Abstract: FR-PO315

Urinary L-Type Fatty Acid-Binding Protein (L-FABP) Reflects the Progression of Autosomal Dominant Polycystic Kidney Disease

Session Information

Category: Genetic Diseases of the Kidney

  • 801 Cystic Kidney Diseases

Authors

  • Watanabe, Shiika, St. Marianna University School, Kawasaki, Kanagawa, Japan
  • Ikemori, Atsuko, St. Marianna University School, Kawasaki, Kanagawa, Japan
  • Sugaya, Takeshi, St. Marianna Univ, Tokyo, Japan
  • Ichikawa, Daisuke, St Marianna University of Medical School, Yokohama City, Kanagawa, Japan
  • Hisamichi, Mikako, St.Marianna university school of medicine, Kawasaki, Japan
  • Kimura, Kenjiro, Tokyo Takanawa Hospital, Tokyo, Japan
  • Shibagaki, Yugo, Division of Nephrology and Hypertension, St Marianna University Hospital, Kawasaki, Japan
Background


Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited progressive kidney disease. Although some imaging modalities, such as ultrasonography, CT or MRI, are useful for diagnosing and staging ADPKD, these modalities are not adequate for monitoring the severity of ADPKD because the modalities detect cyst formation, but not tubulointerstitial inflammation and fibrosis. The aim of this study is to elucidate that urinary L-type fatty acid binding protein (L-FABP) is associated with the severity of ADPKD.

Methods


Male PCK/CrljCrl-Pkhd1pck/Crl (PCK) rats (n=21), of which features are similar to human ADPKD, were used as the ADPKD model. Age and gender-matched Sprague-Dawley rats (n=21) were used as control. Serum, urine, kidneys were obtained at 8, 12 and 16 weeks of age. Serum creatinine, serum L-FABP, urinary L-FABP, urinary KIM-1, urinary NGAL and urinary creatinine were measured.

Results

Serum creatinine and serum L-FABP levels in PCK rats were similar to those in the control rats. Cystic enlargement and progression of both tubulointerstitial inflammation and fibrosis along with age were observed in the PCK rats. Urinary L-FABP levels increased along with the severity of renal pathology, and the levels at 12 and 16 weeks in the PCK rats were significantly higher than in the control rats. Although urinary KIM-1 and urinary NGAL levels at 8, 12 and 16 weeks in the PCK rats were significantly higher than in the control rats, these markers did not increase along with the progression of renal pathology including the degree of cystic enlargement in the PCK rats.

Conclusion


Urinary L-FABP reflects not only the degree of cystic enlargement, but also the progression of tubulointerstitial damage and, therefore, may be useful for monitoring the progression of ADPKD.