Urinary Excretion of Liver Type Fatty Acid Binding Protein Accurately Reflects the Degree of Tubulointerstitial Damage

Yokoyama, Takeshi; Kamijo‐Ikemori, Atsuko; Sugaya, Takeshi; Hoshino, Seiko; Yasuda, Takashi; Kimura, Kenjiro

doi:10.2353/ajpath.2009.080780

Cited by 93 publications

(69 citation statements)

References 34 publications

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“…An indirect immunoperoxidase method was used to identify the antigens, as described previously. 11,12 Macrophages were identified using the rat monoclonal antibody F4/80 (BMA Biomedicals, Augst, Switzerland), and type I or type III collagens were identified using rabbit polyclonal antibodies (Cedarlane Laboratories). Ten nonoverlapping fields from both the cortical and medullary areas were selected.…”

Section: Immunohistological Analysismentioning

confidence: 99%

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Renal Liver-Type Fatty Acid Binding Protein Attenuates Angiotensin II–Induced Renal Injury

et al. 2012

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Studies were conducted in accordance with the St Marianna University School of Medicine Institutional Guide for Animal Experiments. Because renal L-FABP is not expressed in the mouse kidney, hL-FABP Tg mice were generated as described previously (World Intellectual Property Organization patent WO0073791). 10Eight to 10-week-old male hL-FABP Tg mice (n=35; body weight, 23.7±0.2 g) on a C57/BL6 background and wild-type (WT) mice purchased from Japan SLC Inc (Shizuoka, Japan; n=36; body weight, 23.4±0.3 g) were used.Abstract-To investigate the role of human liver-type fatty acid binding protein (hL-FABP) in angiotensin (Ang) II-induced renal injury, Ang II was infused systemically into hL-FABP chromosomal transgenic (Tg) and wild-type (WT) mice (Tg-Ang II and WT-Ang II) for 28 days. Control mice were injected with saline only (Tg-control and WT-control). hL-FABP was expressed in proximal tubules of Tg mice. After a high-dose injection of Ang II, renal gene and protein expressions of hL-FABP in Tg-Ang II mice increased significantly compared with Tg-control mice. Urinary excretion of L-FABP was significantly greater in Tg-Ang II than in Tg-control mice. Blood pressure levels in both groups increased to a similar extent. Upregulation of monocyte chemoattractant protein 1 expression, macrophage infiltration in the interstitium, tubulointerstitial damage, and depositions of type I and III collagens were observed in both Tg-Ang II and WT-Ang II mice. However, these effects were less pronounced in Tg-Ang II compared with WT-Ang II mice. The level of renal N-(hexanoyl)lysine, an oxidative stress marker, was significantly higher in WT-Ang II than in Tg-Ang II mice.In

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Section: Immunohistological Analysismentioning

confidence: 99%

“…Each degree of tubulointerstitial injury and of fibrosis were evaluated as ratios to the entire cortical or medullary area. 11,12 For glomerulosclerosis quantification, the grade of sclerosis in each glomerulus stained with periodic acidSchiff was defined as described previously.…”

Section: Renal Histological and Morphometric Analysismentioning

confidence: 99%

Renal Liver-Type Fatty Acid Binding Protein Attenuates Angiotensin II–Induced Renal Injury

et al. 2012

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“…31 A number of studies have suggested a possible role for urinary FABP in clinical diagnosis of renal disease. 32 Ferguson et al have reported a substantial increment of urinary L-FABP in several etiologies of acute kidney injury (AKI) such as acute tubular necrosis, nephrotoxic exposure, and sepsis. 33 In contrast to previous studies, we did not detect high U L-FABP /Cr levels in our patients.…”

