Two types of fatty acid-binding protein in human kidney. Isolation, characterization and localization

Maatman, R.; Kuppevelt, T. H. M. S. M. Van; Veerkamp, J.H.

doi:10.1042/bj2730759

Cited by 110 publications

(74 citation statements)

References 53 publications

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“…The L-FABP gene is expressed in the renal cortex, and the 14-kD L-FABP protein can be localized predominantly in the proximal tubule (42,43). Elevated urinary L-FABP is detectable immediately postoperatively in patients undergoing cardiac surgery who go on to develop AKI, and it peaks within 6 hours (4,44).…”

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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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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“…Kidney injury molecule-1 (KIM-1), N-acetyl-b-D-glucosaminidase (NAG), cystatin C, and b2-microglobulin (b2MG) were measured as markers for proximal tubular damage (20)(21)(22). As a marker of distal tubular damage, we measured heart-type fatty acid-binding protein (H-FABP) (23,24), whereas neutrophil gelatinase-associated lipocalin (NGAL) and monocyte chemoattractant protein-1 (MCP-1) were measured as markers of inflammation (25,26) For quantification of IgG and IgG4, NGAL, b2MG, MCP-1, and H-FABP, we used direct sandwich-ELISAs as previously described (27). All samples were measured in duplicate in both urine and plasma.…”

Section: Measurement Of Damage Markersmentioning

confidence: 99%

Glomerular and Tubular Damage Markers in Individuals with Progressive Albuminuria

Nauta

Scheven

Meijer

et al. 2013

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Albuminuria is associated with risk for renal and cardiovascular disease. It is difficult to predict which persons will progress in albuminuria. This study investigated whether assessment of urinary markers associated with damage to different parts of the nephron may help identify individuals that will progress in albuminuria.Design, setting, participants, & measurements Individuals were selected from a prospective community-based cohort study with serial follow-up and defined as "progressors" if they belonged to the quintile of participants with the most rapid annual increase in albuminuria, and reached an albuminuria $150 mg/d during follow-up. Patients with known renal disease or macroalbuminuria at baseline were excluded. Each progressor was matched to two control participants, based on baseline albuminuria, age, and sex. Furthermore, damage markers were measured in a separate set of healthy individuals.Results After a median follow-up of 8.6 years, 183 of 8394 participants met the criteria for progressive albuminuria. Baseline clinical characteristics were comparable between progressors and matched controls (n=366). Both had higher baseline albuminuria than the overall population. Urinary excretion of the glomerular damage marker IgG was significantly higher in progressors, whereas urinary excretion of proximal tubular damage markers and inflammatory markers was lower in these individuals compared with controls. Healthy individuals (n=109) had the lowest values for all urinary damage markers measured.Conclusions These data suggest that albuminuria associated with markers of glomerular damage is more likely to progress, whereas albuminuria associated with markers of tubulointerstitial damage is more likely to remain stable.

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“…4,5 L-FABP is expressed in the human proximal tubules of the kidney. 6,7 human L-FABP (hL-FABP) binds fatty acids and transports them to mitochondria or peroxisomes, where fatty acids are ␤-oxidized, and participates in intracellular fatty acid homeostasis. 8,9 Some experimental studies of animal models of kidney disease with tubulointerstitial damage revealed that renal hL-FABP was up-regulated and urinary excretion of hL-FABP was increased.…”

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confidence: 99%

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

Yokoyama

Kamijo‐Ikemori

Sugaya

et al. 2009

The American Journal of Pathology

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To investigate the relationship between liver-type fatty acid-binding protein (L-FABP), a biomarker of chronic kidney disease, in the kidney and the degree of tubulointerstitial damage, folic acid (FA)-induced nephropathy was studied in a mouse model system. As renal L-FABP is not expressed in wild-type mice, human L-FABP (hL-FABP) transgenic mice were used in this study. hL-FABP is expressed in the renal proximal tubules of the transgenic mice that were injected intraperitoneally with FA in NaHCO 3 (the FA group) or only NaHCO 3 (the control group) and oral saline solution daily during the experimental period. The FA group developed severe tubulointerstitial damage with the infiltration of macrophages and the deposition of type I collagen on days 3 and 7 and recovered to the control level on day 14. The gene and protein expression levels of hL-FABP in the kidney were significantly enhanced on days 3 and 7. Urinary hL-FABP in the FA group was elevated on days 3 and 7 and decreased to the control level on day 14. The protein expression levels of hL-FABP in both the kidney and urine significantly correlated with the degree of tubulointerstitial damage, the infiltration of macrophages, and the deposition of type I collagen. In conclusion, renal expression and urinary excretion of hL-FABP significantly reflected the severity of tubulointerstitial damage in FA-induced nephropathy.

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Two types of fatty acid-binding protein in human kidney. Isolation, characterization and localization

Cited by 110 publications

References 53 publications

Biomarkers of AKI

Biomarkers of AKI

Glomerular and Tubular Damage Markers in Individuals with Progressive Albuminuria

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

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