Clinical Significance of Urinary Liver- Type Fatty Acid–Binding Protein in Patients With Diabetic Nephropathy KUMI SUZUKI, MD1,2

Tubulointerstitial damage plays a cru-cial role in the progression of kidneydiseases, including diabetic ne-phropathy (1). Among several distinct types of fatty acid – binding protein (FABP), liver-type FABP (L-FABP) is abundantly expressed in hepatocytes and constitutively expressed in proximal tu-bular cells of the kidney (2). L-FABP in-corporates albumin-bound free fatty acids (FFAs) that are filtered through the glo-meruli into proximal tubular cells and transports FFAs from the cytosol to the nucleus (3). In transgenic mice express-ing human L-FAPB, protein overload, re-su l t ing in mass i ve pro t e inur i a, upregulated renal L-FABP expression and increased its urinary excretion (4), sug-gesting that urinary L-FABP may reflect tubulointerstitial damage. Recently, in patients with nondiabetic glomerular dis-ease, urinary excretion of L-FABP in-creased in parallel with the severity of tubulointerstitial injury and correlated with proteinuria and the rate of progres-sion of renal disease, suggesting that L-FABP may be a useful indicator for the progression of nondiabetic kidney disease (4,5). To determine the clinical signifi-cance of L-FABP in patients with diabetic nephropathy, we conducted a cross-sectional study comparing urinary L-FABP excretion in diabetic patients with serial stages of kidney disease