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confidence: 99%

Urinary early kidney injury molecules in children with beta-thalassemia major

et al. 2015

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Background: The aim of this study was to investigate novel urinary biomarkers including N-acetyl-b-D-glucosaminidase (NAG), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and liver-type fatty acid binding protein (L-FABP) in children with b-thalassemia major (b-TM). Materials and methods: Totally, 52 patients (29 boys, 23 girls) with b-TM and 29 healthy controls (3-17 years) were included. Various demographic characteristics and blood transfusions/year, disease duration, and chelation therapy were recorded. Serum urea, creatinine, electrolytes, and ferritin and urinary creatinine, protein, calcium, phosphorus, sodium, potassium, and uric acid in first morning urine samples were measured and estimated glomerular filtration rate (eGFR) was calculated. Routine serum and urinary biochemical variables, urinary NAG to Creatinine (U NAG/Cr ), U NGAL/Cr , U KIM-1/Cr , and U L-FABP/Cr ratios were determined. Results: Patients had similar mean serum urea, creatinine and eGFR levels compared with controls (p40.05 for all). The mean urinary protein to creatinine (U Protein/Cr ) ratio was significantly higher in patients compared to the healthy subjects (0.13 ± 0.09 mg/mg and 0.07 ± 0.04 mg/mg, respectively; p50.001). Significantly increased U NAG/Cr (0.48 ± 0.58 vs. 0.23 ± 0.16, p ¼ 0.026) and U NGAL/Cr (22.1 ± 18.5 vs. 11.5 ± 6.17, p ¼ 0.01) ratios were found in b-TM patients compared with healthy controls. However, no differences were found in serum and urinary electrolytes or U KIM-1/Cr and U L-FABP/Cr ratios between patients and controls (p40.05). Significant correlations were found between urinary biomarkers and urinary electrolytes (p50.05). Conclusions: Our results suggest that urinary NAG and NGAL may be considered to be reliable markers to monitor renal injury in b-TM patients.

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“…26,27 Real-time quantitative PCR analysis was performed using a TaqMan StepOnePlus system (Thermo Fisher Scientific) to measure the mRNA levels of Nrf2, NAD(P)H quinone oxidoreductase-1, glutathione Stransferase μ1, glutathione S-transferase α4, monocyte chemoattractant protein-1 (MCP-1), regulated on activation, normal T cell expressed and secreted (RANTES), α-1 collagen type I and type III, human L-FABP and glyceraldehyde-3-phosphate dehydrogenase. The expression levels of these transcripts in each sample were normalized to the glyceraldehyde-3-phosphate dehydrogenase expression levels.…”

Section: Real-time Quantitative Pcr Analysismentioning

confidence: 99%

“…An indirect immunoperoxidase method was used to identify the antigens, as described previously. 26,27 Type I and type III collagens were identified using rabbit polyclonal antibodies (Cedarlane Laboratories Ltd, Burlington, ON, Canada). Macrophages were identified using a rat monoclonal antibody against F4/80 (BMA Biomedicals, Augst, Switzerland).…”

Section: Immunohistological Analysismentioning

confidence: 99%

Role of bardoxolone methyl, a nuclear factor erythroid 2-related factor 2 activator, in aldosterone- and salt-induced renal injury

Hisamichi¹,

Kamijo‐Ikemori

Sugaya³

et al. 2017

Hypertens Res

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The aim of this study was to investigate the renoprotective effect of bardoxolone methyl (BM), a nuclear factor erythroid 2-related factor 2 (Nrf2) activator with an antioxidant effect, in a salt-sensitive hypertension model induced by aldosterone (Ald) and salt. Tubulointerstitial damage with urinary liver-type fatty acid-binding protein (L-FABP) was evaluated using human L-FABP chromosomal transgenic (L-FABP +/ − ) male mice. The mice in the Ald group (n = 7) received systemic Ald infusions via an osmotic minipump and were given 1% NaCl water for 35 days. Those in the Ald-BM group (n = 8) were administered BM intraperitoneally in addition to an injection of Ald and salt. The dose of BM was gradually increased every 7 days up to 10 mg kg − 1 per day, which was maintained for 14 days. The administration of BM significantly increased renal expression of the Nrf2 target antioxidant gene. Tubulointerstitial damage was significantly ameliorated in the Ald-BM group compared to the Ald group. The increase in reactive oxygen species (ROS) and upregulation of angiotensinogen expression in the kidneys of the Ald group was significantly prevented in the Ald-BM group. The upregulation of human L-FABP expression induced in the kidneys and increase in urinary L-FABP in the Ald group were significantly suppressed by BM administration. In conclusion, BM ameliorated tubulointerstitial damage in the Ald-and salt-induced hypertension model through suppression of both ROS production and intrarenal renin-angiotensin system activation. Urinary L-FABP may be a useful marker reflecting the therapeutic efficacy of BM.

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Urinary Excretion of Liver Type Fatty Acid Binding Protein Accurately Reflects the Degree of Tubulointerstitial Damage

Cited by 93 publications

References 34 publications

Renal Liver-Type Fatty Acid Binding Protein Attenuates Angiotensin II–Induced Renal Injury

Renal Liver-Type Fatty Acid Binding Protein Attenuates Angiotensin II–Induced Renal Injury

Urinary early kidney injury molecules in children with beta-thalassemia major

Role of bardoxolone methyl, a nuclear factor erythroid 2-related factor 2 activator, in aldosterone- and salt-induced renal injury

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