Angiotensin II receptor antagonist reduces urinary liver-type fatty acid-binding protein levels in patients with diabetic nephropathy and chronic renal failure

To the Editor: The incidence of end-stage renal failure due to diabetic nephropathy has increased dramatically over the past 20 years. It is widely accepted that the rate of functional decline correlates with the severity of renal tubulointerstitial lesions. Previous studies have shown that renal function in patients with type 2 diabetes correlates better with tubulointerstitial changes than with glomerular pathology [1]. Further studies on tubulointerstitial injury in patients with diabetic nephropathy may provide additional insight into the pathogenesis of diabetic nephropathy and lead to the identification of therapeutic targets. Several factors play an important role in the progression of renal injury. Oxidative stress is both a cause and consequence of interstitial inflammation [2]. Tissue hypoxia resulting from angiotensin-induced vasoconstriction or from structural disruption of peritubular capillaries is a final common pathway in the development of tubulointerstitial fibrosis. Liver-type fatty acid-binding protein (L-FABP) is produced in the proximal tubules, where it plays a key role in fatty acid metabolism. Stresses to the proximal tubules tend to overload fatty acids in the cytoplasm and thereby damage tubules with the release of inflammatory factors. In this way, tubulointerstitial inflammation is provoked, and renal function deteriorates over time. Urinary excretion of L-FABP increases with the deterioration of kidney function and is a useful clinical marker for monitoring chronic kidney disease [3]. We have reported that urinary L-FABP may be a useful clinical marker for type 2 diabetic nephropathy [4].