency, sensitivity, and specificity of the existing biomarkers are doubtful. Furthermore, the renal safety of the therapeutic strategies for acute heart failure (AHF) is still ambiguous. Based on these issues, we systematically summarized and depicted the research actualities and predicaments of the pathogenesis, diagnostic markers, and therapeutic strategies of worsening renal function in type-1 cardiorenal syndrome.

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“…Other biomarkers of kidney damage have also been shown to be predictive of acute and chronic cardiac damage (e.g. heart failure) [46,47]. Cardiorenal "connectors" such as erythrocyte superoxide dismutase (SOD1), GSH, and NADPH have also been used to measure kidney and heart injury [48][49][50][51][52][53].…”

Section: Oxidative Stressmentioning

confidence: 99%

New insights into the pathophysiological mechanisms underlying cardiorenal syndrome

Wang

Zhang

et al. 2020

Aging

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Communication between the heart and kidney occurs through various bidirectional pathways. The heart maintains continuous blood flow through the kidney while the kidney regulates blood volume thereby allowing the heart to pump effectively. Cardiorenal syndrome (CRS) is a pathologic condition in which acute or chronic dysfunction of the heart or kidney induces acute or chronic dysfunction of the other organ. CRS type 3 (CRS-3) is defined as acute kidney injury (AKI)-mediated cardiac dysfunction. AKI is common among critically ill patients and correlates with increased mortality and morbidity. Acute cardiac dysfunction has been observed in over 50% of patients with severe AKI and results in poorer clinical outcomes than heart or renal dysfunction alone. In this review, we describe the pathophysiological mechanisms responsible for AKI-induced cardiac dysfunction. Additionally, we discuss current approaches in the management of patients with CRS-3 and the development of targeted therapeutics. Finally, we summarize current challenges in diagnosing mild cardiac dysfunction following AKI and in understanding CRS-3 etiology.

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Increased Urinary Liver-Type Fatty Acid–Binding Protein Level Predicts Worsening Renal Function in Patients With Acute Heart Failure

Cited by 6 publications

References 17 publications

Urinary liver‐type fatty acid‐binding protein as a prognostic marker in patients with acute heart failure

Urinary liver‐type fatty acid‐binding protein as a prognostic marker in patients with acute heart failure

Insights of Worsening Renal Function in Type 1 Cardiorenal Syndrome: From the Pathogenesis, Biomarkers to Treatment

New insights into the pathophysiological mechanisms underlying cardiorenal syndrome

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