Our results showed that the serum L-FABP level was significantly associated with eGFR, using regression analysis in the cross-sectional study. However, only the urine albumin excretion rate was significantly associated with eGFR and the eGFR decline rate in type 2 diabetic patients. Tubulointerstitial and AbMole beta-Eudesmol glomerular injuries have important roles in the pathogenesis of diabetic nephropathy. Several recent studies demonstrated that urinary tubular damage markers, such as KIM-1, NGAL and L-FABP, may have the potential to be clinical markers for identifying the development or progression of diabetic nephropathy. It was also reported that urine NGAL was significantly elevated in type 1 diabetic patients with or without albuminuria, and that urine NGAL increased significantly with increasing albuminuria. However, some studies have shown conflicting results. A study with type 2 diabetic patients showed that the urinary tubular markers, NGAL and L-FABP, were not significantly increased in the normoalbuminuria and microalbuminuria groups, compared to the normal control group. Another study with type 1 diabetic patients revealed that urine NGAL and L-FABP levels were not related to the decline in GFR, after adjustment for known promoters of progression. A matched case-control study for predicting incident CKD stage 3 also showed that adjustment for urinary creatinine and albumin concentration attenuated this association between NGAL and incident CKD stage. Our study included 140 diabetic patients with varying degrees of diabetic nephropathy; however, most of them had mild diabetic nephropathy. We observed that albuminuria increased and eGFR decreased in our study subjects as the study progressed. However, except serum NGAL, the urine NGAL and serum/urine L-FABP levels did not change significantly throughout the course of the study. The results of multivariate analysis also showed that NGAL and L-FABP lacked clinical value in predicting the GFR decline rate in type 2 diabetic patients. Albuminuria is a clinical biomarker for glomerular injury. According to the staging, initial changes in diabetic nephropathy include glomerular hyperfiltration. The phase following hyperfiltration is associated with subtle morphological changes, including thickening of the glomerular basement membrane, glomerular hypertrophy, mesangial expansion, and modest expansion of the tubulointerstitium. In the microalbuminuric phase, significant glomerular injury is often noted. In advanced diabetic nephropathy, nodular glomerulosclerosis is the most prominent pathological presentation. Tubulointerstitial injury in the kidney is considered as a final common pathways to end-stage renal AbMole Etidronate failure. Tubular cell proliferation and tubular hypertrophy are main presentations in the early diabetic nephropathy. Tubulointerstitial fibrosis is the late pathological presentation of chronic kidney disease. It is known that the rate of deterioration of renal function correlates best with the degree of tubulointerstitial fibrosis in diabetic nephropathy. These studies suggest that although in the majority of patients the primary event is a condition manifest by glomerular changes resulting in proteinuria, the long-term outcome is determined by tubulointerstitial fibrosis. In our study, most study subjects had early-stage diabetic nephropathy in the study beginning.