Urinary fatty acid–binding protein as a new clinical marker of the progression of chronic renal disease

• Published in: The Journal of laboratory and clinical medicine 2004, Vol.143 (1), p.23-30
• Main Authors: Kamijo, Atsuko, Kimura, Kenjiro, Sugaya, Takeshi, Yamanouchi, Masaya, Hikawa, Akihisa, Hirano, Norihito, Hirata, Yasunobu, Goto, Atsuo, Omata, Masao
• Format: Article
• Language: English
• Subjects: Animals; Antibodies, Monoclonal - biosynthesis; Biological and medical sciences; Biomarkers - urine; Biopsy; Carrier Proteins - immunology; Carrier Proteins - urine; Creatinine - blood; Disease Progression; Enzyme-Linked Immunosorbent Assay; Fatty Acid-Binding Protein 7; Fatty Acid-Binding Proteins; Female; Follow-Up Studies; General aspects; Humans; Investigative techniques, diagnostic techniques (general aspects); Kidney Failure, Chronic - blood; Kidney Failure, Chronic - pathology; Kidney Failure, Chronic - urine; Liver - metabolism; Male; Medical sciences; Membrane Glycoproteins - urine; Mice; Mice, Inbred BALB C; Middle Aged; Neoplasm Proteins; Nephrology. Urinary tract diseases; Nerve Tissue Proteins; Proteinuria; Trypsin Inhibitor, Kunitz Soybean - urine; Tumor Suppressor Proteins; Urinary system involvement in other diseases. Miscellaneous; Urinary tract. Prostate gland
• ISSN: 0022-2143; 1532-6543
• DOI: 10.1016/j.lab.2003.08.001

Previous studies have indicated that in massive proteinuria, free fatty acids (FFAs) bound to albumin were overloaded in the proximal tubule and exacerbated tubulointerstitial damage. Liver-type fatty acid–binding protein (L-FABP) is an intracellular carrier protein of FFAs that is expressed in the proximal tubule of human kidney. We sought to evaluate urinary L-FABP as a clinical marker in chronic renal disease. Urinary L-FABP was measured in patients with nondiabetic chronic renal disease ( n = 120) with the use of a newly established ELISA method. We then monitored these patients for 15 to 51 months. Clinical data were analyzed with multivariate analysis. Urinary L-FABP was correlated with urinary protein, urinary α 1-microglobulin, and serum creatinine concentrations. Urinary L-FABP at the start of follow-up ( F = 17.1, r = .36, P < .0001) was selected as a significant clinical factor correlated with the progression rate, defined as a slope of a reciprocal of serum creatinine over time. We next selected the patients with mild renal dysfunction ( n = 35) from all 120 patients and divided them into 2 groups according to progression rate: the progression group ( n = 22) and the nonprogression group ( n = 13). Serum creatinine and urinary protein concentrations and blood pressure at the start of follow-up were higher in the progression group than in the nonprogression group, although we detected no significant difference between the 2 groups. Urinary L-FABP was significantly higher in the former group than in the latter ( P < .05). The results showed that urinary L-FABP reflected the clinical prognosis of chronic renal disease. Urinary L-FABP may be a clinical marker that can help predict the progression of chronic glomerular disease.